pituitrin and Hyponatremia

Hyponatremia, especially if acute and severe, can be a life-threatening condition. Several conditions can trigger hyponatremia. In this review, we will discuss two conditions that can determine euvolemic hyponatremia: the cerebral/renal salt wasting (CRSW) syndrome and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), including the two subtypes: reset osmostat (RO) and nephrogenic syndrome of inappropriate antidiuresis (NSIAD) and their differential diagnoses. Despite the passage of over 70 years since its first description, to date, the true etiopathogenesis of CRSW syndrome, a rare cause of hypovolemic/euvolemic hyponatremia, is almost unknown. SIADH, including RO and NSIAD, is sometimes difficult to differentiate from CRSW syndrome; in its differential diagnosis, the clinical approach based on the evaluation of the extracellular volume (ECV) was proven insufficient. We therefore suggest a simple diagnostic algorithm based on the assessment of the degree of hyponatremia, urinary osmolality, and the assessment of the fraction of urate excretion (FEUa) in conditions of hyponatremia and after serum sodium correction, to be applied in children over 1 year of life.

Topics: Algorithms; Child; Diagnosis, Differential; Genetic Diseases, X-Linked; Humans; Hyponatremia; Inappropriate ADH Syndrome; Sodium; Uric Acid; Vasopressins

Hyponatremia is a water-electrolyte balance disorder diagnosed in about 30% of patients after subarachnoid hemorrhage (SAH). The main factors responsible for hyponatremia in these patients are increased plasma concentrations of either vasopressin (leading to water retention and dilutional hyponatremia) or natriuretic peptides (leading to plasma sodium ions deficiency). Data demonstrates that the leading causes of post-SAH disability - delayed cerebrovascular spasm (CVS) and delayed cerebral ischemia (DCI) - are more often diagnosed in patients who develop hyponatremia than in normonatremic patients with SAH. Data also indicates that reducing sodium ion concentration in the blood/perfusate affects the tone and regulation of cerebral blood vessels in a manner that depends on the vessel's location in a vascular tree (intraparenchymal arterioles vs. large vessels on the brain surface) and environmental conditions. In the present article, we review possible mechanisms underlying the effects of hyponatremia on cerebral blood vessels and discuss the potential role of hyponatremia in the development of large vessels and microvascular spasm, taking into consideration the presence of vasopressin and natriuretic peptides.

Topics: Brain Ischemia; Humans; Hyponatremia; Natriuretic Peptides; Risk Factors; Sodium; Spasm; Subarachnoid Hemorrhage; Vasopressins; Vasospasm, Intracranial

Hyponatremia is the most frequent electrolytic disorder in hospitalized patients, and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), the most frequent cause of hiponatremia with clinically normal extracellular volume. It consists of a disorder of the regulation of body water that obeys to different causes, mainly cancer, pulmonary illnesses, disorders of the central nervous system and diverse drugs. As in any hiponatremia it a physiological knowledge of the regulation of body water and sodium is essential as well as the application of precise diagnostic criteria in order to manage the problem with an effective treatment. The available data until the moment show that the clinical diagnosis of SIADH made by professionals is mainly not supported on the established criteria drawn by experts and this lack of accuracy probably hits in the therapeutic result. The basis of the treatment of the SIADH is to correct its cause, water restriction, solutes (sodium chloride) and the use of vaptans in case of failure of the previous measures.

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Sodium; Sodium Chloride; Vasopressins

Linezolid is a synthetic oxazolidinone antimicrobial drug with a broad spectrum and a unique mechanism of inhibiting resistant pathogenic strains, and it was approved by the Food and Drug Administration (FDA) in April 2000. Several different systemic side effects were reported after the use of this medication. In this article, we report a case in which a syndrome of inappropriate antidiuretic hormone (SIADH) was developed after linezolid treatment was started.. We present the case of a 79-year-old woman who developed severe hyponatremia during linezolid treatment (0.6 g i.v. q12 h) after undergoing hemiarthroplasty for left femoral neck fracture. The patient's baseline serum sodium upon admission (138 mmol/L) decreased to 118 mmol/L, urine sodium was 102 mmol/L, plasma osmolality was 248 mOsm/kg and urine osmolarity was 310 mOsm/kg at day 4, thus a diagnosis of SIADH was made. The patient was not taking any other medication known to cause SIADH, and she did not present a comorbidity that could explain her condition. Her serum sodium increased to 135 and 137 mmol/L, respectively, 11 and 12 days after cessation of linezolid, strongly suggesting that SIADH was the cause in this case.. This is the fourth case of linezolid-induced SIADH. A thorough workup was essential for the diagnosis to correctly differentiate between SIADH and other causes of hyponatremia, which helped us properly conducting follow-up treatments. SIADH is a rare but serious side effect of linezolid, and practicing physicians should be aware of this complication. It is necessary to periodically monitor the serum sodium.

Topics: Aged; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Linezolid; Sodium; Vasopressins

The treatment of central diabetes insipidus has not changed significantly in recent decades, and dDAVP and replacement of free water deficit remain the cornerstones of treatment. Oral dDAVP has replaced nasal dDAVP as a more reliable mode of treatment for chronic central diabetes insipidus. Hyponatraemia is a common side effect, occurring in one in four patients, and should be avoided by allowing a regular break from dDAVP to allow a resultant aquaresis. Hypernatraemia is less common, and typically occurs during hospitalization, when access to water is restricted, and in cases of adipsic DI. Management of adipsic DI can be challenging, and requires initial inpatient assessment to establish dose of dDAVP, daily fluid prescription, and eunatraemic weight which can guide day-to-day fluid targets in the long-term.

Topics: Body Weight; Deamino Arginine Vasopressin; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Humans; Hypernatremia; Hyponatremia; Neurophysins; Protein Precursors; Vasopressins

Synthetic phenethylamines are widely abused drugs, comprising new psychoactive substances such as synthetic cathinones, but also well-known amphetamines such as methamphetamine and 3,4-methylenedioxymethamphetamine (MDMA, ecstasy). Cathinones and amphetamines share many toxicodynamic mechanisms. One of their potentially life-threatening consequences, particularly of MDMA, is serotonin-mediated hyponatraemia. Herein, we review the state of the art on phenethylamine-induced hyponatremia; discuss the mechanisms involved; and present the preventive and therapeutic measures. Hyponatraemia mediated by phenethylamines results from increased secretion of antidiuretic hormone (ADH) and consequent kidney water reabsorption, additionally involving diaphoresis and polydipsia. Data for MDMA suggest that acute hyponatraemia elicited by cathinones may also be a consequence of metabolic activation. The literature often reveals hyponatraemia-associated complications such as cerebral oedema, cerebellar tonsillar herniation and coma that may evolve to a fatal outcome, particularly in women. Ready availability of fluids and the recommendation to drink copiously at the rave scene to counteract hyperthermia, often precipitate water intoxication. Users should be advised about the importance of controlling fluid intake while using phenethylamines. At early signs of adverse effects, medical assistance should be promptly sought. Severe hyponatraemia (<130 mmol sodium/L plasma) may be corrected with hypertonic saline or suppression of fluid intake. Also, clinicians should be made aware of the hyponatraemic potential of these drugs and encouraged to report future cases of toxicity to increase knowledge on this potentially lethal outcome.

Topics: Alcohol Drinking; Alkaloids; Amphetamine; Drinking; Humans; Hyponatremia; Illicit Drugs; N-Methyl-3,4-methylenedioxyamphetamine; Neurophysins; Phenethylamines; Protein Precursors; Vasopressins

Hyponatremia is frequently seen in patients with ascites secondary to advanced cirrhosis and portal hypertension. Although not apparent in the early stages of cirrhosis, the progression of cirrhosis and portal hypertension leads to splanchnic vasodilation, and this leads to the activation of compensatory mechanisms such as renin-angiotensin-aldosterone system (RAAS), sympathetic nervous system, and antidiuretic hormone (ADH) to ameliorate low circulatory volume. The net effect is the avid retention of sodium and water to compensate for the low effective circulatory volume, resulting in the development of ascites. These compensatory mechanisms lead to impairment of the kidneys to eliminate solute-free water in decompensated cirrhosis. Nonosmotic secretion of antidiuretic hormone (ADH), also known as arginine vasopressin, further worsens excess water retention and thereby hyponatremia. The management of hyponatremia in this setting is a challenge as conventional therapies for hyponatremia including fluid restriction and correction of hypokalemia are frequently inefficacious. In this review, we discuss the pathophysiology, complications, and various treatment modalities, including albumin infusion, selective vasopressin receptor antagonists, or hypertonic saline for patients with severe hyponatremia and those awaiting liver transplantation.

Topics: Acute Kidney Injury; Acute-On-Chronic Liver Failure; Albumins; Antidiuretic Hormone Receptor Antagonists; Ascites; Fluid Therapy; Hepatic Encephalopathy; Hepatorenal Syndrome; Humans; Hypertension, Portal; Hyponatremia; Liver Cirrhosis; Liver Transplantation; Renin-Angiotensin System; Saline Solution, Hypertonic; Splanchnic Circulation; Tolvaptan; Vasodilation; Vasopressins

Hyponatremia is a frequent complication in patients with advanced cirrhosis. Patients with cirrhosis can develop two types of hyponatremia, hypovolemic or hypervolemic (dilutional) hyponatremia. Hypervolemic hyponatremia is the most common type and it develops as a consequence of an impairment in the renal capacity to eliminate solute-free water. The key mechanism leading to solute-free water retention is a non-osmotic hypersecretion of vasopressin (AVP), secondary to a reduction in effective arterial blood pressure existing in patients with advanced cirrhosis. Hypervolemic hyponatremia is associated with increased morbidity and mortality in patients with cirrhosis, and it has also been associated with increased complications after liver transplantation. Currently, the management of hypervolemic hyponatremia in cirrhosis is based on fluid restriction. Vaptans, oral selective vasopressin V2-receptor antagonists, and particularly tolvaptan, have been investigated as a pharmacological approach for the management of hypervolemic hyponatremia in cirrhosis. However, existing information on its efficacy in cirrhosis is still scarce and a recent warning has been raised about their potential role on inducing liver injury at high doses.

Topics: Antidiuretic Hormone Receptor Antagonists; Humans; Hyponatremia; Liver Cirrhosis; Vasopressins

In the evolutionary process, the successful adaptation of living organisms initially to an aqueous and thereafter to an arid terrestrial environment posed radically different challenges to the maintenance of water balance. Whereas the former required defense against water excess, the latter called for water conservation. To meet such challenges, the mammalian nephron evolved mechanisms for increasing both water excretion by diluting and water conservation by concentrating the urine. This chapter reviews the process whereby the osmosensors control thirst and the secretion of the antidiuretic hormone (vasopressin) to allow for either urinary dilution or concentration and thereby delicately maintain tonicity of body fluids within a very narrow range. Central to this process is the now well-defined cellular pathway whereby vasopressin renders the collecting duct, water permeable. Disorders of vasopressin secretion and action result in disturbances of body fluids tonicity, which are clinically recognized as abnormalities in reduced plasma sodium concentration or hyponatremia.

Topics: Animals; Body Water; Homeostasis; Humans; Hyponatremia; Thirst; Urine; Vasopressins

Nephrogenic syndrome of inappropriate antidiuresis (NSIAD), first described in 2005, is a rare genetic X-linked disease, presenting with hyponatremia, hyposmolarity, euvolemia, inappropriately concentrated urine, increased natriuresis, and undetectable or very low arginine-vasopressine (AVP) circulating levels. It can occur in neonates, infants, or later in life. NSIAD must be early recognized and treated to prevent severe hyponatremia, which can show a dangerous impact on neonatal outcome. In fact, it potentially leads to death or, in case of survival, neurologic sequelae. This review is an update of NSIAD 12 years after the first description, focusing on reported cases of neonatal and infantile onset. The different molecular patterns affecting the AVP receptor 2 (V2R) and determining its gain of function are reported in detail; moreover, we also provide a comparison between the different triggers involved in the development of hyponatremia, the evolution of the symptoms, and modality and efficacy of the different treatments available.

Topics: Age of Onset; Antidiuretic Hormone Receptor Antagonists; Clinical Trials as Topic; Diuretics, Osmotic; Drinking; Gain of Function Mutation; Genetic Diseases, X-Linked; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Infant, Newborn; Mutation, Missense; Receptors, Vasopressin; Renal Reabsorption; Signal Transduction; Sodium; Treatment Outcome; Urea; Vasopressins

ADH is a hormone secreted by neurohypophysis that plays different roles based on the target organ. At the renal level, this peptide is capable of causing electrolyte-free water absorption, thus playing a key role in the hydro-electrolytic balance. There are pathologies and disorders that jeopardize this balance and, in this field, ADH receptor inhibitors such as Vaptans could play a key role. By inhibiting the activation pathway of vasopressin, they are potentially useful in euvolemic and hypervolemic hypotonic hyponatremia. However, clinical trials in heart failure have not given favourable results on clinical outcomes. Even in SIADH, despite their wide use, there is no agreement by experts on their use. Since vaptans inhibit the cAMP pathway in tubular cells, their use has been proposed to inhibit cystogenesis. A clinical trial has shown favourable effects on ADPKD progression. Because vaptans have been shown to be effective in models of renal cysts disorders other than ADPKD, their use has been proposed in diseases such as nephronophthisis and recessive autosomal polycystic disease. Other possible uses of vaptans could be in kidney transplantation and cardiorenal syndrome. Due to the activity of ADH in coagulation and haemostasis, ADH's activation pathway by Desmopressin Acetate could be a useful strategy to reduce the risk of bleeding in biopsies in patients with haemorrhagic risk.

Topics: Antidiuretic Hormone Receptor Antagonists; Cadaver; Cyclic AMP; Forecasting; Humans; Hyponatremia; Kidney Diseases; Kidney Diseases, Cystic; Kidney Transplantation; Kidney Tubules, Collecting; Molecular Targeted Therapy; Neurophysins; Polycystic Kidney, Autosomal Dominant; Protein Precursors; Receptors, Vasopressin; Second Messenger Systems; Tissue Donors; Vasopressins; Water-Electrolyte Imbalance

Despite the introduction of multiple new pharmacological agents over the past three decades in the field of heart failure (HF), overall prognosis remains poor. Hyponatremia is prevalent in HF patients and has been suggested as a contributor to poor response to standard therapy. Elevated levels of arginine vasopressin (AVP), a peptide hormone produced in the hypothalamus, play a role in development of hyponatremia, and AVP and its surrogate, copeptin, are related to changes in osmolality, hemodynamics, neuro-hormones as well as in overall outcome in HF patients. Of current pharmacological interest are the selective and non-selective vasopressin receptor antagonists (VRAs), which inhibit vasoconstriction and cardiac remodeling mediated by the V

Topics: Antidiuretic Hormone Receptor Antagonists; Arginine Vasopressin; Benzazepines; Glycopeptides; Heart Failure; Hemodynamics; Humans; Hyponatremia; Receptors, Vasopressin; Tolvaptan; Vasopressins

Chronic kidney disease (CKD) imposes a significant global health burden. In the United States, one in three adults are at risk for CKD currently affecting over 28 million Americans. While several studies have demonstrated the benefit of treating traditional risk factors in CKD, including hypertension with pharmacologic agents such as blockade of the renin-angiotensin system (RAAS), there is scarce data on the advantages of sodium and fluid management in this population. Both experimental and observational studies have shown improvement in hypertension and cardiovascular outcomes with sodium restriction to ≤2.3 grams per day, however, to date there are very few randomized controlled trials demonstrating a benefit in sodium reduction for the prevention or progression of CKD. Similarly, studies on increasing fluid consumption have shown to be advantageous in polycystic kidney disease as well as chronic nephrolithiasis, yet no randomized controlled trials exist on the fluid management in patients with kidney disease. This review aims to explore the evidence of sodium restriction and fluid management in the CKD population as well as underlying mechanisms and clinical barriers of sodium and water management as conservative therapy.

Topics: Angiotensin-Converting Enzyme Inhibitors; Cardiovascular Diseases; Conservative Treatment; Disease Progression; Fluid Therapy; Humans; Hypertension; Hypertrophy, Left Ventricular; Hyponatremia; Polycystic Kidney Diseases; Renal Insufficiency, Chronic; Renin-Angiotensin System; Risk Factors; Sodium Chloride; United States; Vasopressins

Hyponatremia is a common water balance disorder that often poses a diagnostic or therapeutic challenge. Therefore, guidelines were developed by professional organizations, one from within the United States (2013) and one from within Europe (2014). This review discusses the diagnosis and treatment of hyponatremia, comparing the two guidelines and highlighting recent developments. Diagnostically, the initial step is to differentiate hypotonic from nonhypotonic hyponatremia. Hypotonic hyponatremia is further differentiated on the basis of urine osmolality, urine sodium level, and volume status. Recently identified parameters, including fractional uric acid excretion and plasma copeptin concentration, may further improve the diagnostic approach. The treatment for hyponatremia is chosen on the basis of duration and symptoms. For acute or severely symptomatic hyponatremia, both guidelines adopted the approach of giving a bolus of hypertonic saline. Although fluid restriction remains the first-line treatment for most forms of chronic hyponatremia, therapy to increase renal free water excretion is often necessary. Vasopressin receptor antagonists, urea, and loop diuretics serve this purpose, but received different recommendations in the two guidelines. Such discrepancies may relate to different interpretations of the limited evidence or differences in guideline methodology. Nevertheless, the development of guidelines has been important in advancing this evolving field.

Topics: Acute Disease; Algorithms; Chronic Disease; Diagnosis, Differential; Glycopeptides; Humans; Hyponatremia; Practice Guidelines as Topic; Vasopressins

Copeptin and arginine vasopressin (AVP) are derived from a common precursor molecule and have equimolar secretion and response to osmotic, haemodynamic and stress-related stimuli. Plasma concentrations of copeptin and AVP in relation to serum osmolality are highly correlated. The physiological functions of AVP with respect to homeostasis of fluid balance, vascular tonus and regulation of the endocrine stress response are well known, but the exact function of copeptin is undetermined. Quantification of AVP can be difficult, but copeptin is stable in plasma and can be easily measured with a sandwich immunoassay. For this reason, copeptin has emerged as a promising marker for the diagnosis of AVP-dependent fluid disorders. Copeptin measurements can enable differentiation between various conditions within the polyuria-polydipsia syndrome. In the absence of prior fluid deprivation, baseline copeptin levels >20 pmol/l identify patients with nephrogenic diabetes insipidus. Conversely, copeptin levels measured upon osmotic stimulation differentiate primary polydipsia from partial central diabetes insipidus. In patients with hyponatraemia, low levels of copeptin together with low urine osmolality identify patients with primary polydipsia, and the ratio of copeptin to urinary sodium can distinguish the syndrome of inappropriate antidiuretic hormone secretion from other AVP-dependent forms of hyponatraemia.

Topics: Animals; Body Fluids; Glycopeptides; Homeostasis; Humans; Hyponatremia; Polydipsia; Polyuria; Vasopressins

Hyponatremia is the most frequent electrolyte abnormality seen postoperatively in pediatric patients receiving maintenance fluid therapy. Hyponatremia is also common in acute pediatric illness. The main factors contributing to hyponatremia in these conditions are increased secretion of antidiuretic hormone (ADH) and routine use of sodium hypotonic fluids. An increased ADH secretion results in an impaired ability to excrete free water. If the sodium concentration falls to less than 125 mmol/L hyponatremic encephalopathy might develop, resulting in cerebral edema. This is avoided if hypotonic maintenance fluids are not used perioperatively or for rehydration or maintenance during acute critical illness in children.

Topics: Acute Disease; Child; Critical Illness; Fluid Therapy; Humans; Hyponatremia; Perioperative Care; Postoperative Complications; Practice Guidelines as Topic; Vasopressins

Hyponatraemia is the most common electrolyte abnormality encountered by physicians in the hospital setting. It is associated with increased mortality and length of hospital stay. However, the basis of the relationship of hyponatraemia with clinical outcome is not clear. Doubt remains as to whether the relationship is causal. It may reflect the association of two independent variables both of which are linked with disease severity. Serum sodium concentration is regulated through integrated neuro-humeral mechanisms that overlap with those regulating circulating volume. A mechanistic approach to the classification of hyponatraemia can support a framework for investigation and differential diagnosis based on urine osmolality and urine sodium concentration. Such a framework is more reliable than those based on the clinical assessment of volume status. In the emergency setting, the initial management of hyponatraemia is cause-independent. In other clinical contexts, a cause-specific approach is recommended. Over-rapid correction of serum sodium risks precipitating osmotic demyelination syndrome. Avoiding over-rapid correction is critical in any approach to patient care. Sodium is the major circulating cation and thus a key determinant of overall plasma osmolality. Serum sodium concentration is maintained within a tight physiological range over time, despite wide variation in both sodium and water intake. Hyponatraemia (serum sodium concentration <135 mmols/L) is the most common electrolyte disturbance in clinical practice. All clinicians should be aware of the scope and scale of the problem.

Topics: Aquaporins; Humans; Hyponatremia; Vasopressins

Vasopressin has gained wide support as an adjunct vasopressor in patients with septic shock. This agent exerts its vasoconstriction effects through smooth muscle V1 receptors and also has antidiuretic activity via renal V2 receptors. This interaction with the renal V2 receptors results in the integration of aquaporin 2 channels in the apical membrane of the renal collecting duct leading to free water reabsorption. Thus, water intoxication with subsequent hyponatremia, although rare, is a potentially serious side effect of exogenous vasopressin administration. We present 2 patients who developed hyponatremia within hours of initiation of vasopressin infusion. Extensive diuresis followed its discontinuation with subsequent normalization of serum sodium. One of the patients required the use of hypertonic saline for more rapid normalization of serum sodium due to concerns for potential seizure activity. A review of the literature relevant to the incidence of vasopressin-induced hyponatremia is provided as well as discussion on additional factors relevant to septic shock that should be considered when determining the relative risk of hyponatremia in patients receiving vasopressin.

Topics: Adrenal Cortex Hormones; Diuresis; Female; Humans; Hyponatremia; Male; Receptors, Vasopressin; Shock, Septic; Sodium; Vasoconstrictor Agents; Vasopressins; Water Intoxication; Young Adult

Alterations in water homeostasis can disturb cell size and function. Although most cells can internally regulate cell volume in response to osmolar stress, neurons are particularly at risk given a combination of complex cell function and space restriction within the calvarium. Thus, regulating water balance is fundamental to survival. Through specialized neuronal "osmoreceptors" that sense changes in plasma osmolality, vasopressin release and thirst are titrated in order to achieve water balance. Fine-tuning of water absorption occurs along the collecting duct, and depends on unique structural modifications of renal tubular epithelium that confer a wide range of water permeability. In this article, we review the mechanisms that ensure water homeostasis as well as the fundamentals of disorders of water balance.

Topics: Brain; Cell Size; Diabetes Insipidus; Homeostasis; Humans; Hyponatremia; Kidney Medulla; Kidney Tubules, Collecting; Osmotic Pressure; Sensory Receptor Cells; Thirst; Vasopressins; Water; Water-Electrolyte Balance

Hyponatraemia is the most common electrolyte disbalance in clinical practice, which is associated with increased patients morbidity and mortality. At present the pathophysiology of hyponatraemia is explored in more details, antidiuretic hormone and osmoregulation play the major roles. This article informs about relatively new classification of hyponatraemia for clinical practice based on the severity of clinical symptoms and based on the effective serum osmolality. It also offers diagnostic and treatment guidelines of hyponatraemia, which are based on current recommendations of the world experts and on the evidence based medicine.

Topics: Antidiuretic Agents; Humans; Hyponatremia; Vasopressins

Topics: Antidiuretic Hormone Receptor Antagonists; History, 19th Century; History, 20th Century; History, 21st Century; Humans; Hyponatremia; Practice Guidelines as Topic; Sodium; Vasopressins

Cirrhosis is characterized by systemic and splanchnic vasodilation that leads to excessive nonosmotic secretion of vasopressin (antidiuretic hormone). Hyponatremia is a common electrolyte abnormality in advanced liver disease that results from the impaired ability of the kidney to excrete solute-free water that leads to "dilutional" hyponatremia-water retention disproportionate to the retention of sodium. Hyponatremia in liver diseases carries the prognostic burden, correlates with the severity of cirrhosis, and, in recent studies, has also been implicated in the pathogenesis of hepatic encephalopathy. The current treatment options are limited to conventional therapies like fluid restriction, and the outcomes are unsatisfactory. Although currently available vasopressin (V2 receptors) antagonists have been shown to increase serum sodium concentrations and improve ascites control, their role in the treatment of hyponatremia in liver disease patients remains questionable because of adverse effect profiles, high cost, and poor data on long-term mortality benefits. More information is needed to argue the benefits vs risks of short-term use of vaptans for correction of hyponatremia especially just hours-to-days before liver transplant.

Topics: Drug Therapy, Combination; Female; Humans; Hyponatremia; Liver Cirrhosis; Male; Prognosis; Risk Assessment; Severity of Illness Index; Survival Rate; Treatment Outcome; Vasopressins

Acute kidney injury (AKI) is frequent in patients with cirrhosis. AKI and hyponatraemia are major determinants of the poor prognosis in advanced cirrhosis. The hepatorenal syndrome (HRS) denotes a functional and potential reversible impairment of renal function. Type 1 HRS, a special type of AKI, is a rapidly progressive AKI, whereas the renal function in type 2 HRS decreases more slowly. HRS is precipitated by factors such as sepsis that aggravate the effective hypovolaemia in decompensated cirrhosis, by lowering arterial pressure and cardiac output and enhanced sympathetic nervous activity. Therefore, attempts to prevent and treat HRS should seek to improve liver function and to ameliorate arterial hypotension, central hypovolaemia and cardiac output, and to reduce renal vasoconstriction. Ample treatment of HRS is important to prevent further progression and death, but as medical treatment only modestly improves long-term survival, these patients should always be considered for liver transplantation. Hyponatraemia, defined as serum sodium <130 mmol/L, is common in patients with decompensated cirrhosis. From a pathophysiological point of view, hyponatraemia is related to an impairment of renal solute-free water excretion most likely caused by an increased vasopressin secretion. Patients with cirrhosis mainly develop hypervolaemic hyponatraemia. Current evidence does not support routine use of vaptans in the management of hyponatraemia in cirrhosis.

Topics: Cardiomyopathies; Creatinine; Glomerular Filtration Rate; Hepatorenal Syndrome; Humans; Hyponatremia; Liver Cirrhosis; Vasopressins

Hyponatremia is a known complication in patients with heart failure (HF). HF patients with severe congestion, hyponatremia, and renal insufficiency are difficult to manage and may have worse outcomes. A main cause of hyponatremia is inappropriately elevated level of plasma arginine vasopressin (AVP), which causes water retention at the collecting duct. AVP antagonists have thus been developed to increase aquaresis and serum sodium levels in patients with euvolemic and hypervolemic hyponatremia. Although tolvaptan, an AVP-2 receptor antagonist, did not show outcomes benefit in patients with decompensated HF, prospective studies are ongoing to evaluate its optimal role in targeted HF patients.

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Clinical Trials as Topic; Heart Failure; Humans; Hyponatremia; Prospective Studies; Tolvaptan; Vasopressins

Rapid correction of severe hyponatremia carries the risk of osmotic demyelination. Two recently introduced methods of correction of hyponatremia have diametrically opposite effects on aquaresis. Inhibitors of vasopressin V2 receptor (vaptans) lead to the production of dilute urine, whereas infusion of desmopressin causes urinary concentration. Identification of the category of hyponatremia that will benefit from one or the other treatment is critical. In general, vaptans are effective in hyponatremias presenting with concentrated urine and, with the exception of hypovolemic hyponatremia, can be used as their primary treatment. Desmopressin is effective in hyponatremias presenting with dilute urine or developing urinary dilution after saline infusion. In this setting, desmopressin infusion helps prevent overcorrection of the hyponatremia. Monitoring of the changes in serum sodium concentration as a guide to treatment changes is imperative regardless of the initial treatment of severe hyponatremia.

Topics: Animals; Deamino Arginine Vasopressin; Disease Management; Humans; Hyponatremia; Infusions, Intravenous; Saline Solution, Hypertonic; Severity of Illness Index; Vasopressins

Dysnatremia is among the most common electrolyte disorders in clinical medicine and its improper management can have serious consequences associated with increased morbidity and mortality of patients. The aim of this study is to update the pathophysiology of dysnatremia and review some simple clinical and laboratory tools, easy to interpret, that allow us to make a quick and simple approach. Dysnatremia involves water balance disorders. Water balance is directly related to osmoregulation. There are mechanisms to maintain plasma osmolality control; which are triggered by 1-2% changes. Hypothalamic osmoreceptors detect changes in plasma osmolality, regulating the secretion of Antidiuretic Hormone (ADH), which travels to the kidneys resulting in more water being reabsorbed into the blood; therefore, the kidney is the main regulator of water balance. When a patient is suffering dysnatremia, it is important to assess how his ADH-renal axis is working. There are causes of this condition easy to identify, however, to differentiate a syndrome of inappropriate ADH secretion from cerebral salt-wasting syndrome is often more difficult. In the case of hypernatremia, to suspect insipidus diabetes and to differentiate its either central or nephrogenic origin is essential for its management. In conclusion, dysnatremia management requires pathophysiologic knowledge of its development in order to make an accurate diagnosis and appropriate treatment, avoiding errors that may endanger the health of our patients.

Topics: Child; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins; Water-Electrolyte Imbalance

Excessive secretion of vasopressin in the course of Syndrome of Inappropriate Antidiuretic Hormone Secretion is a common cause of hyponatremia in cancer patients. Clinical symptoms depend on the cause, rate of change of sodium level and their absolute values. Treatment options include fluid restrictions, intravenous administration of hypertonic sodium chloride solutions, loop diuretics and vaptans. The sodium level should not be adjusted too fast, because it may lead to irreversible brain damage. The article presents pathophysiology, diagnostics and recommendations of management of this oncological emergency.

Topics: Emergencies; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infusions, Intravenous; Neoplasms; Saline Solution, Hypertonic; Vasopressins

Disturbances in sodium concentration are common in the critically ill patient and associated with increased mortality. The key principle in treatment and prevention is that plasma [Na+] (P-[Na+]) is determined by external water and cation balances. P-[Na+] determines plasma tonicity. An important exception is hyperglycaemia, where P-[Na+] may be reduced despite plasma hypertonicity. The patient is first treated to secure airway, breathing and circulation to diminish secondary organ damage. Symptoms are critical when handling a patient with hyponatraemia. Severe symptoms are treated with 2 ml/kg 3% NaCl bolus infusions irrespective of the supposed duration of hyponatraemia. The goal is to reduce cerebral symptoms. The bolus therapy ensures an immediate and controllable rise in P-[Na+]. A maximum of three boluses are given (increases P-[Na+] about 6 mmol/l). In all patients with hyponatraemia, correction above 10 mmol/l/day must be avoided to reduce the risk of osmotic demyelination. Practical measures for handling a rapid rise in P-[Na+] are discussed. The risk of overcorrection is associated with the mechanisms that cause hyponatraemia. Traditional classifications according to volume status are notoriously difficult to handle in clinical practice. Moreover, multiple combined mechanisms are common. More than one mechanism must therefore be considered for safe and lasting correction. Hypernatraemia is less common than hyponatraemia, but implies that the patient is more ill and has a worse prognosis. A practical approach includes treatment of the underlying diseases and restoration of the distorted water and salt balances. Multiple combined mechanisms are common and must be searched for. Importantly, hypernatraemia is not only a matter of water deficit, and treatment of the critically ill patient with an accumulated fluid balance of 20 litres and corresponding weight gain should not comprise more water, but measures to invoke a negative cation balance. Reduction of hypernatraemia/hypertonicity is critical, but should not exceed 12 mmol/l/day in order to reduce the risk of rebounding brain oedema.

Topics: Critical Illness; Decision Support Techniques; Diuresis; Diuretics; Humans; Hypernatremia; Hyponatremia; Hypothyroidism; Iatrogenic Disease; Inappropriate ADH Syndrome; Plasma Volume; Sodium Chloride Symporter Inhibitors; Vasopressins

Intravenous maintenance fluid therapy aims to replace daily urinary and insensible losses for ill children in whom adequate enteric administration of fluids is contraindicated or infeasible. The traditional determination of fluid volumes and composition dates back to Holliday and Segar's seminal article from 1957, which describes the relationship between weight, energy expenditure, and physiologic losses in healthy children. Combined with estimates of daily electrolyte requirements, this information supports the use of the hypotonic maintenance fluids that were widely used in pediatric medicine. However, using hypotonic intravenous fluids in a contemporary hospitalized patient who may have complex physiologic derangements, less caloric expenditure, decreased urinary output, and elevated antidiuretic hormone levels is often not optimal; evidence over the last 2 decades shows that it may lead to an increased incidence of hyponatremia. In this review, we present the evidence for using isotonic rather than hypotonic fluids as intravenous maintenance fluid.

Topics: Body Water; Child; Critical Care; Critical Illness; Disease Management; Diuresis; Elective Surgical Procedures; Electrolytes; Energy Metabolism; Fluid Therapy; Humans; Hyponatremia; Hypotonic Solutions; Infusions, Intravenous; Isotonic Solutions; Postoperative Care; Randomized Controlled Trials as Topic; Vasopressins; Water-Electrolyte Imbalance

Hyponatremia is the most common electrolyte disorder in the hospital setting and is defined as a serum sodium concentration less than 135 mmol/l. Most patients have mild hyponatremia (plasma sodium concentration 130-134 mmol/l) and few if any symptoms. Serum sodium concentrations between 120 and 129 mmol/l can be associated with lack of concentration, nausea, forgetfulness, apathy and loss of balance. Severe hyponatremia (<120 mmol/l) can cause coma or grand mal seizure. If hyponatremia occurs acutely (duration <48 h) it will cause more severe symptoms than are observed in chronic hyponatremia (>48 h). It is important to distinguish between different types of hyponatremia: euvolemic hyponatremia causing syndrome of inappropriate antidiuretic hormone secretion(SIADH) also known as Schwartz-Bartter syndrome, hypervolemic hyponatremia (cardiac failure and liver cirrhosis) and hypovolemic hyponatremia (diarrhoea, vomiting or other gastrointestinal fluid losses). Increased levels of ADH and continued fluid intake are the pathogenetic causes of all three types of hyponatremia; nonetheless, infusion of isotonic fluid is the therapy of choice for hypovolemic hyponatremia. In contrast, fluid restriction, lithium carbonate, urea, loop diuretics or demeclocycline have been used as therapeutic options to correct hyponatremia in euvolemic or hypervolemic hyponatremia but most of these therapies have proven to be cumbersome and inefficient. Recently a new class of pharmacological agents has become available, the vaptans, orally taken vasopressin antagonists. Clinical trials showed them to provide effective, specific and safe therapy of hyponatremia. In Europe tolvaptan, the only such agent on the market is now approved for the treatment of euvolemic hyponatremia.

Topics: Critical Care; Diagnosis, Differential; Emergency Service, Hospital; Humans; Hyponatremia; Inappropriate ADH Syndrome; Sodium Chloride; Vasopressins

Hyponatremia is the most common electrolyte disorder in hospitalized patients. According to the Edelman equation, hyponatremia usually develops due to a gain of free water, a loss of serum sodium or a combination of both. Investigating the causes of hyponatremia and consequent correction of the electrolyte disorder can be challenging. In this review we give an overview on the mechanisms leading to hyponatremia and in a further step, the correction of hyponatremia is discussed in detail with sections on: rate of correction, treatment with respect to volume state, risks of correction and a discussion of vasopressin receptor antagonists.

Topics: Antidiuretic Hormone Receptor Antagonists; Body Water; Disease Management; Humans; Hyponatremia; Kidney; Sodium; Vasopressins

The syndrome of inappropriate antidiuresis (SIAD; formerly the syndrome of inappropriate secretion of antidiuretic hormone) is the most frequent cause of hyponatremia. A strong association exists between mortality and hyponatremia, which reflects the severity of the underlying disease. In SIAD, hyponatremia is associated with normovolaemia but the assessment of extracellular volume can be difficult. Clinical features are mainly neurological and can lead to death but mechanisms of adaptation can limit cerebral oedema. The notion of mild asymptomatic hyponatremia was questioned by the observation of subclinical neurocognitive impairment, a greater risk of falls and fractures. Aetiologies are classified into six groups: neurologic disorders, infections mainly cerebral, meningeal and pulmonary, drugs in particular antidepressants, tumors, genetic causes, and idiopathic. Symptomatic acute hyponatremia is a therapeutic emergency that is not specific of SIAD. When hyponatremia is asymptomatic, fluid restriction with salt intake is generally sufficient but urea can be an alternative. In chronic SIAD, there is currently no recommendation. Fluid restriction is not always feasible; urea has proved its efficacy, its good tolerance and its long-term harmlessness. Vaptans have demonstrated their good tolerance and their efficacy on the correction of hyponatremia from SIAD in studies subgroups, for moderate hyponatremia and asymptomatic patients. In the only study having compared vaptans and urea, efficacy and tolerance were similar. Because of the cost difference between vaptans and urea and while waiting for follow-up studies, urea appears at present as the first-line treatment of hyponatremia in SIAD.

Topics: Diagnosis, Differential; Genetic Predisposition to Disease; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infections; Neoplasms; Neurophysins; Protein Precursors; Vasopressins; Water-Electrolyte Balance

Current treatment of acute decompensated heart failure (ADHF) has not reduced the significant morbidity or mortality associated with this disease, and has promoted drug development aimed at neurohormonal targets. Hypervolemic hyponatremia, which is linked to the nonosmotic release of arginine vasopressin, is associated with a poor prognosis in patients with heart failure (HF). Vasopressin acts on V(2) and V(1a) receptors to cause water retention and vasoconstriction, respectively. Clinical trials have demonstrated that vasopressin receptor antagonists (VRAs) are effective in treating hypervolemic hyponatremia in ADHF without a negative impact on renal function. The small hemodynamic benefit seen with VRA use appeared to result from V(2)-receptor antagonist-induced increase in urine output rather than from a vasodilatory drug effect. VRA use in ADHF trials was associated with minimal symptomatic improvement and no impact on morbidity or mortality. At present, clinical trial evidence does not support the routine use of VRAs in ADHF. Given the favorable renal profile of VRAs, studies on the possible benefit of VRAs in ADHF patients with renal insufficiency and diuretic resistance appear warranted.

Topics: Acute Disease; Animals; Antidiuretic Hormone Receptor Antagonists; Benzamides; Benzazepines; Clinical Trials as Topic; Heart Failure; Hemodynamics; Humans; Hyponatremia; Prognosis; Pyrroles; Tolvaptan; Vasoconstriction; Vasopressins

Hyponatremia is an electrolyte disorder that is defined by a serum sodium concentration of less than 135 mmol/L. Hyponatremia occurs at a high incidence. It is commonly associated with mild to moderate mental impairment. Hypoosmolar hyponatremia occurs in the setting of plasma volume deficiency ("hypovolemia", e. g. after gastrointestinal fluid loss), liver cirrhosis and cardiac failure ("hypervolemic" hyponatremia) and syndrome of inappropriate antidiuretic hormone secretion ("euvolemic" hyponatremia). Excessive antidiuretic hormone and continued fluid intake are the pathogenetic causes of these hyponatremias. Whereas hypovolemic hyponatremia is best corrected by isotonic saline, conventional proposals for euvolemic and hypervolemic hyponatremia consist of the following: fluid restriction, lithium carbonate, demeclocycline, urea and loop diuretic. None of these nonspecific treatments is entirely satisfactory. Recently a new class of pharmacological agents - orally available vasopressin antagonists, collectively called vaptans - have been described. A number of clinical trials using vaptans have been performed already. They showed vaptans to be effective, specific and safe in the treatment of euvolemic and hypervolemic hyponatremia. In Europe the vaptanes are currently certified exclusively for the treatment of euvolemic hyponatremia. Hypernatremia is caused by a relative deficit of free water and often occurs in elderly patients, who have an impaired thirst mechanism or are unable to ask for water. The cornerstone of treatment is administration of free water to correct the relative water deficit.

Topics: Adolescent; Child; Diagnosis, Differential; Electrolytes; Hormone Antagonists; Humans; Hypernatremia; Hyponatremia; Sodium; Vasopressins

Although hyponatremia is a recognized complication of several inflammatory diseases, its pathophysiology in this setting has remained elusive until recently. A growing body of evidence now points to an important role for interleukin-6 in the non-osmotic release of vasopressin. Here, we review this evidence by exploring the immuno-neuroendocrine pathways connecting interleukin-6 with vasopressin. The importance of these connections extends to several clinical scenarios of hyponatremia and inflammation, including hospital-acquired hyponatremia, postoperative hyponatremia, exercise-associated hyponatremia, and hyponatremia in the elderly. Besides insights in pathophysiology, the recognition of the propensity for antidiuresis during inflammation is also important with regard to monitoring patients and selecting the appropriate intravenous fluid regimen, for which recommendations are provided.

Topics: Cytokines; Humans; Hyponatremia; Inflammation; Interleukin-6; Signal Transduction; Vasopressins; Water-Electrolyte Balance

Hyponatremia is a marker of different underlying diseases and it can be a cause of morbidity itself; this implies the importance of a correct approach to the problem. The syndrome of inappropriate antidiuresis (SIAD) is one of the most common causes of hyponatremia: it is a disorder of sodium and water balance characterized by urinary dilution impairment and hypotonic hyponatremia, in the absence of renal disease or any identifiable non-osmotic stimulus able to induce antidiuretic hormone (ADH) release; according to its definition, it is diagnosed through an exclusion algorithm. SIAD is usually observed in hospitalized patients and its prevalence may be as high as 35%. The understanding of the syndrome has notably evolved over the last years, as reflected by the significant change in the name, once the syndrome of inappropriate secretion of ADH (SIADH), today SIAD. This review is up to date and it analyses the newest notions about pathophysiological mechanisms, classification, management and therapy of SIAD, including vaptans.

Topics: Animals; Benzazepines; Disease Management; Humans; Hyponatremia; Inappropriate ADH Syndrome; Neurophysins; Protein Precursors; Vasopressins; Water-Electrolyte Balance

Dysnatremias, disorders of sodium concentration, are exceedingly common in critically ill patients and confer increased risk for adverse outcomes including mortality. The physiology that underpins the diagnosis and management of these disorders is complex. This review seeks to discuss current literature regarding the pathophysiology, diagnosis, epidemiology, and management of these disorders.. The role of arginine vasopressin in the maintenance of normal and pathologic plasma osmolality increasingly is refined, improving our ability to diagnose and understand dysnatremia. Identified recent epidemiologic studies highlight the frequent hospital acquisition or exacerbation of dysnatremia, confirm the recognized adverse consequences and explore the potential causality. Despite the complex nature of these disorders, simple consensus treatment strategies have emerged.. Dysnatremia remains a common disorder across the spectrum of critically ill patients. It is frequently hospital acquired. Simplified treatment regimens are proposed and the potential for prevention or earlier recognition and intervention is emphasized. Future directions of interest include further exploration of how dysnatremia contributes to adverse outcomes and new treatment strategies.

Topics: Critical Care; Critical Illness; Humans; Hypernatremia; Hyponatremia; Intensive Care Units; Length of Stay; Prognosis; Risk; United States; Vasopressins

To evaluate acute hemodynamic, short-term, and long-term effects of vasopressin antagonists in patients with heart failure (HF).. Searches of the PubMed database (1966-February 2010) were conducted. Search terms included AVP receptor antagonist, CHF, tolvaptan, conivaptan, lixivaptan, HF, and hyponatremia. Manufacturers' prescribing information, manufacturer Web site searches, and searches made on www.clinicaltrials.gov were also included.. All clinical trials identified from the reference search and data sources were reviewed. Articles were included if they were relevant to short-term and long-term outcomes of patients with HF who were treated with vasopressin antagonists.. Trials of conivaptan, tolvaptan, and lixivaptan were evaluated. The evidence indicates that all agents increase urine output >10 mL/h, and conivaptan and tolvaptan decrease pulmonary capillary wedge pressure (-2.6 +/- 0.7, -5.4 +/- 0.7, and -4.6 +/- 0.7 mm Hg for placebo, conivaptan 20 mg, and conivaptan 40 mg, respectively; -5.67 +/- 4.58 to -6.38 +/- 4.12 mmHg for tolvaptan, and -4.16 +/- 4.57 mm Hg for placebo) in patients with HF. Both of these changes occur without inducing electrolyte abnormalities or renal dysfunction. Trials with conivaptan in acute HF have not demonstrated a benefit in cardiac index, mean arterial pressure, or vascular resistance. Data from clinical trials indicate that tolvaptan may decrease dyspnea (p < 0.05) and pedal edema (p < 0.001). To date, no large-scale trials of any agent have demonstrated an improvement in left ventricular systolic function, rehospitalization, worsening HF, or death.. Vasopressin antagonists cannot be considered routine pharmacotherapy for HF. Further, conivaptan should not be used for the treatment of acute HF. There is not enough literature to advocate for or against the use of lixivaptan in patients with HF. Tolvaptan may be considered for the treatment of hyponatremia.

Topics: Azepines; Benzamides; Benzazepines; Heart Failure; Humans; Hyponatremia; Neurotransmitter Agents; Pyrroles; Tolvaptan; Vasopressins

We review literature from the past 18 months on the treatment of hyponatremia. Therapy must address both the consequences of the untreated electrolyte disturbance (including fatal cerebral edema due to acute water intoxication) and the complications of excessive therapy (the osmotic demyelination syndrome).. Correction of hyponatremia by 4-6 mEq/l within 6 h, with bolus infusions of 3% saline if necessary, is sufficient to manage the most severe manifestations of hyponatremia. Planning therapy to achieve a 6 mEq/l daily increase in the serum sodium concentration can avoid iatrogenic brain damage by staying well clear of correction rates that are harmful. Conservative correction goals are wise because inadvertent overcorrection is common. Administration of desmopressin to halt a water diuresis can help prevent overcorrection; if overcorrection occurs, therapeutic relowering of the serum sodium concentration is supported by data in experimental animals and was found to be safe in a small observational clinical trial. Even mild and apparently asymptomatic hyponatremia may lead to falls because of impaired gait, and an increased likelihood of fracture because of hyponatremia-induced osteoporosis, a newly described entity. Recently approved vasopressin antagonists now make it possible to normalize the serum sodium concentration on a chronic basis, but practical considerations have limited their use.

Topics: Animals; Deamino Arginine Vasopressin; Humans; Hyponatremia; Sodium; Vasopressins

Despite a crucial role in body fluid homeostasis, elevated vasopressin levels can also be pathological in conditions such as congestive heart failure, liver cirrhosis and the syndrome of inappropriate antidiuretic hormone secretion. The result of elevated vasopressin is renal water retention and hyponatremia, a low serum sodium concentration. Hyponatremia is associated with excess morbidity and mortality. Nonpeptide vasopressin-receptor antagonists represent a new drug class of small molecules that competitively inhibit one or more of the vasopressin receptors. There are three vasopressin receptors in humans, including V1a, V1b and V2. Selective V2- and combined V1a/V2-receptor antagonists have been developed for the treatment of hyponatremia resulting from congestive heart failure, liver cirrhosis and the syndrome of inappropriate antidiuretic hormone secretion. Two nonpeptide vasopressin-receptor antagonists, conivaptan and tolvaptan, have recently been approved by American and European drug authorities for clinical use. This article aims to provide a succinct and clinical update on nonpeptide vasopressin-receptor antagonists, including their mechanism of action, performance in randomized clinical trials and current clinical status.

Topics: Antidiuretic Hormone Receptor Antagonists; Clinical Trials as Topic; Humans; Hyponatremia; Vasopressins

Hyponatremia is the most prevalent electrolyte disorder in hospitalized patients. Vasopressin plays an important role in the pathogenesis of this disorder through its action on the vasopressin type 2 receptor (V(2)R), leading to electrolyte-free water reabsorption. Multiple vasopressin receptor antagonists have recently been developed that differ in their specificity for V(2)R and V(1)R. These agents have applications in diseases that can result in hypervolemic and euvolemic hyponatremia, such as the syndrome of inappropriate antidiuretic hormone secretion, congestive heart failure and cirrhosis. V(2)R antagonists have demonstrated promise in the short-term correction of hyponatremia, although the long-term survival benefits of these drugs are less clear. This review discusses the physiology of vasopressin in hyponatremia, the clinical implications of the disorder and examples of individual therapeutics used in treatment strategies.

Topics: Animals; Antidiuretic Agents; Antidiuretic Hormone Receptor Antagonists; Clinical Trials as Topic; Heart Failure; Humans; Hyponatremia; Inappropriate ADH Syndrome; Liver Cirrhosis; Receptors, Vasopressin; Vasopressins

The syndrome of inappropriate ADH secretion (SIADH), also recently referred to as the "syndrome of inappropriate antidiuresis", is an often underdiagnosed cause of hypotonic hyponatremia, resulting for instance from ectopic release of ADH in lung cancer or as a side-effect of various drugs. In SIADH, hyponatremia results from a pure disorder of water handling by the kidney, whereas external Na+ balance is usually well regulated. Despite increased total body water, only minor changes of urine output and modest edema are usually seen. Renal function and acid-base balance are often preserved, while neurological impairment may range from subclinical to life-threatening. Hypouricemia is a distinguishing feature. The major causes and clinical variants of SIADH are reviewed, with particular emphasis on iatrogenic complications and hospital-acquired hyponatremia. Effective treatment of SIADH with water restriction, aquaretics, or hypertonic saline + loop diuretics, as opposed to worsening of hyponatremia during parenteral isotonic fluid administration, underscores the importance of an early accurate diagnosis and careful follow-up of these patients.

Topics: Algorithms; Humans; Hyponatremia; Inappropriate ADH Syndrome; Models, Biological; Neurophysins; Osmolar Concentration; Protein Precursors; Vasopressins; Water-Electrolyte Balance

Hyponatremia is the most common electrolyte disorder in patients with cirrhosis. This disorder can be a result of substantial loss of extracellular fluid "hypotonic or hypovolemic hyponatremia" or develop in the context of an increase in extracellular fluid volume and in the absence of major sodium losses; this situation occurs in patients with advanced cirrhosis and is known as "dilutional or hypervolemic hyponatremia". In dilutional or hypervolemic hyponatremia, serum sodium concentration is reduced, plasma volume is increased (although the effective plasma volume is decreased due to marked arterial vasodilation in the splanchnic circulation) and extracellular fluid volume is increased, with ascites and edema in the absence of signs of dehydration. This is a result of the marked deterioration in renal excretion of solute-free water, leading to disproportionate water retention in relation to sodium retention. Hypotonic hyponatremia represents 10% of all hyponatremias in patients with cirrhosis. Since hypervolemic hyponatremia is by far the most frequent form of this disorder, the present chapter will concentrate specifically on hypervolemic hyponatremia in cirrhosis.

Topics: Antidiuretic Hormone Receptor Antagonists; Ascites; Blood Volume; Contraindications; Disease Progression; Diuresis; Extracellular Fluid; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Liver Cirrhosis; Liver Transplantation; Natriuresis; Prognosis; Saline Solution, Hypertonic; Splanchnic Circulation; Vasodilation; Vasopressins

The non-peptide vasopressin antagonists (VPA), called vaptans, were developed in the 1990s to antagonize both the pressor and antidiuretic effects of vasopressin. There are three subtypes of VPA receptors: V1a, V1b and V2. V1a receptors are widely distributed in the body, mainly the blood vessels and myocardium. The V1b receptors are located mainly in the anterior pituitary gland and play a role in ACTH release. V2 receptors are located in the collecting tubular renal cells. Both V1a and V1b receptors act through the intracellular phosphoinositol signalling pathway, Ca(++) being the second messenger. V2 receptors work through AMPc generation, which promotes aquaporin 2 (AQP2) trafficking and allows water to enter the cell. The vaptans act competitively at the AVP receptor. The most important are mozavaptan, lixivaptan, satavaptan and tolvaptan, all of which are selective V2 antagonists and are administered through the oral route. In contrast, conivaptan is a dual V1 and V2 antagonist administered through the endovenous route. The main characteristics of vaptans are their effect on free water elimination without affecting electrolyte excretion. There are several studies on the effects of these drugs in hypervolemic hyponatremia (heart failure, hepatic cirrhosis) as well as in normovolemic hyponatremia (inappropriate secretion of ADH [SIADH]). Current studies show that the vaptans are effective and well tolerated, although knowledge of these drugs remains limited. There are no studies of the use of vaptans in severe hyponatremia. Osmotic demyelination syndrome due to excessively rapid correction of hyponatremia has not been described.

Topics: Adult; Antidiuretic Hormone Receptor Antagonists; Aquaporin 2; Benzamides; Benzazepines; Calcium Signaling; Clinical Trials as Topic; Cyclic AMP; Double-Blind Method; Drug Therapy, Combination; Heart Failure; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney Tubules, Collecting; Liver Cirrhosis; Morpholines; Multicenter Studies as Topic; Neoplasms; Pituitary Gland, Anterior; Pyrroles; Randomized Controlled Trials as Topic; Receptors, Vasopressin; Second Messenger Systems; Spiro Compounds; Tolvaptan; Vasopressins

Hyponatremia is the most common electrolyte abnormality found in hospitalized patients with heart failure. It may occur in patients who have hypovolemic, hypervolemic, or euvolemic state. It is usually not corrected by available therapies. It is a major predictor of prognosis, and correction of hyponatremia can be effectively accomplished by vasopressin antagonists. However, it still remains to be seen whether the normalization of serum sodium with vasopressin antagonists will also lead to an improved long-term prognosis.

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Heart Failure; Humans; Hyponatremia; Prognosis; Sodium; Tolvaptan; Treatment Outcome; Vasopressins

The pathogenesis of cardiac failure involves activation of the neurohumoral axis including stimulation of the sympathetic nervous system, the renin-angiotensin-aldosterone, and nonosmotic vasopressin systems. While these responses are critical in maintaining arterial pressure, they are associated with renal vasoconstriction, as well as sodium and water retention. In advanced circumstances, renal dysfunction and hyponatremia occur with cardiac failure. Even a modest rise in serum creatinine related to diminished renal function in heart failure patients is associated with increased risk for cardiovascular morbidity and mortality. Similarly, increased thirst and the nonosmotic stimulation of vasopressin in advanced cardiac failure leads to hyponatremia, which is also a major risk factor for mortality. Currently, V2 vasopressin receptor antagonists have been shown to correct hyponatremia in cardiac failure. One such agent, conivaptan, also is a V1 receptor antagonist which could theoretically benefit heart failure patients by decreasing cardiac afterload and remodeling. The effect of V2 receptor antagonists to correct hyponatremia in heart failure patients appears to be quite safe. However, to date no effect on mortality has been demonstrated.

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Heart Failure; Humans; Hyponatremia; Kidney; Kidney Diseases; Vasopressins

Abnormalities in thirst and vasopressin (AVP) release play key roles in the genesis of hyponatremia; both processes are under the control of osmoreceptive neurons in the central nervous system (CNS). The acute development of hyponatremia in turn leads to profound cerebral edema, whereas treatment of chronic hyponatremia can be associated with osmotic demyelination syndrome (ODS). The brain is thus both "culprit" and "victim" in hyponatremia. This review summarizes recent advances in the understanding of osmoreception in the brain, the CNS response to acute and chronic hyponatremia, and the pathophysiology of ODS.

Topics: Animals; Brain; Demyelinating Diseases; Humans; Hyponatremia; Models, Biological; Osmosis; Thirst; Vasopressins

Cerebral salt-wasting (CSW), or renal salt-wasting (RSW), has evolved from a misrepresentation of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) to acceptance as a distinct entity. Challenges still confront us as we attempt to differentiate RSW from SIADH, ascertain the prevalence of RSW, and address reports of RSW occurring without cerebral disease. RSW is redefined as 'extracellular volume depletion due to a renal sodium transport abnormality with or without high urinary sodium concentration, presence of hyponatremia or cerebral disease with normal adrenal and thyroid function.' Our inability to differentiate RSW from SIADH lies in the clinical and laboratory similarities between the two syndromes and the difficulty of accurate assessment of extracellular volume. Radioisotopic determinations of extracellular volume in neurosurgical patients reveal renal that RSW is more common than SIADH. We review the persistence of hypouricemia and increased fractional excretion of urate in RSW as compared to correction of both in SIADH, the appropriateness of ADH secretion in RSW, and the importance of differentiating renal RSW from SIADH because of disparate treatment goals: fluid repletion in RSW and fluid restriction in SIADH. Patients with RSW are being incorrectly treated by fluid restriction, with clinical consequences. We conclude that RSW is common and occurs without cerebral disease, and propose changing CSW to RSW.

Topics: Animals; Atrial Natriuretic Factor; Biomarkers; Brain; Diagnosis, Differential; Extracellular Fluid; Fluid Therapy; Humans; Hyponatremia; Kidney; Natriuretic Peptide, Brain; Pituitary ACTH Hypersecretion; Sodium; Terminology as Topic; Uric Acid; Vasopressins; Water-Electrolyte Balance

Copeptin denominates the C-terminal fragment of the vasopressin (AVP) precursor hormone. Circulating copeptin levels reflect the activity of the AVP system and correlate closely with plasma osmolality. The measurement of stimulated plasma AVP levels is crucial in the differential diagnosis of diabetes insipidus, particularly the characterization of partial forms, and is used to diagnose primary polydipsia. However, determination of AVP levels is technically demanding, and validated assays are not readily available for clinical routine. Recently, a reliable sandwich immunoassay for measurement of serum or plasma copeptin levels has been introduced. Assaying stimulated copeptin levels will be helpful in the differential diagnosis of diabetes insipidus. Recent studies suggest that measurement of copeptin, once the assay is commercially available, might prove useful in the workup of hyponatremic disorders. Moreover, copeptin has been found to be a prognostically relevant biomarker in a variety of illnesses such as sepsis, shock, pneumonia, acute exacerbation of COPD, heart failure, and myocardial infarction.

Topics: Biomarkers; Diabetes Insipidus; Glycopeptides; Humans; Hyponatremia; Immunoassay; Prognosis; Protein Precursors; Vasopressins; Water-Electrolyte Imbalance

Hyponatremia, defined by a serum sodium concentration of less than 135 mmmol/l, is a complex clinical occurrence frequently manifested in newborns admitted to the neonatal intensive care unit. The pathogenetic mechanisms and clinical timing underlying the onset of hyponatremia have not been well established in the newborn. Aim of this review is to present a practical approach and management of hypotonic hyponatremia in newborns, with particular emphasis on nephrogenic syndrome of inappropriate antidiuresis, recently described by us for the first time in the literature in a newborn.

Topics: Administration, Oral; Diabetes Insipidus, Nephrogenic; Female; Fluid Therapy; Humans; Hyponatremia; Hypoxia-Ischemia, Brain; Inappropriate ADH Syndrome; Infant; Infant, Newborn; Male; Neurophysins; Polymorphism, Single Nucleotide; Protein Precursors; Syndrome; Urea; Vasopressins

The tools available to physicians for the treatment of hyponatremia, the most common of electrolyte disorders, are limited by lack of effectiveness, compliance difficulties, and toxicity problems. For this reason the development of novel oral antagonists of vasopressin provide a new approach to the management of these disorders. Since vasopressin plays a central role in the pathogenesis of most hyponatremic disorders, the inhibition of binding of the hormone to its receptors is likely to provide a most reliable and reproducible response leading to increases in free water excretion. This article reviews many of the studies that have been undertaken with this new class of agents, both in hypovolemic and hypervolemic settings.

Topics: Body Water; Heart Failure; Humans; Hyponatremia; Vasopressins

Impaired urinary dilution leading to water retention and hyponatremia may occur in patients with cardiac failure, cirrhosis, pregnancy, oxytocin administration, hypothyroidism, glucocorticoid, and mineralocorticoid deficiency. The mechanisms for these defects predominantly involve the nonosmotic stimulation of arginine vasopressin release with up-regulation of aquaporin 2 water channel expression and trafficking to the apical membrane of the principal cells of the collecting duct. These perturbations are reversed by V2 vasopressin receptor antagonists. In contrast, urinary concentration defects leading to polyuria are vasopressin resistant. They may involve several factors, such as impaired countercurrent concentration secondary to down-regulation of Na-K-2Cl cotransporter. Vasopressin-resistant down-regulation of aquaporin 2 expression has also been described as a factor in impaired urinary concentration.

Topics: Aquaporin 2; Body Water; Homeostasis; Humans; Hyponatremia; Polyuria; Vasopressins

Etiopathogenesis, diagnostics and therapy of hyponatremias are summarized for clinicians. Hyponatremia is the most common electrolyte abnormality. Mild to moderate hyponatremia and severe hyponatremia are found in 15-30% and 1-4% of hospitalized patients, respectively. Pathophysiologically, hyponatremias are classified into two groups: hyponatremia due to non-osmotic hypersecretion of vasopressin (hypovolemic, hypervolemic, euvolemic) and hyponatremia of non-hypervasopressinemic origin (pseudohyponatremia, water intoxication, cerebral salt wasting syndrome). Patients with mild hyponatremia are almost always asymptomatic. Severe hyponatremia is usually associated with central nervous system symptoms and can be life-threatening. Diagnostic evaluation of patients with hyponatremia is directed toward identifying the extracellular fluid volume status, the neurological symptoms and signs, the severity and duration of hyponatremia, the rate at which hyponatremia developed. The first step to determine the probable cause of hyponatremia is the differentiation of the hypervasopressinemic and non-hypervasopressinemic hyponatremias with measurement of plasma osmolality, glucose, lipids and proteins. For further differential diagnosis of hyponatremia, the determination of urine osmolality, the clinical assessment of extracellular fluid volume status and the measurement of urine sodium concentration provide important information. The most important representative of euvolemic hyponatremias is SIADH. The diagnosis of SIADH is based on the exclusion of other hyponatremic conditions; low plasma osmolality (<275 mosmol/kg) and inappropriate urine concentration (urine osmolality >100 mosmol/kg) are of pathognomic value. Acute (<48 hrs) severe hyponatremia (<120 mmol/l) necessitates emergency care with rapid restoration of normal osmotic milieu (1 mmol/l/hr increase rate of serum sodium). Patients with chronic symptomatic hyponatremia have a high risk of osmotic demyelination syndrome in brain if rapid correction of the plasma sodium occurs (maximal rate of correction of serum sodium should be 0.5 mmol/l/hr or less). The conventional treatments for chronic asymptomatic hyponatremia (except hypovolemic patients) include water restriction and/or the use of demeclocycline or lithium or furosemide and salt supplementation. Vasopressin receptor antagonists have opened a new forthcoming therapeutic era. V2 receptor antagonists, such as lixivaptan, tolvaptan, satavaptan and the V2+

Topics: Antidiuretic Hormone Receptor Antagonists; Azepines; Benzamides; Benzazepines; Blood Volume; Brain Diseases; Central Nervous System; Chronic Disease; Demeclocycline; Demyelinating Diseases; Diagnosis, Differential; Diuretics; Extracellular Fluid; Furosemide; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lithium Compounds; Morpholines; Osmolar Concentration; Osmosis; Pyrroles; Severity of Illness Index; Sodium; Spiro Compounds; Time Factors; Tolvaptan; Vasopressins

Causes of hyponatremia in children include the syndrome of appropriate antidiuretic hormone secretion, the syndrome of inappropriate antidiuretic hormone secretion and cerebral salt wasting. The purpose of this review is to distinguish these possibilities, focusing on cerebral salt wasting.. Most cases of hyponatremia in children are due to the syndrome of appropriate antidiuretic hormone secretion. The syndrome of inappropriate antidiuretic hormone secretion can be seen with neurological injury, pain and medication use. Recent studies suggest that cerebral salt wasting is a rare cause of hyponatremia. When cerebral salt wasting is diagnosed, it is often difficult to make a direct link with the central nervous system insult.. The clinical condition, assessment of extracellular fluid space volume status, measurement of urinary electrolytes and responses to infusion of saline solutions can distinguish between syndrome of appropriate antidiuretic hormone secretion, syndrome of inappropriate antidiuretic hormone secretion and cerebral salt wasting. The word 'cerebral' in 'cerebral salt wasting syndrome' can thus be inappropriate, conveying inaccurate causation.

Topics: Brain Injuries; Child; Diagnosis, Differential; Humans; Hyponatremia; Hypovolemia; Inappropriate ADH Syndrome; Sodium; Vasopressins

Topics: Arginine Vasopressin; Heart Failure; Humans; Hyponatremia; Receptors, Vasopressin; Vasopressins

Oxytocin (OT) and vasopressin (AVP) mediate their biological actions by acting on four known receptors: The OT (uterine) and the AVP V(1a) (vasopressor), V(1b) (pituitary), V(2) (renal) receptors and a fifth putative AVP V(1c)? (vasodilating) receptor. This presentation will summarize some highlights of the recent progress, in the design and synthesis of selective peptide agonists, antagonists, radioiodinated ligands, fluorescent ligands and bivalent ligands for these receptors. Here we present published and unpublished pharmacological data on the most widely used agonists, antagonists and labelled ligands. The pharmacological properties of promising new selective OT antagonists and V(1b) agonists are also presented. This review should serve as a useful guide for the selection of the most appropriate ligand for a given study. The current status of non-peptide OT and AVP antagonists and agonists is also summarized. The relative merits of peptide and non-peptide AVP and OT agonists and antagonists as: (1) research tools and (2) therapeutic agents will be evaluated. Many of the receptor selective peptide agonists and antagonists from this and other laboratories are far more widely used as pharmacological tools for studies on the peripheral and central effects of OT and AVP than their non-peptide counterparts. In addition to OT and to a lesser extent AVP (pitressin), a number of OT and AVP analogues; such as carbetocin (OT agonist) dDAVP (desmopressin, V(2) agonist), terlipressin (V(1a) agonist), felypressin (V(1a) agonist) and atosiban (Tractocile OT antagonist) are also in clinical use. Despite much early promise, no non-peptide V(1a) or OT antagonists are currently in clinical trials. While a number of orally active non-peptide V(2) antagonists (Vaptans); notably, Tolvaptan, Lixivaptan and Satavaptan, are currently in Phase III clinical trials; to date, only the mixed V(2)/V(1a), antagonist Conivaptan (Vaprisol), has been approved by the US FDA for clinical use (by i.v. administration), for the treatment of euvolemic and hypervolemic hyponatremia in hospitalized patients. Promising new non-peptide V(1b) and OT antagonists, as well as non-peptide V(2) and OT agonists are now in pre-clinical development.

Topics: Animals; Antidiuretic Agents; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Clinical Trials as Topic; Deamino Arginine Vasopressin; Female; Humans; Hyponatremia; Lypressin; Oligopeptides; Oxytocin; Peptides; Rats; Receptors, Oxytocin; Receptors, Vasopressin; Structure-Activity Relationship; Terlipressin; Uterus; Vasodilator Agents; Vasopressins

Hyponatremia is the most common electrolyte disorder present in hospitalized patients. Acute and severe hyponatremia can cause significant morbidity and mortality. The present review discusses the epidemiology, causes, and a practical approach to the diagnosis and management of acute and chronic hyponatremia, including the appropriate use of hypertonic saline and potential future use of the new V2 vasopressin receptor antagonists in critically ill patients.. The increasing knowledge of aquaporin water channels and the role of vasopressin in water homeostasis have enhanced our understanding of hyponatremic disorders. Increased vasopressin secretion due to nonosmotic stimuli leads to decreased electrolyte-free water excretion with resulting water retention and hyponatremia. Vasopressin receptor antagonists induce electrolyte-free water diuresis without natriuresis and kaliuresis. Phase three trials indicate that these agents predictably reduce urine osmolality, increase electrolyte-free water excretion, and raise serum sodium concentration. They are likely to become a mainstay of treatment of euvolemic and hypervolemic hyponatremia.. The correct diagnosis and management of hyponatremia is complex and requires a systematic approach. Vasopressin receptor antagonists are potential tools in the management of hyponatremia. Further studies are needed to determine their role in the treatment of acute, severe, life-threatening hyponatremia as well as chronic hyponatremia.

Topics: Acute Disease; Humans; Hyponatremia; Osmolar Concentration; Osmotic Pressure; Receptors, Vasopressin; Vasoconstrictor Agents; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

In pregnancy, blood volume increases greatly and plasma osmolality is reduced, due to mild hyponatraemia despite sodium retention. In rats, both vasopressin and oxytocin neurones in the supraoptic nucleus are osmosensitive and have contrasting roles in these adaptations. Increased vasopressin secretion stimulates water retention by renal actions, while oxytocin is natriuretic, partly by stimulating cardiac atrial natriuretic peptide (ANP) secretion. In pregnancy, relaxin from the corpora lutea, acting via the lamina terminalis in the presence of pregnancy levels of oestrogen and progesterone, stimulates vasopressin secretion and drinking, resulting in hypervolaemia and hyponatraemia. Initial stimulation of oxytocin secretion by relaxin is lost in late pregnancy, and oxytocin neurone responses to modest osmotic stimulation are reduced. Consequently, with reduced ANP secretion and action, sodium is retained and hypervolaemia maintained. Oxytocin neurone responses to other inputs, from hypervolaemia, immune or satiety signals, are reduced in late pregnancy by up-regulated central endogenous opioid mechanisms. Neither inhibition by opioid nor nitric oxide explains reduced responses to osmotic stimulation. Increased activity of GABA input, by allopregnanolone action, might be involved. However, the lack of a shift in threshold for hyperosmotic stimulation of oxytocin secretion in pregnancy, despite the hyponatraemia caused by relaxin, seems a sufficient explanation.

Topics: Animals; Estrogens; Female; Humans; Hyponatremia; Osmolar Concentration; Oxytocin; Pregnancy; Pregnancy, Animal; Progesterone; Rats; Relaxin; Vasopressins

While electrolyte measurements after death may be confounded by a number of variables, vitreous humor sodium tends to remain stable for some time, enabling correlation between ante- and postmortem levels. Review of natural and unnatural causes of reduced vitreous humor sodium levels at autopsy was undertaken to demonstrate the range of diseases that may result in this finding. Natural diseases affecting the vasopressin-renin-angiotensin axis may cause reduction in sodium levels with associated hypovolemia, euvolemia, and hypervolemia. Low sodium measurements may also occur with redistribution of water, and artefactually when there are underlying lipid and protein disorders. Unnatural causes of hyponatremia at autopsy include water intoxication from psychogenic polydipsia, environmental polydipsia, ingestion of dilute infant formulas, beer potomania, endurance exercise, fresh water immersion (including water births) and iatrogenic causes including drug and parenteral fluid administration, and surgical irrigation. A knowledge of the range of conditions that may result in lowered postmortem sodium levels will help to exclude or confirm certain diseases at autopsy. In addition, significant vitreous hyponatremia may be a useful finding to help clarify mechanisms of unnatural deaths.

Topics: Drinking Behavior; Exercise; Humans; Hyponatremia; Hypovolemia; Iatrogenic Disease; Immersion; Infant Formula; Physical Endurance; Renin-Angiotensin System; Vasopressins

Total body water and tonicity is tightly regulated by renal action of antidiuretic hormone (ADH), reninangiotensin-aldosterone system, norepinephrine and by the thirst mechanism. Abnormalities in water balance are manifested as sodium disturbances--hyponatremia and hypernatremia. Hyponatremia ([Na+ < 136 meq/ l]) is a common abnormality in hospitalized patients and is associated with increased morbidity and mortality. A common cause of hyponatremia is impaired renal water excretion either due to low extracellular fluid volume or inappropriate secretion of ADH. Clinical assessment of total body water and urine studies help in determining cause and guiding treatment of hyponatremia. Acute and severe hyponatremia cause neurological symptoms necessitating rapid correction with hypertonic saline. Careful administration and monitoring of serum [Na+] is required to avoid overcorrection and complication of osmotic demyelination. Vasopressin receptor antagonists are being evaluated in management of euvolemic and hypervolemic hyponatremia. Hypematremia ([Na+] > 145 meq/l) is caused by primary water deficit (with or without Na+ loss) and commonly occurs from inadequate access to water or impaired thirst mechanism. Assessment of the clinical circumstances and urine studies help determine the etiology, while management of hypernatremia involves fluid resuscitation and avoiding neurological complications from hypernatremia or its correction. Frequent monitoring of [Na+] is of paramount importance in the treatment of sodium disorders that overcomes the limitations of prediction equations.

Topics: Antidiuretic Agents; Antidiuretic Hormone Receptor Antagonists; Fluid Therapy; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Sodium Chloride; Vasopressins; Water-Electrolyte Balance

As vasopressin receptors are found in many different tissues, vasopressin antagonists may benefit the treatment of numerous disorders. Effects of vasopressin via V1(a) and V2 receptors are closely implicated in a variety of water-retaining diseases and cardiovascular diseases, including heart failure, hyponatremia, hypertension, renal diseases, syndrome of inappropriate antidiuretic hormone secretion, cirrhosis, and ocular hypertension. Furthermore, V1(a) vasopressin antagonists might be useful in cerebral ischemia and stroke, Raynaud's disease, dysmenorrhoea and tocolytic treatment. V1(b) selective vasopressin antagonists are discussed in terms of their usefulness in the treatment of emotional and psychiatric disorders. The vaptans are vasopressin receptor antagonists with V1(a) (relcovaptan) or V2 (tolvaptan, lixivaptan, satavaptan) selectivity or non-selective activity (conivaptan). Conivaptan is the first vaptan which has been approved by the FDA for the treatment of euvolemic hyponatremia. For further indications such as congenital heart failure, studies are going on.

Topics: Antidiuretic Agents; Antidiuretic Hormone Receptor Antagonists; Heart Failure; Humans; Hyponatremia; Vasopressins

Topics: Body Water; Diagnosis, Differential; Humans; Hypernatremia; Hyponatremia; Osmolar Concentration; Potassium; Sodium; Vasopressins

Hyponatremia is the most common electrolyte abnormality in hospitalized patients. When symptomatic (hyponatremic encephalopathy), the overall morbidity is 34%. Individuals most susceptible to death or permanent brain damage are prepubescent children and menstruant women. Failure of the brain to adapt to the hyponatremia leads to brain damage. Major factors that can impair brain adaptation include hypoxia and peptide hormones. In children, physical factors--discrepancy between skull size and brain size--are important in the genesis of brain damage. In adults, certain hormones--estrogen and vasopressin (usually elevated in cases of hyponatremia)--have been shown to impair brain adaptation, decreasing both cerebral blood flow and oxygen utilization. Initially, hyponatremia leads to an influx of water into the brain, primarily through glial cells and largely via the water channel aquaporin (AQP)4. Water is thus shunted into astrocytes, which swell, largely preserving neuronal cell volume. The initial brain response to swelling is adaptation, utilizing the Na(+)-K(+)-ATPase system to extrude cellular Na(+). In menstruant women, estrogen + vasopressin inhibits the Na(+)-K(+)-ATPase system and decreases cerebral oxygen utilization, impairing brain adaptation. Cerebral edema compresses the respiratory centers and also forces blood out of the brain, both lowering arterial Po(2) and decreasing oxygen utilization. The hypoxemia further impairs brain adaptation. Hyponatremic encephalopathy leads to brain damage when brain adaptation is impaired and is a consequence of both cerebral hypoxia and peptide hormones.

Topics: Adaptation, Physiological; Age Factors; Blood-Brain Barrier; Brain; Brain Edema; Cell Size; Estrogens; Humans; Hyponatremia; Hypoxia; Organ Size; Sex Factors; Vasopressins

Vasopressin antagonists have been studied in a variety of clinical settings, including patients with acute and chronic heart failure. The clinical trials published to date have sought to describe the clinical and physiologic effects of these agents in an effort to prove clinical efficacy and safety. A variety of agents with varying effects on V2 and V1a vasopressin receptor subtype have been studied. They have been shown to reduce bodyweight and improve serum sodium without worsening renal function. They may also decrease the need for loop diuretic use and may be particularly useful in patients with hyponatremia in the setting of volume overload. Further studies are underway that are powered to assess for morbidity and mortality benefits. The beneficial effects have been well documented but, until outcomes are understood more fully, the use of these agents should be limited to currently approved indications. In the USA, this includes only the treatment of euvolemic hyponatremia.

Topics: Antidiuretic Hormone Receptor Antagonists; Dose-Response Relationship, Drug; Drug Administration Schedule; Female; Follow-Up Studies; Heart Failure; Humans; Hyponatremia; Male; Randomized Controlled Trials as Topic; Receptors, Vasopressin; Risk Factors; Severity of Illness Index; Survival Rate; Treatment Outcome; Vasopressins

Hyponatremia is a common clinical problem in hospitalized patients and nursing home residents. It also may occur in healthy athletes after endurance exercise. The majority of patients with hyponatremia are asymptomatic and do not require immediate correction of hyponatremia. Symptomatic hyponatremia is a medical emergency requiring rapid correction to prevent the worsening of brain edema. How fast we should increase the serum sodium levels depends on the onset of hyponatremia and still remains controversial. If the serum sodium levels are corrected too rapidly, patients may develop central pontine myelinolysis, but if they are corrected too slowly, patients may die of brain herniation. We review the epidemiology and mechanisms of hyponatremia, the sensitivity of women to hyponatremic injury, the adaptation and maladaptation of brain cells to hyponatremia and its correction, and the practical ways of managing hyponatremia. Because the majority of hyponatremia is caused by the non-osmotic release of vasopressin, the recent approval of the vasopressin receptor antagonist conivaptan for euvolemic hyponatremia may simplify hyponatremia management. However, physicians should be aware of the risk of rapid correction of hyponatremia, hypotension, and excessive fluid intake.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Brain; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Kidney Concentrating Ability; Kidney Tubules, Collecting; Male; Osmolar Concentration; Vasopressins

Disorders of water balance are a common feature of clinical practice. An understanding of the physiology and pathophysiology of the key endocrine regulator of water balance vasopressin (VP) is key to diagnosis and management of these disorders. Diabetes insipidus is the result of a lack of VP or (less commonly) resistance to the renal effects of the hormone. Diagnostic testing can clarify aetiology and direct appropriate management. VP production can be associated with hyponatraemia. A comprehensive assessment of cardiovascular status and pharmacological influences are needed in these circumstances to differentiate between primary (inappropriate) and secondary (appropriate) physiological VP production. As with diabetes insipidus, diagnostic testing can help define the aetiology of hyponatraemia and direct appropriate management. Patients with disorders of water balance benefit from a joint clinical and laboratory medicine approach to diagnosis and management.

Topics: Aquaporins; Body Water; Diabetes Insipidus; Diuresis; Humans; Hypernatremia; Hyponatremia; Kidney; Molecular Structure; Polyuria; Receptors, Vasopressin; Sodium; Thirst; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

In a national heart failure registry, hyponatremia (serum sodium < 130 mEq/L) was initially reported in 5% of patients and considered a risk factor for increased morbidity and mortality. In a chronic heart failure study, serum sodium level on admission predicted an increased length of stay for cardiovascular causes and increased mortality within 60 days of discharge. Hyponatremia in patients with congestive heart failure (CHF) is associated with a higher mortality rate. Also, by monitoring and increasing serum sodium levels during hospitalization for CHF, patient outcomes may improve. This review describes the pathophysiology of hyponatremia in relation to CHF, including the mechanism of action of vasopressin receptors in the kidney, and assesses the preclinical and clinical trials of vasopressin receptor antagonists--agents recently developed to treat hyponatremia. In hospitalized patients with CHF, hyponatremia plays a major role in poor outcomes. Vasopressin receptor antagonists have been shown to be safe and effective in clinical trials in patients with hyponatremia.

Topics: Arginine Vasopressin; Azepines; Benzamides; Benzazepines; Chronic Disease; Clinical Trials as Topic; Diuretics; Heart Failure; Humans; Hyponatremia; Models, Biological; Pyrroles; Registries; Renin-Angiotensin System; Sodium; Tolvaptan; Treatment Outcome; Vasopressins

Mild hyponatremia is common in patients hospitalized for worsening heart failure, and it is a major predictor of post-discharge mortality and morbidity irrespective of left ventricular ejection fraction. Recent data also suggest that standard therapy for heart failure does not improve or normalize serum sodium concentration during hospitalization. There are conclusive data that vasopressin antagonists improve or normalize serum sodium in this patient population. However, it is not known if this improvement or normalization in serum sodium is associated with an improvement in post-discharge outcomes. Future trials with vasopressin antagonists in patients hospitalized with worsening heart failure and hyponatremia are in order.

Topics: Heart Failure; Humans; Hyponatremia; Sodium; Survival Rate; Treatment Outcome; Vasopressins

Hyponatremia is frequently associated with neurological disease, neurosurgical procedures, and use of psychoactive drugs. Arginine vasopressin (AVP), or antidiuretic hormone, is the principal physiological regulator of water and electrolyte balance, and disruption of the normal AVP response to osmotic stimuli is a common cause of dilutional hyponatremia in neurological disorders. The hyponatremia-induced shift in water from the extracellular to the intracellular compartment can lead to cerebral edema and serious neurological complications, especially if the decrease in serum sodium concentration ([Na+]) is large or rapid. Overly rapid correction of the serum [Na+] may lead to osmotic demyelination and irreversible brain injury. Fluid restriction is considered first-line treatment and pharmacological agents currently used in the treatment of hyponatremia are limited by inconsistent response and adverse side effects. AVP receptor antagonists represent a new approach to the treatment of hyponatremia by blocking tubular reabsorption of water by binding to V2 receptors in the renal collecting ducts, resulting in aquaresis. Initial clinical experience with AVP receptor antagonists for hyponatremia has shown that these agents augment free water clearance, decrease urine osmolality, and correct serum [Na+] and serum osmolality. Controlled clinical trials now underway will help elucidate the role of AVP receptor antagonism in the treatment of hyponatremia.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Humans; Hyponatremia; Models, Biological; Nervous System Diseases; Osmolar Concentration; Receptors, Vasopressin; Sodium; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Topics: Cushing Syndrome; Edema; Humans; Hyperaldosteronism; Hypertension; Hypokalemia; Hyponatremia; Inappropriate ADH Syndrome; Mineralocorticoid Excess Syndrome, Apparent; Renin-Angiotensin System; Vasopressins

The first non-peptide vasopressin receptor antagonist (VRA) was recently approved by the United States Food and Drug Administration, and several others are now in late stages of clinical development. Phase 3 trials indicate that these agents predictably reduce urine osmolality, increase electrolyte-free water excretion, and raise serum sodium concentration. They are likely to become a mainstay of treatment of euvolemic and hypervolemic hyponatremia. Although tachyphylaxis to the hydro-osmotic effect of these agents does not appear to occur, their use is accompanied by an increase in thirst, and they do not always eliminate altogether the need for water restriction during treatment of hyponatremia. Experience with use of these agents for treatment of acute, severe, life-threatening hyponatremia as well as chronic hyponatremia is limited. Further studies are needed to determine how they are best used in these situations, but the risk of overly rapid correction of hyponatremia seems low. Results of long-term trials to determine the ability of VRAs to reduce morbidity or mortality in congestive heart failure or to slow the progression of polycystic kidney disease are awaited with great interest.

Topics: Antidiuretic Hormone Receptor Antagonists; Azepines; Benzamides; Benzazepines; Clinical Trials as Topic; Diabetes Insipidus, Nephrogenic; Fibrosis; Heart Failure; Humans; Hyponatremia; Osmolar Concentration; Polycystic Kidney Diseases; Pyrroles; Receptors, Vasopressin; Sodium; Tolvaptan; United States; United States Food and Drug Administration; Vasopressins

Pre-operative central diabetes insipidus has been reported in 8-35% of patients affected with craniopharyngioma, and in 70-90% after surgery. The management of postoperative polyuria and polydipsia can be challenging and fluid balance needs to be closely monitored. The classical triphasic pattern of endogenous vasopressin secretion--an initial phase of symptomatic diabetes insipidus occurring 24 hours after surgery; a second phase of inappropriate vasopressin secretion potentially causing hyponatraemia; and a third phase with a return to diabetes insipidus occurring up to 2 weeks later--is often complicated by cerebral salt wasting and thirst disorders. Inadequate adrenal replacement therapy and anticonvulsant agent treatment may increase the risk of life-threatening hyponatraemia in the course of desmopressin (DDAVP) treatment. Appropriate management, in order to avoid life-threatening or disabling electrolyte disturbances, requires a good grasp of the relevant pathophysiology. We review here the pathophysiology and management of the multiple fluid disorders encountered following surgery for craniopharyngiomas.

Topics: Child; Craniopharyngioma; Diabetes Insipidus; Humans; Hyponatremia; Neurosurgical Procedures; Pituitary Neoplasms; Postoperative Complications; Thirst; Vasopressins; Water-Electrolyte Imbalance

Hyponatremia is a frequent and symptomatic electrolyte disorder for which specific treatments have been lacking. Hyponatremia is attributable to nonosmotic vasopressin stimulation and continued increased fluid intake. In the past, peptidic derivatives of arginine vasopressin proved that blockade of vasopressin V-2 receptors served to improve hyponatremia, however, these antagonists had intrinsic agonistic activity, too. In the past decade, random screening of molecules uncovered nonpeptide, orally available vasopressin antagonists without agonistic properties. The agents show competitive binding to the vasopressin V-2 receptor at an affinity comparable with that of arginine vasopressin. Four antagonists have undergone extensive study. Three of these agents--lixivaptan or VPA 985; SR 121 463 B; tolvaptan or OPC 41,061--are specific V-2 antagonists whereas conivaptan or YM 087 is a V-1/V-2 mixed antagonist. In animal and clinical studies all of the agents were able to correct water retention and hyponatremia in a dose-dependent manner. There was no tachyphylaxis, even when the agents were given over many weeks. It is expected that the clinical use of the agents will lead to a major improvement in the treatment of hyponatremia.

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Humans; Hyponatremia; Tolvaptan; Vasopressins; Water

Topics: Aquaporin 2; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Humans; Hyponatremia; Hypothalamus; Inappropriate ADH Syndrome; Mutation; Receptors, Vasopressin; Vasopressins

Topics: Arginine Vasopressin; Body Water; Diabetes Insipidus, Neurogenic; Diagnosis, Differential; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Kidney Tubules, Collecting; Osmolar Concentration; Vasopressins

Increased arginine vasopressin (AVP) secretion in heart failure may lead to vasoconstriction, left ventricular remodeling, and water retention-actions that promote afterload, preload, and hyponatremia and thereby cause disease progression. Interfering with AVP-mediated signaling pharmacologically may be beneficial in heart failure. Selective antagonism of the vasopressin 2 (V2) receptor may facilitate a safe diuresis and normalize low serum sodium levels, as demonstrated in preliminary clinical trials. Pure V2 antagonism, however, may stimulate AVP secretion and enhance V1a signaling, while pure V1a receptor antagonism may lead to unwanted V2 stimulation and secondary water retention and volume expansion. Combined V1a and V2 receptor antagonism could potentially prove advantageous as a therapy for heart failure by acting synergistically to facilitate diuresis and improve hemodynamics.

Topics: Antidiuretic Hormone Receptor Antagonists; Aquaporin 2; Arginine Vasopressin; Disease Progression; Heart Failure; Humans; Hyponatremia; Treatment Outcome; Vasopressins

Hyponatremia is a common electrolyte disorder associated with potentially serious or life-threatening consequences. Serum osmolality and sodium concentration [Na+] are regulated by thirst, the hormone arginine vasopressin (AVP), and renal water and sodium handling. Hyponatremia is frequently caused by dysregulation of AVP, which accompanies disorders of water retention, such as congestive heart failure (CHF) and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Clinical trials with AVP receptor antagonists have confirmed the important role of AVP in the pathophysiology of hyponatremia and suggest these agents are efficacious in treating hyponatremia associated with SIADH, cirrhosis, and CHF. Acting directly at AVP receptors in the renal tubules, these agents promote aquaresis - the electrolyte-sparing excretion of free water - in patients with hyponatremia. In clinical trials, AVP receptor antagonists have been shown to increase the serum [Na+] and urine output while decreasing urine osmolality.

Topics: Antidiuretic Hormone Receptor Antagonists; Humans; Hyponatremia; Receptors, Vasopressin; Vasopressins; Water-Electrolyte Balance

This article discusses the pathophysiology of sodium and water retention in edematous disorders with a particular focus on cardiac failure, cirrhosis, and pregnancy. The body fluid volume hypothesis, which emphasizes the dominant role of arterial baroreceptors in renal sodium and water excretion, is reviewed. With arterial underfilling, either due to a decrease in cardiac output or peripheral arterial vasodilation, the normal central inhibition of the sympathetic nervous system activity and baroreceptor-mediated, nonosmotic arginine vasopressin (AVP) release is attenuated. The resultant increase in renal adrenergic activity stimulates the renin-angiotensin-aldosterone system. Although the resultant increase in systemic vascular resistance compensates for the primary arterial underfilling, this activation of the neurohumoral axis results in diminished sodium and water delivery to the renal collecting duct sites of aldosterone, AVP, and natriuretic peptide action. This diminished distal sodium and water delivery will be discussed as an important factor in the failure to escape from the sodium-retaining effects of aldosterone, the resistance to the natriuretic and diuretic effects of natriuretic peptides, and the diminished maximal solute-free water excretion in patients with edema. The role of the nonosmotic AVP release in water retention and hypo-osmolality/hyponatremia has been demonstrated in patients and experimental animals by administering nonpeptide, orally active vasopressin V2 receptor antagonists. These agents have been found to increase solute-free water excretion in patients with water-retaining, hyponatremic edema as well as in experimental animals.

Topics: Aldosterone; Body Water; Edema; Female; Heart Failure; Humans; Hyponatremia; Liver Cirrhosis; Pregnancy; Pregnancy Complications; Renin-Angiotensin System; Vasodilation; Vasopressins

Hyponatremia is the most frequent electrolyte disorder encountered in hospitalized patients. It is a state of relative water excess due to stimulated arginine vasopressin (AVP) and fluid intake greater than obligatory losses. This kind of hyponatremia occurs in the syndrome of inappropriate antidiuretic hormone secretion, congestive heart failure, and liver cirrhosis. Fluid restriction is the presently recommended treatment for hyponatremia. However, fluid restriction may be very difficult for patients to achieve, is slow to work, and does not allow a graded therapeutic approach. More efficient and specific treatments of hyponatremia are needed. In this respect, pharmacologic research has yielded a number of compounds exhibiting antagonistic qualities at the vasopressin V2 receptor. Among these agents, peptidic derivatives of AVP turned out to have intrinsic antidiuretic properties in vivo when given over days or weeks. The development of such agents for use in patients has not been pursued. However, several promising nonpeptide, vasopressin receptor antagonists have been described; these agents are VPA-985 (lixivaptan), YM-087 (conivaptan), OPC-41061 (tolvaptan), and SR-121463. Prospective, randomized, placebo-controlled trials performed with these agents found that they corrected hyponatremia efficiently and safely. Most of the studies were conducted over a 4- to 28-day period. Long-term studies will be needed in the future to address such issues as the eventual benefit to patients and the effects of vasopressin antagonists on morbidity and mortality of patients with hyponatremia.

Topics: Antidiuretic Hormone Receptor Antagonists; Azepines; Benzamides; Benzazepines; Humans; Hyponatremia; Inappropriate ADH Syndrome; Morpholines; Pyrroles; Randomized Controlled Trials as Topic; Spiro Compounds; Tolvaptan; Vasopressins

Hyponatremia is an important and common electrolyte disorder in critically ill neurosurgical patients that has been reported in association with a number of different primary diagnoses. The correct diagnosis of the pathophysiological cause is vital because it dramatically alters the treatment approach.. We review the epidemiology and presentation of patients with hyponatremia, the pathophysiology of the disorder with respect to sodium and fluid balance, and the diagnostic procedures for determining the correct cause.. We then present the various treatment options, including discussion of one of the newest groups of agents, the arginine vasopressin receptor antagonists, currently under study for the treatment of hyponatremia in neurosurgical patients.. Hyponatremia is a serious comorbidity in neurosurgical patients that requires particular attention as its treatment varies by cause and its consequences can affect neurological outcome.

Topics: Antidiuretic Hormone Receptor Antagonists; Brain Diseases; Comorbidity; Humans; Hyponatremia; Natriuretic Peptides; Prevalence; Receptors, Vasopressin; Sodium; Vasopressins; Water-Electrolyte Balance

Disorders of sodium and water homeostasis are among the most commonly encountered disturbances in the critical care setting, because many disease states cause defects in the complex mechanisms that control the intake and output of water and solute. Because body water is the primary determinant of extracellular fluid osmolality, disorders of body water balance can be categorized into hypoosmolar and hyperosmolar disorders depending on the presence of an excess or a deficiency of body water relative to body solute. Because the main constituent of plasma osmolality is sodium, hypoosmolar and hyperosmolar disease states are generally characterized hy hyponatremia and hypernatremia, respectively. After a brief review of normal water metabolism, this article focuses on the diagnosis and treatment of hyponatremia and hypernatremia in the critical care setting.

Topics: Body Water; Critical Illness; Homeostasis; Humans; Hypernatremia; Hyponatremia; Osmolar Concentration; Vasopressins

The usual diagnostic approach to a patient with hyponatraemia is based on the clinical assessment of the extracellular fluid (ECF) volume, and laboratory parameters such as plasma osmolality, urine osmolality and/or urine sodium concentration. Several clinical diagnostic algorithms (CDA) applying these diagnostic parameters are available to the clinician. However, the accuracy and utility of these CDAs has never been tested. Therefore, we performed a survey in which 46 physicians were asked to apply all existing, unique CDAs for hyponatraemia to four selected cases of hyponatraemia. The results of this survey showed that, on average, the CDAs enabled only 10% of physicians to reach a correct diagnosis. Several weaknesses were identified in the CDAs, including a failure to consider acute hyponatraemia, the belief that a modest degree of ECF contraction can be detected by physical examination supported by routine laboratory data, and a tendency to diagnose the syndrome of inappropriate secretion of antidiuretic hormone prior to excluding other causes of hyponatraemia. We conclude that the typical architecture of CDAs for hyponatraemia represents a hierarchical order of isolated clinical and/or laboratory parameters, and that they do not take into account the pathophysiological context, the mechanism by which hyponatraemia developed and the clinical dangers of hyponatraemia. These restrictions are important for physicians confronted with hyponatraemic patients and may require them to choose different approaches. We therefore conclude this review with the presentation of a more physiology-based approach to hyponatraemia, which seeks to overcome some of the limitations of the existing CDAs.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Algorithms; Diuresis; Extracellular Fluid; Female; Humans; Hyponatremia; Kidney; Male; N-Methyl-3,4-methylenedioxyamphetamine; Sensitivity and Specificity; Sodium; Vasopressins

Charles Darwin, in his Origin of the Species, noted that different species of finches on the Galapagos Islands had adapted their beak size based on where they sought their food. Homer Smith, in his book From Fish to Philosopher, discussed the evolution of the nephron from a single conduit in salt water vertebrates, to nephrons with large glomerular capillaries and proximal and distal tubules in fresh water vertebrates, to smaller glomerular capillaries in amphibians, to nephrons with loops of Henle to allow for urinary concentration and dilution in mammals. The kidney with its million nephrons has emerged as the vital organ for regulating body fluid composition and volume. With the recent discovery of aquaporin water channels, our understanding of volume regulation has been greatly enhanced. This article reviews current knowledge regarding: 1) the unifying hypothesis of body fluid volume regulation; 2) brain aquaporins and their role in pathophysiologic states; and 3) function and regulation of renal aquaporins in the syndrome of inappropriate antidiuretic hormone secretion (SIADH).

Topics: Animals; Aquaporins; Body Water; Brain; Finches; Fishes; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Vasopressins; Water-Electrolyte Balance

We present a case of acute, symptomatic hyponatremia in a young woman that developed after use of 3,4-methylenedioxymethylamphetamine (MDMA), more commonly known as "ecstasy." The patient was treated with 5% saline and had complete recovery. The pathogenesis of MDMA-associated hyponatremia involves excessive water intake and inappropriately elevated antidiuretic hormone (ADH) levels. It seems that young, premenopausal women are at particularly high risk for the development of severe, symptomatic hyponatremia after use of this drug. Review of the literature revealed 4 fatal outcomes from MDMA-associated hyponatremia. All were women and all died from cerebellar tonsillar herniation. We suggest that acute hyponatremia that develops after MDMA use may be a life-threatening condition. Recent recommendation that MDMA users should drink large volumes of water may not be appropriate.

Topics: Adolescent; Female; Humans; Hyponatremia; N-Methyl-3,4-methylenedioxyamphetamine; Sodium Chloride; Substance-Related Disorders; Vasopressins

Topics: Dehydration; Fluid Therapy; Glucose; Humans; Hyponatremia; Infections; Meningitis; Pediatrics; Sodium Chloride; Vasopressins

Osmotic demyelination of the brain (ODS) is a dreaded complication that typically occurs several days after aggressive therapy for chronic hyponatraemia, but is eminently avoidable. In this teaching exercise, Professor McCance, an imaginary consultant, is asked to explain how he would have treated a 28-year-old female who had hyperkalaemia, hypoglycaemia, hypotension and hyponatraemia (118 mM) to prevent the development of ODS. He begins with a review of the physiology, including his own landmark work on chronic hyponatraemia associated with a contracted extracellular fluid volume. Adding quantitative analysis, the cause of the excessive rise in plasma sodium concentration is revealed, and a better plan for therapy is proposed.

Topics: Addison Disease; Adult; Brain Diseases; Demyelinating Diseases; Female; Humans; Hyperkalemia; Hypoglycemia; Hyponatremia; Hypotension; Renal Agents; Syndrome; Vasopressins; Water-Electrolyte Imbalance

This discussion emphasizes two aspects of hyponatremia: classification according to effective osmolality of the body fluid, and distinction between appropriate and inappropriate ADH secretion. Assessment of the effective osmolality is important because the main deleterious effect of hyponatremia is cell overhydration, which occurs only when the effective osmolality is reduced. Since most cases of hyponatremia are associated with low effective osmolality, cell overhydration is a hallmark of acute hyponatremia. On the other hand, one must be aware of other types of hyponatremia in which effective osmolality is either normal or even increased. Inappropriateness of ADH secretion is defined as ADH secretion that occurs despite low effective osmolality and normal or expanded effective vascular volume. ADH secretion that occurs in hyponatremia is deemed appropriate if the effective vascular volume is low. The use of laboratory parameters is much more reliable in determining effective vascular volume than is careful physical examination.

Topics: Body Water; Extracellular Space; Glucocorticoids; Glucose; Homeostasis; Humans; Hyponatremia; Hypothyroidism; Neurophysins; Osmolar Concentration; Protein Precursors; Transurethral Resection of Prostate; Vasopressins

The development of selective oral V2 receptor antagonists has led to confirmation of established concepts of the pathogenesis of hyponatremia and to new approaches to its treatment. V2 receptor antagonists are effective and promising agents. Their properties as specific pharmacologic tools will facilitate the treatment of the different types of hyponatremia because of the improved predictability of response, and improved control of fine tuning of responses, compared with what is achieved by current therapies. In addition, the quality of life of hyponatremic patients will improve because there will be less need for severe fluid restrictions. It is likely that these agents can be administered over prolonged periods of time.

Topics: Antidiuretic Hormone Receptor Antagonists; Humans; Hyponatremia; Kidney; Receptors, Vasopressin; Vasopressins

Topics: Azepines; Benzamides; Brain Diseases, Metabolic; Humans; Hyponatremia; Inappropriate ADH Syndrome; Liver Cirrhosis; Pyrroles; Vasopressins

Lixivaptan is a non-peptide, orally-active vasopressin antagonist under development by American Home Products for the potential treatment of hyponatremia associated with diseases such as heart failure, liver cirrhosis and nephrotic syndrome. By 1997, it was in phase II trials in the US and elsewhere for hyponatremia [2424051. It selectively prevents vasopressin-dependent water resorption, increasing water excretion with low electrolyte loss [266993] and is selective towards the human V2 versus V1 receptors [295987].

Topics: Animals; Azepines; Benzamides; Clinical Trials as Topic; Humans; Hyponatremia; Pyrroles; Structure-Activity Relationship; Vasopressins

Patients who drink more electrolyte-free water than they can excrete may develop hyponatremia. A subgroup of hyponatremic patients has a reduced excretion of electrolyte-free water and a low rate of excretion of solutes even though vasopressin is not detected in their plasma. Basal water permeability in the distal nephron, by permitting a limited volume of electrolyte-free water to be reabsorbed, offers a way to help explain these findings. Basal water permeability will also be considered from the perspective of integrative physiology in evolutionary and developmental biology settings. Its possible clinical importance will be explored in patients with chronic hyponatremia who have a low distal volume delivery. These patients may develop osmotic demyelination if a large solute load leads to a very rapid excretion of electrolyte-free water.

Topics: Capillary Permeability; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney Tubules, Collecting; Nephrons; Syndrome; Vasopressins; Water-Electrolyte Balance

Hyponatraemia is a frequent electrolyte disorder. It is primarily attributable to vasopressin excess plus sustained fluid intake. Hyponatraemia causes CNS symptoms, especially during the first 2-4 days; these symptoms are related to brain swelling. Hyponatraemia occurs in the setting of liver cirrhosis and congestive cardiac failure, in which it is related to stimulation by low arterial blood pressure acting through baroreceptors. Hyponatraemia also occurs in the syndrome of inappropriate antidiuretic hormone secretion, usually from neoplasms releasing vasopressin. The conventional treatment of hyponatraemia used to be fluid restriction and treatment of the underlying disorder. This kind of treatment has been unreliable, cumbersome and difficult to comply with for the patient. In the future, effective vasopressin V2 antagonists will become available for clinical use in the treatment of hyponatraemia, and are expected to improve the management of hyponatraemia. Pharmacological characteristics and observations of biological effects of three antagonists are reported in the present article.

Topics: Antidiuretic Hormone Receptor Antagonists; Azepines; Benzamides; Benzazepines; Humans; Hyponatremia; Morpholines; Pyrroles; Receptors, Vasopressin; Spiro Compounds; Vasopressins

Disorders of the serum sodium concentration (hypo- and hypernatremia) are amongst the most frequent electrolyte disorders in clinical medicine. They are attributable to disturbance of to water metabolism. Hyponatremia is almost always a condition of water excess while hypernatremia is due water deficiency. Physiological normonatremia (normal plasma osmolality) is maintained by an integrated system involving regulated water intake via thirst and control of water excretion via antidiuretic hormone secretion. Therefore hypo- and hypernatremia should be analyzed in terms of dysregulated ADH secretion, fluid intake and renal water excretion. Hyponatremia is usually a disorder of vasopressin excess, due to 'non-osmotic' vasopressin release. The latter may occur in two different settings: (I) SIADH, (II) baroreceptor mediated vasopressin secretion (cardiac failure, liver cirrhosis). This entities are easy to distinguish in clinical practice. SIADH is associated with striking lower plasma concentrations of urate, creatinine and urea. In SIADH the blood pressure is normal and there is no edema. In contrast in the hyponatremia of liver cirrhosis and heart failure the plasma measurements indicated are usually slightly elevated, the blood pressure is low and there is edema. The typical patient with hypernatremia is old and has no thirst sensation. Hypo- or hypernatremia may cause major neurologic symptoms. These symptoms are more related to the rate of change in the serum sodium concentration than to the absolute level of a hypo- or hypernatremia reached. The traditional treatment for hyponatremia used to be water restriction. However V2-Vasopressin-Antagonists may provide a better treatment modality in the future. Hypernatremia is treated by slow rehydratation.

Topics: Diagnosis, Differential; Drinking; Fluid Therapy; Heart Failure; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Liver Cirrhosis; Vasopressins

Topics: Diagnosis, Differential; Humans; Hyponatremia; Inappropriate ADH Syndrome; Neoplasms; Osmotic Pressure; Plasma Volume; Prognosis; Vasopressins; Water Deprivation

Topics: Animals; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Kidney Concentrating Ability; Vasopressins; Water-Electrolyte Balance

The changes in sodium homeostasis most frequently are expression of water-electrolyte balance disturbances in patients with liver cirrhosis. Hyponatremia of water excess is found in 35% of the patients with cirrhosis and ascites. This disturbance is most frequently connected with raised antidiuretic hormone (vasopressin) secretion and is realized by including of nonosmotic stimulating mechanisms. The vasopressin plays a leading role in pathogenesis of disturbed water metabolism in the liver cirrhosis. Some patients with hepatorenal syndrome are established with highest plasma vasopressin concentrations. Gene expression of the regulation of kidney vasopressin-sensitive water channels (aquaporin-2 proteins) is also raised in the liver cirrhosis. Using in practice vasopressin-type 2 (V-2) receptor antagonists gives hopeful results in medical treatment of water-electrolyte disturbances in patients with advanced liver cirrhosis.

Topics: Gene Expression; Humans; Hyponatremia; Liver Cirrhosis; Renal Insufficiency; Sodium; Vasopressins; Water-Electrolyte Imbalance

Hyponatremia in virtually all patients results from water retention due to an inability to excrete ingested water. In most cases, this defect represents the persistent secretion of ADH (such as in effective circulating volume depletion, and in the syndrome of inappropriate ADH secretion), although free water excretion can also be limited in disorders in which ADH levels may be appropriately suppressed (such as in advanced renal failure, and in primary polydipsia). The symptoms of hyponatremia primarily reflect neurologic dysfunction induced by cerebral edema and are related both to the severity and to the rapidity of reductions in the plasma sodium concentration. The degree of cerebral edema which occurs in acute hyponatremia is much less with chronic hyponatremia, because the brain cells lose solutes, leading to the osmotic movement of water out the cells and less brain swelling. In general, hyponatremia is corrected acutely by giving Na+ to patients who are volume-depleted and by restricting water intake in patients who are normovolemic or edematous. The optimal rate of correction should be defined to prevent the risk of central demyelinating lesions.

Topics: Adrenal Insufficiency; Adult; Brain Edema; Edema; Female; Humans; Hyponatremia; Hypothyroidism; Inappropriate ADH Syndrome; Kidney Failure, Chronic; Models, Biological; Osmolar Concentration; Potassium; Pregnancy; Syndrome; Vasopressins

Topics: Antidiuretic Hormone Receptor Antagonists; Body Water; Humans; Hyponatremia; Kidney; Liver Cirrhosis; Receptors, Vasopressin; Vasopressins

Topics: Adult; Animals; Congenital Hypothyroidism; Diseases in Twins; Female; Humans; Hyponatremia; Hypothyroidism; Infant; Infant, Newborn; Infant, Premature, Diseases; Male; Pregnancy; Thyroxine; Vasopressins

Topics: Age Factors; Aged; Aged, 80 and over; Body Water; Edema; Female; Homeostasis; Humans; Hyponatremia; Kidney Tubules; Male; Osmolar Concentration; Risk Factors; Sodium; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

An impairment in the renal capacity to excrete water is a common finding in patients with cirrhosis and ascites. In some patients this abnormality is minor since it is only detectable by measuring urine volume or free water clearance after a water load and is not associated with changes in plasma osmolality and serum sodium concentration. In other patients the intensity of the disorder is such that they are not able to eliminate their regular water intake, and develop dilutional hyponatremia and hypoosmolality. The renal capacity to excrete water is one of the most useful prognostic indicators in patients with cirrhosis and ascites. The main pathogenic factors of the impaired water excretion in human cirrhosis are an increased plasma concentration of AVP, a reduced renal synthesis of prostaglandins and a reduced delivery of filtrate to the ascending limb of the loop of Henle. At present, no effective therapy exists for the management of this complication. Two types of drugs have recently been reported that selectively increase renal water excretion, antagonists of the AVP V2 receptors and kappa-opioid agonists. Experimental studies have shown that both substances improve water excretion in rats with cirrhosis and ascites. Therefore, these drugs may represent a novel therapeutic tool in the management of spontaneous hyponatremia in cirrhosis and in the treatment or prevention of diuretic-induced hyponatremia in these patients.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Diuresis; Diuretics; Humans; Hyponatremia; Liver Cirrhosis; Receptors, Opioid, kappa; Vasopressins

Hyponatremia is the most frequent electrolyte disorder in clinical medicine. It is usually attributable to primary vasopressin excess, causing the syndrome of inappropriate antidiuresis (SIAD), or to secondary vasopressin stimulation, involving a baroreceptor mechanism. The latter is regularly found in the hyponatremia of liver cirrhosis, cardiac failure and volume contraction. In the first kind of setting the concentrations of creatinine, urea and urate in plasma will be low because of the associated volume expanded state. In the second type of setting they will be elevated because of the circulatory compromise of these patients. The hyponatremia of SIAD may be treated by water restriction, furosemide and substitution of the inadvertent sodium losses by giving 3% NaCl. Baroreceptor hyponatremia is best treated by fluid restriction together with judiciously administered saline. In correcting severe chronic hyponatremia, the rate of correction should not exceed 1 mM/l/h and the corrected serum sodium concentration should not be higher than 130 mM/l. In the foreseeable future oral non-peptide oral vasopressin antagonists will become available. They are expected to become new tools for the treatment of hyponatremia.

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Pressoreceptors; Vasopressins

Hyponatraemia is very common in AIDS patients. It is observed in about 40-50% of hospitalized patients. It may contribute to overall mortality in advanced disease. Vasopressin measurements in these patients basically present two distinct syndromes: hyponatraemia and 'normal' vasopressin levels (i.e. measurable vasopressin) and hyponatraemia with suppressed vasopressin. Hyponatraemia with suppressed vasopressin is very rare and has only been observed in AIDS patients with dementia and primary polydipsia. Hyponatraemia and measurable vasopressin can be also divided into two syndromes. In some patients vasopressin is 'appropriately' elevated, i.e. in those with body fluid losses (diarrhoea) or chronic hypovolaemia (adrenal failure); these patients also present with hyperuricaemia and other signs of low blood volume. In other patients vasopressin is 'inappropriately' elevated in those with no clinical evidence of hypovolaemia (typically characterized by low serum uric acid levels) such as in Pneumocystis carinii pneumonia and other opportunistic infections leading to SIADH. CSWS is a relatively frequent complication in some patients with cerebral infection or tumour. High-dose trimethoprim (for Pneumocystis carinii prevention) acts as an amiloride-like drug and induces a clinical state characterized by hyponatraemia and hyperkalaemia which is indistinguishable from hyporeninaemic hypoaldosteronism. The mechanism of the hyponatraemia caused by other drugs (miconazole, pentamidine, amphotericin, vidarabine) is not as yet known.

Topics: Acquired Immunodeficiency Syndrome; Adrenal Insufficiency; Humans; Hyponatremia; Inappropriate ADH Syndrome; Sodium; Vasopressins; Water-Electrolyte Balance

The kidney and its response to the antidiuretic hormone (ADH) are the principal protective mechanisms necessary to maintain a normal plasma tonicity (osmolality). Hence, determination of the response of the ADH-renal axis to an abnormal plasma tonicity is an important step to understanding water homeostasis. Determination of free water clearance is the most direct clinical method to measure the ability of the kidney to reabsorb or excrete water; it can be used as a sensitive method to study water metabolism, describing the abnormal water homeostasis in simple quantitative terms. A positive electrolyte-free water clearance denotes the excretion of excess free water. A negative electrolyte-free water clearance indicates reabsorption of excess free water. During hypertonicity, an increased concentration of ADH enhances renal reabsorption of free water. With diminished ADH secretion and normal renal function, a substantial volume of free water is cleared in response to hypotonic stimuli. A positive free water clearance > 0.4 L/day in hypertonic conditions or a negative free water clearance during hypotonicity confirms an abnormal ADH-renal axis response.

Topics: Adult; Body Water; Female; Humans; Hypernatremia; Hyponatremia; Kidney; Male; Metabolic Clearance Rate; Osmolar Concentration; Reference Values; Urine; Vasopressins

Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; Child; Child, Preschool; Female; Humans; Hypernatremia; Hyponatremia; Infant; Male; Middle Aged; Renin-Angiotensin System; Sodium; Vasopressins; Water-Electrolyte Imbalance

Heart failure is a syndrome characterized by the activation of neurohumoral mechanisms (sympathoadrenergic, renin-angiotensin, vasopressin) which cause peripheral vasoconstriction, sodium retention and myocardial hypertrophy. In acute myocardial disfunction these systems can play a critical role in patient survival, however, they can directly worsen myocardial function and patient prognosis on a long-term basis. Other neurohumoral systems activated in heart failure (atrial natriuretic factor, prostaglandins, dopamine) tend to counterbalance the vasoconstrictive, sodium retentive mechanisms. Though their secretion is increased in heart failure, it is however not sufficient, and peripheral vasoconstriction and sodium retention prevail. Moreover the role of local factors, such as tissue renin-angiotensin system, EDRF and endothelin secretion has been recently pointed out. Neurohumoral activation is directly related to the severity of the clinical and hemodynamic impairment and prognosis of the patient with heart failure. A thorough evaluation of the neurohumoral mechanisms is therefore of paramount importance for the assessment of patients with heart failure. Neurohumoral activation can be roughly assessed using some simple laboratory measurements: plasma sodium concentration, for example, is inversely related to the degree of activation of many neurohormones such as norepinephrine, angiotensin II, vasopressin and atrial natriuretic factor. The method most commonly used to assess neurohumoral activity relies on the direct measurement of the plasma concentrations. It must be noted, however, that plasma levels are critically dependent on many factors besides hormone secretion and metabolism. For example, 3-4 days on a low sodium diet or standing for at least 2 hours can increase plasma renin activity in a normal subject from 1.5 to 5-10 pg/ml/hr. Plasma concentrations of neurohormones are related to the factors controlling their secretion: for example, "normal" values of plasma renin activity in presence of fluid retention and edema are to be judged as excessively elevated. Autonomic nervous system activity can also be assessed studying reflexes in which this system is involved (orthostasis, cold pressor test, phenylephrine test...). Another method consists in the study of the spontaneous variability of some parameters controlled by this system, such as heart rate and blood pressure. The most reliable method is based on the power spectral analysis of heart rat

Topics: Adrenal Glands; Atrial Natriuretic Factor; Heart Failure; Humans; Hyponatremia; Neurotransmitter Agents; Renin-Angiotensin System; Sympathetic Nervous System; Vasopressins

Discussion of abnormal plasma sodium concentrations with an emphasis on the pathogenesis, diagnosis, and treatment.. Relevant literature in the English language and the authors' clinical experience.. No special study has been carried out for the present discussion.. The information from the literature and the data from the authors' clinical experience have been used to illustrate important points in the discussion.. A most important aspect in the approach to hypernatremia is determination of the mechanism responsible for impaired water intake. Various mechanisms of abnormal water loss can be determined from measurement of urine osmolality. Hypernatremia is treated by water replacement and measures to reduce abnormal water loss. In most instances, hyponatremia is caused by inappropriate concentration of urine because of either appropriate or inappropriate antidiuretic hormone secretion. The determination of appropriateness of antidiuretic hormone secretion requires the assessment of effective arterial volume. Treatment depends on the pathogenetic mechanism.. Abnormal plasma sodium concentration results from abnormal water intake or water output. Treatment is guided by determining the pathogenetic mechanism.

Topics: Diagnosis, Differential; Fluid Therapy; Furosemide; Humans; Hypernatremia; Hyponatremia; Sodium; Vasopressins; Water-Electrolyte Balance

Plasma sodium concentration depends on water balance, and is normally maintained in a narrow range by an integrated system involving the precise regulation of water intake via thirst mechanism and control of water output via vasopressin secretion. Anything that interferes with the full expression of either osmoregulatory function exposes the patient to the hazards of abnormal decreases or increases in plasma sodium level. Hyponatraemia is almost always due to a defect in water excretion. Increased intake may contribute to the problem but is rarely, if ever, a sufficient cause. Hypernatraemia is almost always due to deficient water intake; excessive water losses may contribute to the problem, but they are never a sufficient cause. The most dangerous and usually the most blatant clinical effects of the disturbed water balance are those involving the central nervous system. Complex adaptive mechanisms have been developed to mitigate the impact of both hypo- and hypernatraemia on brain cells. However, the same protective changes render the brain more susceptible to severe neuropathology that may arise from inappropriate treatment of these disorders.

Topics: Diagnosis, Differential; Emergencies; Humans; Hypernatremia; Hyponatremia; Vasopressins; Water-Electrolyte Balance

Topics: Adrenocorticotropic Hormone; Aged; Aged, 80 and over; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Vasopressins

In tuberculous meningitis there is a disturbance of control involving hyponatraemia and increased urinary elimination of antidiuretic hormone resulting in hypersecretion of vasopressin. This inappropriate secretion of antidiuretic hormone should not be confused with the Schwartz-Bartter syndrome, which is reserved for paraneoplastic syndromes. The pathophysiology remains poorly understood but its recognition in cases of lymphocytic meningitis is improved as the correct diagnosis has precise therapeutic implications.

Topics: Aged; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Tuberculosis, Meningeal; Vasopressins

Disorders of water homeostasis are common in psychiatric patients and include compulsive water drinking, the syndrome of inappropriate antidiuretic hormone secretion (SIADH), and the syndrome of self-induced water intoxication (SIWI). Although water intoxication was recognized nearly 70 years ago, the physiological basis of these disorders of water metabolism still remains elusive. This review will provide a historical overview, critique current studies on compulsive water drinking and SIWI, discuss possible etiologies, and present current approaches to treatment of these disorders. Because of the complexity of the subject, a review of normal water homeostasis and the SIADH will be included.

Topics: Drinking; Humans; Hyponatremia; Inappropriate ADH Syndrome; Mental Disorders; Psychotropic Drugs; Thirst; Vasopressins; Water Intoxication

Hyponatremia occurs frequently in the elderly. During aging, mechanisms which regulate the renal handling of water are modified, making easier the occurrence of hyponatremia: osmotic and non osmotic release of ADH is increased whereas renal diluting capacity is depressed. Hyponatremia occurs predominantly during administration of diuretic therapy and/or in congestive cardiac failure. In those circumstances, hyponatremia results from increased non osmotic release of ADH, changes in renal hemodynamics and excessive water intake, as compared to renal diluting capacity. Intracellular hyperhydratation may lead to neurologic damage resulting either from the disorder itself or from a too rapid correction. The latter may be complicated by a cerebral demyelination syndrome. This risk makes necessary to define rules for correction of hyponatremia.

Topics: Aged; Blood; Drinking; Humans; Hyponatremia; Intracellular Fluid; Osmolar Concentration; Vasopressins; Water-Electrolyte Balance

Topics: Blood Volume; Combined Modality Therapy; Heart Failure; Humans; Hyponatremia; Inappropriate ADH Syndrome; Liver Cirrhosis; Nephrotic Syndrome; Vasopressins

Hyponatremia complicates ascitic hepatic cirrhosis with frequency and gravity related to the gravity of the cirrhosis itself. When hyponatremia develops, it worsens the already present secondary hyperaldosteronism and makes therapy with spironolactone inefficacious. From a pathophysiologic viewpoint a pathogenetic role in determining hyponatremia is attributable to the reduced plasmatic renal perfusion; in several patients a syndrome of inappropriate ADH secretion develops. Other neurohormonal systems (catecholamines, prostaglandins, natriuretic hormones) are probably very important in modifying renal hemodynamics and renal tubular function. In some patients a causative role for hyponatremia is attributable to iatrogenic factors (e.g.: diuretics). From a therapeutic viewpoint, we examine some schedules, pharmacologic or not, that, however, are far from being useful for all patients. We discuss, mainly, water restriction, osmotic diuretics with or without loop diuretics, loop diuretics followed by sodium reintegration and concentration-reinfusion of ascites or application of peritoneovenous shunt.

Topics: Ascites; Humans; Hyponatremia; Liver Cirrhosis; Vasopressins

The serum sodium concentration reflects the osmolality of the extracellular fluid and provides no direct information about total body sodium content. Patients with hyponatremia may have decreased, normal, or increased total body sodium content. The first step in the approach to the patient with hyponatremia is measurement of plasma osmolality. Hyponatremia with normal plasma osmolality results from hyperlipemia or hyperproteinemia whereas hyponatremia with increased plasma osmolality results from hyperglycemia or mannitol infusion. Patients with hyponatremia and decreased plasma osmolality may be hypovolemic, hypervolemic, or normovolemic. The volume status of the patient is best determined by history, physical examination, and a few ancillary tests (e.g., total plasma protein concentration, hematocrit, blood pressure, central venous pressure). The clinical signs of hyponatremia are related more to the rapidity of onset than to the severity of the associated plasma hypoosmolality and reflect influx of water into the central nervous system. The main goals of treatment in hyponatremia are to manage the underlying disease and, if necessary, to increase serum sodium concentration and plasma osmolality.

Topics: Animals; Dog Diseases; Dogs; Hyponatremia; Osmolar Concentration; Sodium; Vasopressins; Water-Electrolyte Balance

A male quadriplegic (C6--complete) with persistent chronic hyponatremia (serum sodium values ranging consistently from 117-132 mmol/L) developed acute hyponatremia with a serum sodium concentration of 98 mmol/L. This extreme hyponatremia related, in part, to a reversible defect in the excretion of a water load, while on a low (46 mmol/day) sodium diet. Subsequent ingestion of a normal sodium diet (150 mmol/day), with or without 0.1 mg of fludrocortisone (Florinef), reestablished his ability to excrete a water load normally. The etiology of this patient's hyponatremia is discussed as well as the unique concordance of factors which make hyponatremia a common occurrence among spinal-cord injured patients.

Topics: Acute Disease; Diet, Sodium-Restricted; Fludrocortisone; Humans; Hyponatremia; Male; Middle Aged; Osmolar Concentration; Sodium, Dietary; Spinal Cord Injuries; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Antineoplastic Agents; Diuretics; Drug-Related Side Effects and Adverse Reactions; Humans; Hypokalemia; Hyponatremia; Natriuresis; Potassium; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Aged; Female; Humans; Hyponatremia; Male; Middle Aged; Pneumonia; Vasopressins; Water-Electrolyte Imbalance

It was observed that hyponatremia has been evaluated by many studies of patients and laboratory animals. In virtually all of these the presence of nonosmotic ADH has been shown, but several details of this relationship remain controversial at this time. The role of specific receptor areas for ADH stimulation requires further study, particularly in the hyponatremia of a decreased effective arterial blood volume. In addition, it will be important to define the suspected vascular effects of nonosmotic ADH more specifically. Other areas of uncertainty include: the degree to which the tubular effect of ADH in hyponatremia may be modified by a decreased delivery of fluid to the loops of Henle; the potential stimulation of ADH by stress in clinical hyponatremia; and the meaning of very low or non-measurable concentrations of ADH in hyponatremia. New experimental tools such as vasopressin antagonists and agonists, measurements of baroreceptor input, and tests of proximal fluid reabsorption can be expected to clarify some of these questions in the near future.

Topics: Animals; Blood Volume; Humans; Hyponatremia; Receptors, Angiotensin; Receptors, Vasopressin; Vasopressins

Topics: Animals; Body Water; Homeostasis; Humans; Hyponatremia; Inappropriate ADH Syndrome; Nutritional Physiological Phenomena; Sodium Chloride; Thirst; Vasopressins; Water-Electrolyte Balance

Normal osmoregulation is maintained by the proper function and interplay of factors influencing thirst, renal water metabolism, and vasopressin secretion. In pathophysiologic states, body water homeostasis is disrupted and hyponatremia ensures. Hyponatremia associated with cardiac failure, hepatic failure, respiratory failure, diabetes mellitus, the postoperative state, and other disorders is commonly found in the critical care setting. The pathophysiology, diagnosis, and treatment of hyponatremia are discussed.

Topics: Body Water; Humans; Hyponatremia; Kidney Diseases; Multiple Organ Failure; Osmolar Concentration; Thirst; Vasopressins

It is apparent that renal water retention in patients with advanced liver disease constitutes a fascinating clinical constellation with numerous and diverse causes and an elusive pathophysiology. The dissociation between elevated AVP levels and the attendant changes in renal water handling under diverse experimental conditions, and the demonstration of an impairment in renal water excretion in response to prostaglandin synthetase inhibition, underscore the multifactorial nature of the derangement. It is likely that the development of impaired renal water handling is attributable to a panoply of several hormonal or neural mediators, or both, acting in concert. Additional insight into this fascinating problem must await further characterization of some of the mediators and a delineation of their pathophysiologic role.

Topics: Body Water; Catecholamines; Glomerular Filtration Rate; Humans; Hyponatremia; Kidney; Liver Cirrhosis; Liver Diseases; Prostaglandins; Sympathetic Nervous System; Vasopressins; Water-Electrolyte Imbalance

Topics: Demeclocycline; Humans; Hyponatremia; Vasopressins

Topics: Body Water; Extracellular Space; Humans; Hyponatremia; Kidney; Kidney Concentrating Ability; Osmolar Concentration; Sodium; Vasopressins

Topics: Body Water; Diuretics; Extracellular Space; Glucocorticoids; Humans; Hyperlipidemias; Hyponatremia; Inappropriate ADH Syndrome; Kidney Failure, Chronic; Lithium; Lithium Carbonate; Osmolar Concentration; Sodium; Vasodilator Agents; Vasopressins

Topics: Age Factors; Aged; Benzothiadiazines; Body Water; Body Weight; Diuretics; Female; Furosemide; Humans; Hyponatremia; Iatrogenic Disease; Inappropriate ADH Syndrome; Male; Middle Aged; Potassium; Prognosis; Risk; Sex Factors; Sodium; Sodium Chloride; Sodium Chloride Symporter Inhibitors; Vasopressins

Topics: Animals; Body Water; Demeclocycline; Diuretics; Humans; Hyponatremia; In Vitro Techniques; Kidney Tubules; Lithium; Structure-Activity Relationship; Vasopressins

Topics: Animals; Blood; Blood Pressure; Blood Volume; Diabetes Insipidus; Diuresis; Female; Humans; Hyperaldosteronism; Hypernatremia; Hyponatremia; Hypothalamus; Lung Neoplasms; Nausea; Osmolar Concentration; Pituitary Gland, Posterior; Pregnancy; Pressoreceptors; Sodium; Thirst; Urine; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Topics: Animals; Central Nervous System Diseases; Diagnosis, Differential; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Inappropriate ADH Syndrome; Neoplasms; Nephrons; Vasopressins; Water-Electrolyte Imbalance

Vasopressin is capable of being stimulated by several nonosmotic factors such as hypovolemia, hypotension, pharmacologic agents and stress. Vasopressin levels of only 1-2 pg/ml are capable of decreasing substantially renal water excretion. If water is ingested or given intravenously in this setting, positive water balance with hypotonicity and hyponatremia of extracellular fluid (ECF) occur. Such dilution of the ECF results in water movement into cells and potential central nervous system complications [3]. Many disorders (see Tab. 1) may be associated with nonosmotic stimulation of vasopressin release. In these clinical settings, judicious administration of free water and monitoring of serum sodium concentration is necessary. A knowledge of clinical conditions associated with vasopressin-mediated water retention may have therapeutic implications as well. Thus, in recent years it has become appreciated that selected pharmacologic agents such as lithium and demeclocycline can impair the water retaining property of vasopressin [26]. Although lithium appears too toxic for routine usage, demeclocycline has proved to be efficacious therapy in some patients with high vasopressin levels and hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone who are unable to limit their water intake [9]. More recently, other compounds that selectively antagonize the hydro-osmotic effect of vasopressin are being tested and soon may be available [13].

Topics: Adrenal Cortex Diseases; Blood Volume; Diuresis; Extracellular Space; Humans; Hyponatremia; Hypothyroidism; Inappropriate ADH Syndrome; Liver Cirrhosis; Osmosis; Respiratory Insufficiency; Vasopressins

Topics: Adrenal Cortex Hormones; Arrhythmias, Cardiac; Cardiovascular Diseases; Catecholamines; Cerebrovascular Disorders; Humans; Hyperglycemia; Hypertension; Hyponatremia; Models, Biological; Pulmonary Edema; Vasopressins

Nonsteroidal antiinflammatory drugs can adversely affect the kidney. They may induce sodium retention and antagonize the action of diuretics, impair free-water clearance and cause hyponatremia, and prevent aldosterone production and cause hyperkalemic hyperchloremic acidosis. If patients taking these drugs are exposed to a renal insult, acute renal failure becomes more likely. Similarly, patients with chronic renal disease who are taking them appear to be at greater risk of chronic renal failure. However, not all renal effects of nonsteroidal antiinflammatory drugs are adverse. Beneficial effects have been reported in patients with Bartter's syndrome and in those with severe orthostatic hypotension.

Topics: Acidosis; Acute Kidney Injury; Aged; Anti-Inflammatory Agents; Bartter Syndrome; Female; Humans; Hyponatremia; Hypotension, Orthostatic; Ibuprofen; Indomethacin; Kidney; Kidney Failure, Chronic; Lupus Erythematosus, Systemic; Nephrotic Syndrome; Prostaglandin Antagonists; Sodium; Vasopressins

Topics: Benzothiadiazines; Diuretics; Humans; Hyponatremia; Hypotonic Solutions; Iatrogenic Disease; Parenteral Nutrition; Sodium Chloride Symporter Inhibitors; Vasopressins; Vincristine

Topics: Acute Disease; Arginine Vasopressin; Chronic Disease; Hyponatremia; Osmolar Concentration; Sodium Chloride; Urine; Vasopressins; Water; Water-Electrolyte Balance

Topics: Adrenocorticotropic Hormone; Chorionic Gonadotropin; Cushing Syndrome; Erythropoietin; Gastrointestinal Hormones; Hormones, Ectopic; Hypercalcemia; Hypoglycemia; Hyponatremia; Melanocyte-Stimulating Hormones; Neurologic Manifestations; Paraneoplastic Endocrine Syndromes; Parathyroid Hormone; Polycythemia; Prostaglandins E; Somatomedins; Vasopressins

Topics: Brain Diseases; Diabetes Insipidus; Electrolytes; Humans; Hypernatremia; Hyponatremia; Postoperative Complications; Vasopressins; Water; Water Intoxication; Water-Electrolyte Imbalance

Topics: Angiotensin II; Animals; Blood Pressure; Hypertension, Malignant; Hypertension, Renal; Hyponatremia; Juxtaglomerular Apparatus; Osmolar Concentration; Pepstatins; Plasma Volume; Rats; Renin; Saralasin; Vasopressins; Water-Electrolyte Imbalance

Topics: Benzothiadiazines; Body Water; Diabetes Insipidus; Diuretics; Humans; Hypernatremia; Hypertension, Renal; Hyponatremia; Hypothalamus; Infusions, Parenteral; Kidney Concentrating Ability; Osmotic Pressure; Pituitary Gland; Sodium; Sodium Chloride; Sodium Chloride Symporter Inhibitors; Vasopressins

SIADH consists of hyponatremia and hyposmolality, continued urinary loss of sodium, excretion of an inappropriately concentrated urine, and absence of dehydration, usually in the presence of normal renal and adrenal function. The retention of excess water caused by the inappropriate secretion of antidiuretic hormone is central to the development of the syndrome. In pediatrics, SIADH is most commonly seen in patients with meningitis or postoperatively. Fluid restriction is vital in such patients to prevent the development of symptomatic SIADH. Fluid restriction alone will also result in the correction of serum electrolyte composition in patients with SIADH. Hypertonic saline should be used only in severely symptomatic patients.

Topics: Adult; Aldosterone; Blood Volume; Child; Diuresis; Drinking; Ethanol; Humans; Hyponatremia; Kidney Concentrating Ability; Kidney Tubules, Distal; Kidney Tubules, Proximal; Lithium; Osmolar Concentration; Saline Solution, Hypertonic; Sodium; Syndrome; Vasopressins; Water Intoxication; Water-Electrolyte Imbalance

Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Animals; Blood Volume; Diabetes Insipidus; Feedback; Hormones, Ectopic; Humans; Hyponatremia; Kidney; Osmolar Concentration; Pancreas; Paraneoplastic Endocrine Syndromes; Stress, Physiological; Sweat Glands; Vasopressins; Water-Electrolyte Balance

Topics: Adrenocortical Hyperfunction; Adult; Carcinoid Heart Disease; Cushing Syndrome; Endocrine System Diseases; Gynecomastia; Humans; Hypercalcemia; Hyperparathyroidism; Hyperthyroidism; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Osmolar Concentration; Osteoarthropathy, Secondary Hypertrophic; Syndrome; Vasopressins

Topics: Adult; Blood Proteins; Diabetic Coma; Diuresis; Female; Humans; Hypertonic Solutions; Hyponatremia; Kidney Diseases; Lipids; Male; Mannitol; Middle Aged; Osmolar Concentration; Peritoneal Dialysis; Renal Dialysis; Sodium Chloride; Vasopressins; Water Intoxication

Topics: Humans; Hyponatremia; Syndrome; Vasopressins

Topics: Adenylyl Cyclases; Adrenal Glands; Adult; Animals; Body Water; Chlorpropamide; Dehydration; Diabetes Insipidus; Genes; Growth Hormone; Heterozygote; Humans; Hyponatremia; Hypothalamus; Oxytocin; Pituitary Gland; Pituitary Gland, Posterior; Rats; Sodium; Vasopressins

Topics: Abdomen; Autonomic Nervous System; Axons; Constipation; Cranial Nerves; Depression; Diabetic Neuropathies; Drug Interactions; Hallucinations; Humans; Hyponatremia; Hypotension, Orthostatic; Intestinal Obstruction; Muscular Atrophy; Nervous System Diseases; Neural Conduction; Norepinephrine; Pain; Paresthesia; Parkinson Disease; Peripheral Nervous System Diseases; Seizures; Vasopressins; Vincristine

Topics: Acetaminophen; Amitriptyline; Animals; Anura; Body Fluids; Carbamazepine; Chlorpropamide; Clofibrate; Cyclophosphamide; Diabetes Insipidus; Diabetes Mellitus; Diazoxide; Drug-Related Side Effects and Adverse Reactions; Humans; Hypoglycemic Agents; Hyponatremia; Kidney; Rats; Sodium; Sulfonylurea Compounds; Tolbutamide; Urinary Bladder; Vasopressins; Vincristine; Water Intoxication; Water-Electrolyte Balance

Topics: Addison Disease; Ascites; Edema; Extracellular Space; Heart Failure; Humans; Hyponatremia; Intestinal Secretions; Kidney Failure, Chronic; Liver Cirrhosis; Potassium; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adrenal Insufficiency; Diet, Sodium-Restricted; Diuretics; Humans; Hyponatremia; Neoplasms; Nephritis; Paraneoplastic Endocrine Syndromes; Sodium; Vasopressins

Topics: Animals; Body Fluids; Cell Membrane Permeability; Chlorides; Dogs; Extracellular Space; Heart Failure; Humans; Hyponatremia; Infant Nutrition Disorders; Kidney; Liver Cirrhosis; Neoplasms; Osmolar Concentration; Potassium; Respiratory Insufficiency; Sodium; Vasopressins; Water; Whipple Disease

Topics: Adolescent; Bronchial Neoplasms; Carcinoma, Small Cell; Child, Preschool; Cushing Syndrome; Diagnosis, Differential; Hormones, Ectopic; Humans; Hyperaldosteronism; Hypercalcemia; Hyperparathyroidism; Hyponatremia; Kidney Neoplasms; Paraneoplastic Endocrine Syndromes; Renin; Sodium Chloride; Syndrome; Vasopressins

Topics: Carcinoma, Small Cell; Central Nervous System Diseases; Endocrine System Diseases; Hormones, Ectopic; Humans; Hyponatremia; Kidney; Lung Diseases; Lung Neoplasms; Osmolar Concentration; Paraneoplastic Endocrine Syndromes; Syndrome; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Adrenal Gland Diseases; Diabetes Insipidus; Diabetic Nephropathies; Diagnosis, Differential; Diuresis; Glomerular Filtration Rate; Humans; Hypercalcemia; Hyponatremia; Kidney; Kidney Concentrating Ability; Kidney Diseases; Natriuresis; Osmolar Concentration; Urologic Diseases; Vasopressins; Water-Electrolyte Balance

Topics: Acute Kidney Injury; Animals; Blood; Cardiac Glycosides; Dehydration; Diuretics; Glomerular Filtration Rate; Heart Failure; Hyponatremia; Kidney Failure, Chronic; Liver Cirrhosis; Mineralocorticoid Receptor Antagonists; Nephrotic Syndrome; Sodium; Syndrome; Vasopressins; Water

Topics: 5-Hydroxytryptophan; Acanthosis Nigricans; Carcinoid Tumor; Carotid Body Tumor; Catecholamines; Cushing Syndrome; Dermatomyositis; Endocrine System Diseases; Gynecomastia; Hormones, Ectopic; Humans; Hypercalcemia; Hyperthyroidism; Hypoglycemia; Hyponatremia; Neoplasms; Neuromuscular Diseases; Osteoarthropathy, Secondary Hypertrophic; Peripheral Nervous System Diseases; Polycythemia; Puberty, Precocious; Syndrome; Toxins, Biological; Vascular Diseases; Vasopressins; Zollinger-Ellison Syndrome

Topics: Adrenal Glands; Aldosterone; Feedback; Glomerular Filtration Rate; Humans; Hyponatremia; Kidney; Kidney Diseases; Kidney Neoplasms; Mixed Function Oxygenases; Natriuresis; Sodium; Vasopressins; Water Intoxication

Topics: Adrenal Insufficiency; Carcinoma, Bronchogenic; Diagnosis, Differential; Hormones, Ectopic; Humans; Hyponatremia; Lung Neoplasms; Neurologic Manifestations; Phenytoin; Syndrome; Vasopressins

Topics: Chlorides; Humans; Hydrogen-Ion Concentration; Hypernatremia; Hyponatremia; Infusions, Parenteral; Sodium; Vasopressins; Water Intoxication

Topics: Brain Diseases; Bronchial Neoplasms; Deficiency Diseases; Diuresis; Ethanol; Hyponatremia; Kidney Concentrating Ability; Natriuresis; Respiratory Tract Diseases; Vasopressins

Topics: Carcinoma, Bronchogenic; Diuresis; Ethacrynic Acid; Hormones, Ectopic; Humans; Hyponatremia; Kidney Function Tests; Vasopressins

Topics: Adrenal Gland Diseases; Central Nervous System Diseases; Diagnosis, Differential; Humans; Hyponatremia; Hypothalamus; Vasopressins; Water Intoxication

Topics: Adult; Aged; Blood; Body Fluids; Central Nervous System Diseases; Child; Female; Hormones, Ectopic; Humans; Hypernatremia; Hyponatremia; Male; Osmolar Concentration; Pituitary Gland; Vasopressins

Topics: Brain Diseases; Female; Humans; Hypernatremia; Hypokalemia; Hyponatremia; Male; Metabolic Diseases; Vasopressins; Water-Electrolyte Balance

Topics: Central Nervous System Diseases; Child; Edema; Endocrine System Diseases; Humans; Hyponatremia; Hypopituitarism; Lung Diseases; Male; Middle Aged; Neoplasms; Vasopressins

Topics: Adrenocorticotropic Hormone; Endocrine System Diseases; Erythropoietin; Gynecomastia; Hormones, Ectopic; Humans; Hypercalcemia; Hyperthyroidism; Hypoglycemia; Hyponatremia; Insulin; Luteinizing Hormone; Melanocyte-Stimulating Hormones; Neoplasms; Parathyroid Hormone; Polycythemia; Puberty, Precocious; Thyrotropin; Vasopressins

Topics: Arginine; Diabetes Insipidus; Diuresis; Humans; Hyponatremia; Lung Neoplasms; Pituitary Diseases; Pituitary Gland, Posterior; Vasopressins; Water-Electrolyte Balance

Topics: Bloodletting; Carbonic Anhydrase Inhibitors; Chlorides; Diet, Sodium-Restricted; Digitalis Glycosides; Diuresis; Diuretics; Ethacrynic Acid; Furosemide; Heart Failure; Humans; Hyperkalemia; Hypokalemia; Hyponatremia; Kidney Glomerulus; Kidney Tubules; Mineralocorticoid Receptor Antagonists; Organomercury Compounds; Spironolactone; Steroids; Thiazines; Triamterene; Uracil; Vasopressins; Water-Electrolyte Balance; Xanthenes

Topics: Humans; Hyponatremia; Lung Neoplasms; Vasopressins

Topics: Alcohols; Body Water; Central Nervous System Diseases; Child; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diuresis; Edema; Ethanol; Histiocytosis, Langerhans-Cell; Homeostasis; Humans; Hyponatremia; Infant; Infant, Newborn; Kidney Diseases; Nicotine; Physiology; Pituitary Gland; Pituitary Gland, Posterior; Potassium Deficiency; Prednisone; Pyloric Stenosis; Vasopressins; Water

Topics: Adenoma, Islet Cell; Adrenocortical Hyperfunction; Adrenocorticotropic Hormone; Alkalosis; Cushing Syndrome; Electrolytes; Endocrinology; Humans; Hypernatremia; Hypokalemia; Hyponatremia; Neoplasms; Pancreatic Neoplasms; Vasopressins; Water-Electrolyte Balance

Previous trials have suggested that vasopressin and methylprednisolone administered during in-hospital cardiac arrest might improve outcomes.. To determine whether the combination of vasopressin and methylprednisolone administered during in-hospital cardiac arrest improves return of spontaneous circulation.. Multicenter, randomized, double-blind, placebo-controlled trial conducted at 10 hospitals in Denmark. A total of 512 adult patients with in-hospital cardiac arrest were included between October 15, 2018, and January 21, 2021. The last 90-day follow-up was on April 21, 2021.. Patients were randomized to receive a combination of vasopressin and methylprednisolone (n = 245) or placebo (n = 267). The first dose of vasopressin (20 IU) and methylprednisolone (40 mg), or corresponding placebo, was administered after the first dose of epinephrine. Additional doses of vasopressin or corresponding placebo were administered after each additional dose of epinephrine for a maximum of 4 doses.. The primary outcome was return of spontaneous circulation. Secondary outcomes included survival and favorable neurologic outcome at 30 days (Cerebral Performance Category score of 1 or 2).. Among 512 patients who were randomized, 501 met all inclusion and no exclusion criteria and were included in the analysis (mean [SD] age, 71 [13] years; 322 men [64%]). One hundred of 237 patients (42%) in the vasopressin and methylprednisolone group and 86 of 264 patients (33%) in the placebo group achieved return of spontaneous circulation (risk ratio, 1.30 [95% CI, 1.03-1.63]; risk difference, 9.6% [95% CI, 1.1%-18.0%]; P = .03). At 30 days, 23 patients (9.7%) in the intervention group and 31 patients (12%) in the placebo group were alive (risk ratio, 0.83 [95% CI, 0.50-1.37]; risk difference: -2.0% [95% CI, -7.5% to 3.5%]; P = .48). A favorable neurologic outcome was observed in 18 patients (7.6%) in the intervention group and 20 patients (7.6%) in the placebo group at 30 days (risk ratio, 1.00 [95% CI, 0.55-1.83]; risk difference, 0.0% [95% CI, -4.7% to 4.9%]; P > .99). In patients with return of spontaneous circulation, hyperglycemia occurred in 77 (77%) in the intervention group and 63 (73%) in the placebo group. Hypernatremia occurred in 28 (28%) and 27 (31%), in the intervention and placebo groups, respectively.. Among patients with in-hospital cardiac arrest, administration of vasopressin and methylprednisolone, compared with placebo, significantly increased the likelihood of return of spontaneous circulation. However, there is uncertainty whether this treatment results in benefit or harm for long-term survival.. ClinicalTrials.gov Identifier: NCT03640949.

Topics: Aged; Cardiovascular Agents; Confidence Intervals; Denmark; Double-Blind Method; Epinephrine; Female; Glucocorticoids; Heart Arrest; Humans; Hyperglycemia; Hyponatremia; Male; Methylprednisolone; Neurologic Examination; Placebos; Return of Spontaneous Circulation; Treatment Outcome; Uncertainty; Vasoconstrictor Agents; Vasopressins

The purpose of this study was to determine the efficacy and safety of tolvaptan in Japanese patients with hyponatremia secondary to syndrome of inappropriate secretion of antidiuretic hormone (SIADH). This multicenter, open-label, dose-escalation, phase III study enrolled Japanese patients (20-85 years old) with hyponatremia secondary to SIADH who were unresponsive to fluid restriction. Oral tolvaptan was administered for up to 30 days, initially at 7.5 mg/day, but escalated daily as necessary, based on the serum sodium concentration and safety, over the first 10 days until the optimal maintenance dose was determined for each patient (maximum 60 mg/day). The primary endpoint was the proportion of patients with normalized serum sodium concentration on the day after the final tolvaptan dose. Secondary endpoints included the mean change in serum sodium concentration from baseline on the day after the final dose. Sixteen patients (male, 81.3%; mean ± standard deviation age 71.9 ± 6.1 years) received tolvaptan treatment and 11 patients completed the study with one patient re-administered tolvaptan in the treatment period. Serum sodium concentrations normalized in 13 of 16 (81.3%) patients on the day after the final tolvaptan dose. The mean change in serum sodium concentration from baseline on the day after the final dose was 11.0 ± 4.3 mEq/L. Adverse events considered related to tolvaptan (10 [62.5%] patients) were generally of mild to moderate severity. Oral tolvaptan corrects hyponatremia in Japanese patients with SIADH with a similar efficacy and safety profile as that noted in non-Japanese patients.

Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Dose-Response Relationship, Drug; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Japan; Male; Middle Aged; Tolvaptan; Treatment Outcome; Vasopressins; Young Adult

The approach to hyponatremia is in a state of flux, especially in differentiating syndrome of inappropriate antidiuretic hormone secretion (SIADH) from cerebral-renal salt wasting (RSW) because of diametrically opposite therapeutic goals. Considering RSW can occur without cerebral disease, we determined the prevalence of RSW in the general hospital wards.. To differentiate SIADH from RSW, we used an algorithm based on fractional excretion (FE) of urate and nonresponse to saline infusions in SIADH as compared to excretion of dilute urines and prompt increase in serum sodium in RSW.. Of 62 hyponatremic patients, (A) 17 patients (27%) had SIADH, 11 were nonresponsive to isotonic saline, and 5 normalized a previously high FEurate after correction of hyponatremia; (B) 19 patients (31%) had a reset osmostat based on normal FEurates and spontaneously excreted dilute urines; (C) 24 patients (38%) had RSW, 21 had no clinical evidence of cerebral disease, 19 had saline-induced dilute urines; 2 had undetectable plasma ADH levels when urine was dilute, 10 required 5% dextrose in water to prevent rapid increase in serum sodium, 11 had persistently increased FEurate after correction of hyponatremia and 10 had baseline urinary sodium < 20 mEq/L; (D) 1 patient had Addison disease with a low FEurate and (E) 1 patient (1.6%) had hyponatremia due to hydrochlorothiazide.. Of the 24 patients with RSW, 21 had no cerebral disease, supporting our proposal to change cerebral-renal salt wasting to renal salt wasting. Application of established pathophysiological standards and a new algorithm based on determination of FEurate were superior to the volume approach for determination of urinary sodium when identifying the cause of hyponatremia.

Topics: Aged; Aged, 80 and over; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Prevalence; Saline Solution; Uric Acid; Vasopressins

Depressed hemodynamics stimulates arginine vasopressin (AVP) release, but the relationship between plasma AVP levels (P-AVP) and cardiac parameters, especially in patients with stage D heart failure (HF) receiving guideline-directed medical therapy, has not examined. METHODS AND RESULTS: Data including P-AVP were obtained from 162 in-hospital patients with stage D HF and from 80 patients receiving ventricular assist device (VAD, n=46) or heart transplantation (HTx, n=34) at 3 months after surgery. In the HF group, considerably high P-AVP (5.9±6.1 pg/ml) negatively correlated with serum sodium concentration (S-Na, 135.3±5.8 mEq/L, r=-0.548 [P<0.01]) and cardiac index (CI, 2.2±0.5 L·min(-1)·m(-2), r=-0.458 [P<0.01]). After VAD/HTx treatment, improvement in the CI (2.7±0.5 L·min(-1)·m(-2)[P<0.01] vs. HF) was accompanied by normalization of serum sodium concentration (S-Na; 138.2±2.0 mEq/L [P<0.01] vs. HF) and suppressed release of AVP (1.7±3.4 pg/ml [P<0.01] vs. HF). P-AVP positively correlated with only S-Na (r=0.454 [P<0.01]), whereas no correlation was observed with CI after VAD/HTx treatment. P-AVP ≥5.3 pg/ml well predicted poor 2-year survival in HF group (60% [P<0.01] vs. 90%).. Low cardiac output stimulates AVP release via a non-osmotic process that results in hyponatremia and poor prognosis in patients with stage D HF. After sufficient recovery of cardiac output by cardiac replacement therapy, AVP release is suppressed and is mainly regulated by serum osmolality.

Topics: Adult; Aged; Cardiac Output, Low; Heart Failure; Humans; Hyponatremia; Middle Aged; Vasopressins; Water-Electrolyte Balance

Medical textbooks often list Legionnaires' disease as a differential diagnosis of the syndrome of inappropriate secretion of anti-diuretic hormone (ADH) (SIADH), but evidence supporting this association is largely lacking. We tested the hypothesis whether hyponatremia in patients with Legionnaires' disease would be caused by increased CT-ProVasopressin.. We measured CT-ProVasopressin and sodium levels in a prospective cohort of 873 pneumonia patients from a previous multicentre study with 27 patients having positive antigen tests for Legionella pneumophila.. Patients with Legionnaires' disease more frequently had low sodium levels (Na < 130 mmol/L) (44.4% vs 8.2%, p < 0.01), but similar mean CT-ProVasopressin levels (pmol/l) (39.4 [±7] vs 51.2 [±2.7], p = 0.43) as compared to patients with pneumonia of other etiologies. In patients with Legionnaires' disease, CT-ProVasopressin levels showed a positive correlation with sodium (r = 0.42, p < 0.05). Independent of pneumonia etiology, CT-ProVasopressin correlated significantly with the pneumonia severity index (r = 0.56, p < 0.05), ICU admission (adjusted odds ratio per decile, 95% CI) (1.6, 1.2 - 2.0), and 30-day-mortality (1.8, 1.3 - 2.4).. While Legionnaires' disease was associated with hyponatremia, no concurrent increase in CT-ProVasopressin levels was found, which argues against elevated ADH levels as the causal pathway to hyponatremia. Rather, Vasopressin precursors were upregulated as response to stress in severe disease, which seems to overrule the osmoregulatory regulation of ADH.

Topics: Aged; Calcitonin; Female; Humans; Hyponatremia; Legionnaires' Disease; Male; Middle Aged; Pneumonia; Prospective Studies; Protein Precursors; Sodium; Vasopressins

Arginine vasopressin (AVP) V(2) receptor antagonism is a new approach to the management of hyponatraemia in congestive heart failure (CHF). The aim of this study was to investigate the efficacy and safety of satavaptan, an oral AVP V(2)-receptor antagonist, in patients with dilutional hyponatraemia.. A total of 118 patients (90 with CHF) with dilutional hyponatraemia (serum sodium 115-132 mmol/L) were randomized to double-blind treatment with placebo or to 25 or 50 mg/day of satavaptan for 4 days, followed by non-comparative open-label satavaptan therapy for up to 343 days. The response rate (sodium ≥ 135 mmol/L and/or an increase in ≥ 5 mmol/L above baseline) was significantly higher with satavaptan 50 mg than with placebo (61.0 vs. 26.8%; P= 0.0035), with a trend towards significance with satavaptan 25 mg (48.6%, P= 0.0599). Median times to response were 3.30 and 2.79 days with satavaptan 25 and 50 mg/day, respectively, both shorter than placebo (>4 days; P= 0.0278 and P= 0.0004, respectively). Satavaptan therapy was effective in CHF patients, with response rates higher with both satavaptan 25 mg/day (53.6%) and 50 mg/day (57.1%) than with placebo (23.5%; P= 0.019 and P= 0.009, respectively). Sodium responses were maintained during open-label therapy after a temporary study drug discontinuation period. Higher rates of adverse events occurred with the 50 mg/day dose, including rapid correction of hyponatraemia.. In patients with dilutional hyponatraemia, V(2) receptor antagonism with satavaptan was effective in increasing serum sodium concentrations. The long-term open-label treatment results demonstrate sustained efficacy of satavaptan in maintaining normal sodium levels. Trial Registration clinicaltrials.gov Identifier: NCT00274326.

Topics: Adult; Aged; Antidiuretic Hormone Receptor Antagonists; Body Weight; Double-Blind Method; Female; Heart Failure; Humans; Hyponatremia; Kaplan-Meier Estimate; Male; Middle Aged; Morpholines; Sodium; Spiro Compounds; Treatment Outcome; Vasopressins; Young Adult

To determine the importance of sodium content versus administration rate of intravenous fluids in the development of hyponatremia in postoperative children.. In this prospective, randomized, nonblinded study, 124 children admitted for surgery received 0.9% (NS) or 0.45% (N/2) saline solution at 100% or 50% maintenance rates. Plasma electrolytes, osmolality, and ADH at induction of anesthesia were compared with values 8 hours (T(8)), and 24 hours (T(24); n = 67) after surgery. Blood glucose and ketones were measured every 4 hours. Electrolytes and osmolality were measured in urine samples.. Plasma sodium concentrations fell in both N/2 groups at T(8) (100%: -1.5 +/- 2.3 mmol/L 50%: -1.9 +/- 2.0 mmol/L; P < .01) with hyponatremia more common than in the NS groups at T(8) (30% vs 10%; P = .02) but not T(24). Median plasma antidiuretic hormone concentrations increased 2- to 4-fold during surgery (P < or = .001) and only reattained levels at induction of anesthesia by T(24) in the N/2 100% group. On multiple linear regression analysis, fluid type, not rate determined risk of hyponatremia (P < .04). Two children on 100% developed SIADH (1NS). Fourteen (23%; 7NS) on 50% maintenance were assessed as dehydrated. Dextrose content was increased in 18 for hypoglycemia or ketosis.. The risk of hyponatremia was decreased by isotonic saline solution but not fluid restriction.

Topics: Adolescent; Child; Child, Preschool; Female; Fluid Therapy; Humans; Hyponatremia; Infant; Infusions, Intravenous; Isotonic Solutions; Linear Models; Male; Multivariate Analysis; Osmolar Concentration; Postoperative Care; Prospective Studies; Sodium Chloride; Vasopressins; Water-Electrolyte Balance

This study investigated the development of hyponatremia and its underlying mechanism in elderly patients prescribed paroxetine. Patients were 15 men and women (mean age, 75.7 +/- 5.3 years) who were participants in a treatment study of late-life depression and who were without medical illness or other medications known to cause hyponatremia or alter antidiuretic hormone (ADH) secretion. Blood samples for measurement of plasma sodium, ADH, blood urea nitrogen (BUN), creatinine, glucose, and osmolality were determined prior to initiation of paroxetine (week 0) and at 2, 4, 6, and 12 weeks of treatment with paroxetine. Hyponatremia (serum sodium < 135 mEq/L) was identified in 6 of 15 patients after 2 weeks of treatment with paroxetine. Despite low plasma osmolality, ADH levels were not suppressed appropriately. Data suggest hyponatremia is a common adverse event in elderly patients prescribed paroxetine and implicates inappropriate secretion of ADH as the potential mechanism.

Topics: Aged; Depressive Disorder, Major; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Osmolar Concentration; Paroxetine; Pilot Projects; Prospective Studies; Selective Serotonin Reuptake Inhibitors; Severity of Illness Index; Vasopressins

The mechanism(s) of hyponatremia of cirrhosis is not completely clarified. Although increased vasopressin activity has been proposed in some studies, there have been reports disputing its role in the pathogenesis of profound hyponatremia in patients with decompensated liver disease. Methodologic flaws and lack of correlation with indices of circulatory dysfunction may have contributed to these discrepancies. The aims of the present study were to measure levels of vasopressin both in plasma and in urine and to correlate them with the volume-dependent hormonal systems of plasma renin activity (PRA) and atrial natriuretic factor (ANF).. Plasma vasopressin, ANF, and PRA were measured by radioimmunoassay in 19 patients with cirrhosis, ascites, and severe hyponatremia (mean serum sodium, 121.8 mmol/l) and 11 patients with cirrhosis and normal serum sodium (mean, 137.6 mmol/l). Vasopressin levels were also assessed by radioimmunoassay in urine.. Patients with hyponatremia had higher plasma and urine vasopressin levels than patients with normal serum sodium concentrations (plasma, 2.9 versus 1.0 pg/ml, P = 0.0009; urine, 38.3 versus 12.3 ng/g creatinine, P = 0.0008). PRA was higher (4.8 versus 1.0 ng/ml/h, P = 0.0004) and plasma ANF lower (111.1 versus 148.7 pg/ml, P = 0.01) in patients with hyponatremia.. These results indicate that plasma and urine vasopressin levels are inappropriately increased in patients with cirrhosis and severe hyponatremia. The concomitant increase of PRA and decrease of plasma ANF suggest that decreased 'effective' plasma volume generates nonosmotic stimuli for vasopressin hypersecretion in these patients.

Topics: Adult; Aged; Atrial Natriuretic Factor; Diuretics; Female; Humans; Hyponatremia; Kidney Function Tests; Liver Cirrhosis; Male; Middle Aged; Plasma Volume; Prognosis; Radioimmunoassay; Reference Values; Renin; Survival Rate; Urinalysis; Vasopressins

1. The effects of intravenous chlorthiazid and frusemide on urinary osmolality were compared in 19 hyponatraemic oedematous patients. 2. Frusemide (1 mg/kg) caused production of a dilute urine (urine/plasma osmolality ratio, Uosm./Posm., 1.64-0.84, P less than 0.01) whereas chlorthiazid (10 mg/Kg) did not (Uosm./Posm, 1.54-1.34, not significant. 3. The Osmolar clearance (Cosm.) was higher after frusemide than after chlorthiazid (11.45 vs 4.99 ml/min, P less than 0.01). When the doses of frusemide (0.25-0.5 mg/Kg) and chlorthiazid (20 mg/Kg) were chosen to give a similar Cosm. (7.25 vs 7.48 ml/min, not significant), the Uosm./Posm. was still lower after frusemide (2.20-1.00, P less than 0.001) than after chlorthiazid (1.75-1.26, P less than 0.01). 4. Exogenous vasopressin did not increase the low Uosm./Posm. after frusemide (1.00-1.00, not significant) but increased the ratio after chlorthiazid (1.34-1.68, p less than 0.01). 5. These results indicate that frusemide, but not chlorthiazid, lead to the excretion of a dilute urine in hyponatraemic oedematous patients. This dilution is not due to a greater solution excretion but is associated with a resistance to the action of vasopressin.

Topics: Adult; Chlorothiazide; Edema; Furosemide; Humans; Hyponatremia; Middle Aged; Osmolar Concentration; Vasopressins

The activity of demeclotetracyclin, and ADH antagonist, is studied in 11 ethylic patients with cirrhosis of the liver, under a large hydric diet (1500 cm3). The prescription of the cyclin (600 mg daily) is always determined by a fall of the urinary osmolarity (-36%) and by a dramatic improvement of the free water clearance (+ 60%); consecutively, we observe an increase of natremia in 8 out of 9 cases. Associated with Spironolactone (200 mg daily) the anti-ADH activity persists (the free water clearance becomes positive in 5 out of 10 patients), in spite of the natriuretic activity of anti-aldosterone ; a minimal fall of the natremia is observed in only 2 cases. The indication of Demeclotetracyclin in the curative or preventive treatment of the hyponatremia of the liver cirrhosis is discussed.

Topics: Adult; Aged; Ascites; Clinical Trials as Topic; Demeclocycline; Drug Therapy, Combination; Edema; Female; Humans; Hyponatremia; Liver Cirrhosis; Male; Middle Aged; Natriuresis; Spironolactone; Vasopressins

Vasopressin is increasingly used in infants following cardiac surgery. Hyponatremia is a noted adverse event, but incidence and risk factors remain undefined.. The primary objective was to identify the incidence of vasopressin-induced hyponatremia. Secondary objectives included comparing baseline and change in serum sodium concentrations between infants receiving vasopressin with and without hyponatremia, and comparing vasopressin dose, duration, and clinical characteristics in those with and without hyponatremia.. This Institutional Review Board-approved, retrospective case-control study included infants <6 months following cardiac surgery receiving vasopressin for ≥6 hours at a tertiary care, academic hospital. Patients who developed hyponatremia, cases, were matched to controls in a 1:2 fashion. Demographics and clinical characteristics were collected. Descriptive and inferential statistics were employed. A conditional logistic regression was used to assess odds of hyponatremia.. Of the included 142 infants, 20 (14.1%) developed hyponatremia and were matched with 40 controls. There was significant difference in median nadir between controls and cases, 142.0 versus 128.5 mEq/L (<0.001). A significantly higher number of cases received corticosteroids, loop diuretics, and chlorothiazide versus controls. The regression analysis demonstrated that each additional hour of vasopressin increased the odds of developing hyponatremia by 5% (adjusted odds ratio 1.05 [confidence interval 1-1.1]).. Vasopressin-induced hyponatremia incidence was <15%. Vasopressin duration was independently associated with hyponatremia development.

Topics: Case-Control Studies; Humans; Hyponatremia; Infant; Retrospective Studies; Risk Factors; Vasopressins

Primary central nervous system lymphoma (PCNSL) rarely originates in the hypothalamus. Hypothalamic PCNSL can present with various symptoms specific to dysfunction of the hypothalamus, including consciousness disturbance, cognitive impairment, hypopituitarism, and diabetes insipidus (DI). However, it remains unclear whether syndrome of inappropriate secretion of antidiuretic hormone (SIADH) can present as an initial sign of hypothalamic PCNSL.. Ninety-nine patients with PCNSL were diagnosed between January 2006 and December 2020 at our institutes. The initial symptoms and signs, hypothalamic-pituitary functions, serum sodium (Na) value, Karnofsky Performance Status (KPS) score on admission, and duration from onset to diagnosis were retrospectively investigated from the medical charts.. Eight and 91 patients had hypothalamic PCNSL (hypothalamic group) and PCNSL located in other regions (control group), respectively. Patients' pathological diagnoses were diffuse large B-cell lymphoma (97 patients) and intravascular lymphoma (two patients). Six patients presented with hyponatremia derived from SIADH or suspected SIADH, and one presented with DI. Statistically significant differences between the hypothalamic and control groups were detected only in the preoperative serum Na values and KPS scores.. SIADH can be an initial presentation of hypothalamic PCNSL. Early detection of hypothalamic PCNSL from SIADH may lead to proper management and improved prognosis.

Topics: Diabetes Insipidus; Humans; Hyponatremia; Hypothalamus; Inappropriate ADH Syndrome; Retrospective Studies; Vasopressins

We report a case of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) after total proctocolectomy followed with ileal pouch-anal anastomosis (TPC-IPAA) for ulcerative colitis (UC). The patient was a 46-year-old woman. She was diagnosed with UC of pancolitis in 2000. High grade dysplasia was detected in the transverse colon after a surveillance colonoscopy in 2021. She underwent laparoscopy-assisted TPC-IPAA. On the sixth postoperative day, she had a decreased level of consciousness that worsened on the following day. Her laboratory data showed a serum sodium level of 108 mEq/L and the plasma osmolality was 234 mOsm/kg. We did not find any other abnormalities in the laboratory examination that could cause hyponatremia. Computed tomography scan showed no central nervous system disturbances such as a pituitary tumor, antidiuretic hormone-producing tumors, or pulmonary diseases. The patient was diagnosed with Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) caused by surgical invasion. We started to administer 3% sodium chloride slowly to improve the hyponatremia. Her serum sodium level became normal and stable. Although it is rare for SIADH to be caused by abdominal surgery, if hyponatremia is observed after surgery, the possibility of postoperative SIADH should be considered.

Topics: Colitis, Ulcerative; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Middle Aged; Proctocolectomy, Restorative; Sodium; Vasopressins

Classic treatment for syndrome of inappropriate antidiuretic hormone (SIADH) is fluid restriction. However, this is not ideal for infants who need large fluid volumes to ensure adequate caloric intake for growth. The use of urea has not been thoroughly studied in children.. This infant had SIADH complicated by poor growth, solitary central incisor, and NF1. Following failed attempts to correct hyponatremia with fluid restriction and other therapeutics, urea normalized sodium levels and allowed liberalization of formula volumes, which resulted in improved weight gain.. Urea is a safe, cost-effective, long-term treatment for SIADH in infants who are unable to fluid restrict due to caloric goals.

Topics: Child; Humans; Hyponatremia; Inappropriate ADH Syndrome; Incisor; Infant; Neurofibromatosis 1; Urea; Vasopressins

Hyponatremia is the most frequent electrolytic disorder in clinical practice. In addition to neurological symptoms, hyponatremia, even when mild/moderate and chronic, has been related to other manifestations, such as bone demineralization and increased risk of fractures. To better elucidate tissue alterations associated with reduced serum sodium concentration [Na. Overall, these findings shed new light on the possible consequences of chronic hyponatremia and prompt a more thorough evaluation of hyponatremic patients.

Topics: Animals; Deamino Arginine Vasopressin; Hyponatremia; Inappropriate ADH Syndrome; Liver; Male; Mice; Sodium; Spermatogenesis; Vasopressins

Fructose has recently been proposed to stimulate vasopressin secretion in humans. Fructose-induced vasopressin secretion is not only postulated to result from ingestion of fructose-containing drinks but may also occur from endogenous fructose production via activation of the polyol pathway. This raises the question of whether fructose might be involved in some cases of vasopressin-induced hyponatremia, especially in situations where the cause is not fully known such as in the syndrome of inappropriate secretion of diuretic hormone (SIADH) and exercise-associated hyponatremia, which has been observed in marathon runners. Here we discuss the new science of fructose and vasopressin, and how it may play a role in some of these conditions, as well as in the complications associated with rapid treatment (such as the osmotic demyelination syndrome). Studies to test the role of fructose could provide new pathophysiologic insights as well as novel potential treatment strategies for these common conditions.

Topics: Diuretics; Humans; Hyponatremia; Inappropriate ADH Syndrome; Running; Vasopressins

Hypothalamic hamartoma (HH) typically presents with gonadotrophin-dependent precocious puberty and/or seizures. Other endocrine disturbances are rare. We describe an infant with syndrome of inappropriate secretion of anti-diuretic hormone (SIADH) and a HH.. A 6-week-old infant presented with seizures and life-threatening hyponatremia. A HH was identified on magnetic resonance imaging. Clinical examination and biochemistry were consistent with SIADH, and serum copeptin was high during hyponatremia, further supporting this diagnosis. Tolvaptan was effective in normalizing plasma sodium and enabling liberalization of fluids to ensure sufficient nutritional intake and weight gain and manage hunger.. Hyponatremia due to SIADH is novel at presentation of a HH, and can be challenging to diagnose and manage. Successful management of hyponatremia in this case was achieved using tolvaptan.

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Diuretics; Humans; Hyponatremia; Inappropriate ADH Syndrome; Seizures; Tolvaptan; Vasopressins

Dilutional hyponatremia due to increased plasma arginine vasopressin (AVP) is associated with liver cirrhosis. However, plasma AVP remains elevated despite progressive hypoosmolality. This study investigated changes to inhibitory control of supraoptic nucleus (SON) AVP neurons during liver cirrhosis. Experiments were conducted with adult male Sprague-Dawley rats. Bile duct ligation was used as a model of chronic liver cirrhosis. An adeno-associated virus containing a construct with an AVP promoter and either green fluorescent protein (GFP) or a ratiometric chloride indicator, ClopHensorN, was bilaterally injected into the SON of rats. After 2 weeks, rats received either BDL or sham surgery, and liver cirrhosis was allowed to develop for 4 weeks. In vitro, loose patch recordings of action potentials were obtained from GFP-labeled and unlabeled SON neurons in response to a brief focal application of the GABA

Topics: Animals; Arginine Vasopressin; Bile Ducts; Chlorides; gamma-Aminobutyric Acid; Green Fluorescent Proteins; Hyponatremia; Liver Cirrhosis; Male; Muscimol; Neurons; Rats; Rats, Sprague-Dawley; Supraoptic Nucleus; Vasopressins

The syndrome of inappropriate ADH-secretion (SIADH) is a common cause of low sodium levels with diverse aetiology. Here, we report a case of a 41 years old male patient diagnosed with SIADH and a good response to Tolvaptan therapy. Of interest, as a potential unique cause, magnetic resonance imaging revealed a micronodular structure in the posterior pituitary, while no other common cause of SIADH could be identified. Hence, to the best of our knowledge, this is the first case of a Tolvaptan-responsive SIADH associated with a pituitary micronodular structure.

Topics: Adult; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Pituitary Gland, Posterior; Tolvaptan; Vasopressins

Patients with secondary adrenal insufficiency can present with impaired free water excretion and hyponatremia, which is due to the enhanced secretion of vasopressin (AVP) despite increased total body water. AVP is produced in magnocellular neurons in the paraventricular nucleus of the hypothalamus (PVH) and supraoptic nucleus and in parvocellular corticotropin-releasing factor (CRF) neurons in the PVH. This study aimed to elucidate whether magnocellular AVP neurons or parvocellular CRF neurons coexpressing AVP are responsible for the pathogenesis of hyponatremia in secondary adrenal insufficiency. The number of CRF neurons expressing copeptin, an AVP gene product, was significantly higher in adrenalectomized AVP-floxed mice (AVPfl/fl) than in sham-operated controls. Adrenalectomized AVPfl/fl mice supplemented with aldosterone showed impaired water diuresis under ad libitum access to water or after acute water loading. They became hyponatremic after acute water loading, and it was revealed under such conditions that aquaporin-2 (AQP2) protein levels were increased in the kidney. Furthermore, translocation of AQP2 to the apical membrane was markedly enhanced in renal collecting duct epithelial cells. Remarkably, all these abnormalities observed in the mouse model for secondary adrenal insufficiency were ameliorated in CRF-AVP-/- mice that lacked AVP in CRF neurons. Our study demonstrates that CRF neurons in the PVH are responsible for the pathogenesis of impaired water excretion in secondary adrenal insufficiency.

Topics: Adrenal Insufficiency; Adrenocorticotropic Hormone; Animals; Aquaporin 2; Arginine Vasopressin; Corticotropin-Releasing Hormone; Diuresis; Hyponatremia; Hypothalamus; Mice; Neurons; Paraventricular Hypothalamic Nucleus; Pituitary Hormone-Releasing Hormones; Vasopressins

A 1-year-old spayed female Miniature Schnauzer had chronic hyponatremia, accompanied by polyuria and polydipsia. Blood tests and urinalysis revealed severe hyponatremia, low plasma osmolality with euvolemia, and increased sodium excretion in urine. Hypothyroidism and hypoadrenocorticism were ruled out as causes. These findings led to the diagnosis of syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Magnetic resonance imaging (MRI) showed dilation of the lateral ventricles, indicating severe hydrocephalus. Tolvaptan, a vasopressin V2 receptor antagonist commonly used in human SIADH, was administered along with water restriction. This treatment resulted in a consistent increase in plasma sodium levels without any adverse effects. This case report represents the first documented evidence of the therapeutic efficacy of tolvaptan in treating SIADH in a dog.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Dog Diseases; Dogs; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Sodium; Tolvaptan; Vasopressins

Perioperative hyponatremia, due to non-osmotic release of the antidiuretic hormone arginine vasopressin, is a serious electrolyte disorder observed in connection with many types of surgery. Since blood loss during surgery contributes to the pathogenesis of hyponatremia, we explored the effect of bleeding on plasma sodium using a controlled hypotensive hemorrhage pig model. After 30-min baseline period, hemorrhage was induced by aspiration of blood during 30 min at mean arterial pressure <50 mmHg. Thereafter, the animals were resuscitated with retransfused blood and a near-isotonic balanced crystalloid solution and monitored for 180 min. Electrolyte and water balances, cardiovascular response, renal hemodynamics, and markers of volume regulation and osmoregulation were investigated. All pigs (n = 10) developed hyponatremia. All animals retained hypotonic fluid, and none could excrete net-free water. Urinary excretion of aquaporin 2, a surrogate marker of collecting duct responsiveness to antidiuretic hormone, was significantly reduced at the end of the study, whereas lysine vasopressin, i.e., the pig antidiuretic hormone remained high. In this animal model, hyponatremia developed due to net positive fluid balance and generation of electrolyte-free water by the kidneys. A decreased urinary aquaporin 2 excretion may indicate an escape from antidiuresis.

Topics: Animals; Aquaporin 2; Electrolytes; Hemorrhage; Hyponatremia; Sodium; Swine; Vasopressins; Water

Duloxetine is widely used for pain control and depressive syndromes. One of its potential side effects is syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Duloxetine-induced SIADH causes hyponatremia, which leads to a variety of symptoms and has previously been reported in the elderly. In the present case, we experienced a case of the rapid onset of SIADH in a super-elderly woman receiving low-dose duloxetine. Elderly patients tend to have lower duloxetine doses and an earlier onset than non-elderly patients. When hyponatremia occurs after duloxetine administration, duloxetine-induced SIADH should be considered, especially in high-risk elderly patients, regardless of the duloxetine dose or duration of treatment.

Topics: Aged; Duloxetine Hydrochloride; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Middle Aged; Vasopressins

To describe a case of inappropriate antidiuretic hormone (ADH) secretion in a dog secondary to trauma.. A 14-year-old neutered female mixed breed dog presented for evaluation of bite wounds. The dog sustained multiple puncture wounds to the cervical area, stifle, and elbow. Treatment was initiated with isotonic crystalloid fluids, analgesia, broad-spectrum antimicrobials, and gastroprotectants. The dog developed hyponatremia with concurrent serum hypoosmolality and inappropriate urine hyperosmolality and urine sodium secretion, leading to a diagnosis of the syndrome of inappropriate ADH secretion. The hyponatremia improved, and the dog improved clinically and was discharged 3 days after admission.. This is the first case description of the syndrome of inappropriate ADH secretion in a dog suffering from trauma. Inappropriate ADH secretion is largely under-recognized in veterinary patients. Increased awareness of this syndrome can lead to initiation of appropriate treatment and improved outcomes.

Topics: Animals; Dog Diseases; Dogs; Female; Hospitalization; Hyponatremia; Inappropriate ADH Syndrome; Osmolar Concentration; Vasopressins

Copeptin concentrations are a useful component of the diagnostic workup of paediatric patients with polyuria and polydipsia, but the value of measuring copeptin in patients with hyponatraemia is less clear.. We report 5 children with hyponatraemia in the context of different underlying pathologies. Copeptin concentrations were elevated in 4 cases (13.7, 14.4, 26.1, and 233 pmol/L; reference range 2.4-8.6 pmol/L), suggesting that non-osmoregulated vasopressin release (syndrome of inappropriate antidiuretic hormone) was the underlying mechanism for low sodium levels. In one of the patients, there was an underlying diagnosis of Schaaf-Yang syndrome (MAGEL2 gene mutation) with a clinical picture suggestive of dysregulated vasopressin production with inappropriately high and then low copeptin release. In one hyponatraemic patient, low copeptin concentrations indicated that non-osmoregulated arginine vasopressin release was not the cause of hyponatraemia and oliguria.. Copeptin measurement did not influence management acutely but helped to clarify the mechanism leading to hyponatraemia when the result was available. Relatively high and low copeptin concentrations in association with hypo- and hypernatraemia indicate dysregulated vasopressin production in Schaaf-Yang syndrome.

Topics: Arthrogryposis; Child; Craniofacial Abnormalities; Female; Glycopeptides; Humans; Hyponatremia; Hypopituitarism; Intellectual Disability; Male; Polydipsia; Proteins; Vasopressins

Topics: Duloxetine Hydrochloride; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

Topics: Duloxetine Hydrochloride; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

To evaluate serum antidiuretic hormone (ADH), its receptors, and renin levels in cerebral salt wasting (CSW) in tuberculous meningitis (TBM).. Patients diagnosed with definite (n = 30) or probable TBM (n = 47) who developed hyponatremia (CSW, SIADH, or miscellaneous causes) were included. Sequential measurement of serum ADH, ADH-R, and renin activity by enzyme-linked immunosorbent assay was done and correlated with serum sodium level, urinary output, and fluid balance.. Out of 79 TBM patients, CSW was observed in 36, SIADH in four, and miscellaneous hyponatremia in eight patients. CSW patients had a longer hospital stay (P < 0.001), lower GCS score (P < 0.007), higher MRC grade (P < 0.007), and a lower serum Na (P < 0.001) compared to non-CSW TBM patients. In severe CSW patients, serum ADH and ADH-R were correlated with hyponatremia and returned to baseline on correction; however, serum renin levels remained elevated. Serum ADH was related to hyponatremia but ADH-R and renin were not. ADH-R and renin levels did not significantly differ in CSW and SIADH.. CSW is the commonest cause of hyponatremia in TBM and correlates with disease severity. ADH is related to hyponatremia, but ADH receptor and renin are not.

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Renin; Tuberculosis, Meningeal; Vasopressins

A 67-year-old man with a history of esophageal cancer resection was referred to our hospital because of nausea and appetite loss. Laboratory findings showed severe hyponatremia and were compatible with syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Chest computed tomography (CT) revealed a nodule measuring 13 mm in the lower lobe of the right lung. Right thoracotomy was performed, and the histopathological diagnosis was small-cell lung cancer (T1bN0M0; Stage 1b). Although SIADH is frequently associated with small-cell lung cancer, it is extremely rare as the initial clinical feature in stage I small-cell lung cancer.

Topics: Aged; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Small Cell Lung Carcinoma; Vasopressins

To report on an unusual case of ketamine-precipitated syndrome of inappropriate antidiuretic hormone secretion (SIADH) in an individual managed by an outpatient pain specialty team.. A 78-yr-old male presented to the emergency department with lethargy, malaise, nausea, and abdominal bloating three days following intravenous ketamine infusion for intractable postsurgical lumbar radicular pain with neuropathic features. The patient had a history of resected prostate cancer, hyperlipidemia, chronic kidney disease, and spinal stenosis and the cause of his symptoms was investigated. He was found to be hyponatremic and the treating team excluded reversible surgical and medical causes. A Naranjo score of 7 was calculated, suggesting that the correlation between ketamine and hyponatremia was "likely." Hence, a diagnosis of ketamine-precipitated SIADH was made. The patient was treated with fluid restriction and symptoms were controlled with antiemetics. He returned to baseline function with resolution of the hyponatremia within three days of discharge.. This case is of clinical importance for providers using ketamine in the field of pain management as the effect of this medication reaction can be profound. Clinicians should develop an awareness that ketamine can potentiate adverse effects such as SIADH and they should monitor, detect, and manage as appropriate.. RéSUMé: OBJECTIF: Nous signalons un cas inhabituel de syndrome de sécrétion inappropriée d’hormones antidiurétiques (SIADH - syndrome of inappropriate antidiuretic hormone secretion) précipité par la kétamine chez une personne prise en charge par une équipe spécialisée en douleur en soins ambulatoires. CARACTéRISTIQUES CLINIQUES: Un homme de 78 ans s’est présenté à l’urgence souffrant de léthargie, de malaise, de nausées et de ballonnements abdominaux trois jours après avoir reçu une perfusion intraveineuse de kétamine pour le traitement d’une douleur radiculaire lombaire postopératoire rebelle avec des caractéristiques neuropathiques. Le patient avait des antécédents de résection de cancer de la prostate, d’hyperlipidémie, d’insuffisance rénale chronique et de sténose du canal rachidien, et la cause de ses symptômes a été évaluée. Il s’est avéré hyponatrémique et l’équipe soignante a exclu les causes chirurgicales et médicales réversibles. Un score Naranjo de 7 a été calculé, suggérant que la corrélation entre la kétamine et l’hyponatrémie était « probable ». Par conséquent, un diagnostic de SIADH précipité par la kétamine a été posé. Le patient a été traité par restriction hydrique et les symptômes ont été contrôlés par des antiémétiques. Il est revenu à son fonctionnement de référence avec la résolution de l’hyponatrémie dans les trois jours suivant son congé. CONCLUSION: Ce cas est important d’un point de vue clinique pour les praticiens qui utilisent la kétamine pour la prise en charge de la douleur, car l’effet de cette réaction médicamenteuse peut être profond. Les cliniciens devraient prendre conscience que la kétamine peut augmenter des effets indésirables tels que le SIADH et ils devraient monitorer, dépister et prendre en charge le patient, le cas échéant.

Topics: Drug-Related Side Effects and Adverse Reactions; Humans; Hyponatremia; Inappropriate ADH Syndrome; Ketamine; Male; Pain; Vasopressins

Topics: Humans; Hyponatremia; Hypothyroidism; Inappropriate ADH Syndrome; Vasopressins

A 9-year-old girl with remarkable hyponatremia was diagnosed with SIADH that was likely secondary to varicella. Under appropriate treatment, her serum sodium returned to the normal level. There was no evidence of hyponatremia at a 3-month follow-up. We propose that medical professionals need to consider the existence of that SIADH when treating patients with varicella who present with severe hyponatremia.

Topics: Chickenpox; Child; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

Hyponatremia and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) are associated with and can be caused by tuberculosis (TB) through meningitis by locally invading the hypothalamus, adrenal, or pituitary glands or possibly through ectopic ADH production. This study assessed the association of TB mortality with hyponatremia and SIADH in a large cohort of a university hospital in Austria.. This retrospective study enrolled patients with hyponatremia and patients diagnosed with TB from 01/2001-11/2019 to assess the prevalence of TB in hyponatremia and TB morbidity and mortality in patients with and without hyponatremia. Sex, age, microbiological results, laboratory tests and comorbidities were analysed and used to calculate survival rates.. Of 107.532 patients with hyponatremia (0.07%) and 186 patients with TB (43%), 80 patients were diagnosed with both-hyponatremia and TB. Only three TB patients had SIADH, precluding further SIADH analysis. In hyponatremia, young age and high CRP levels showed significant associations with TB diagnosis (p<0.0001). Survival rates of patients diagnosed with TB with moderate to profound hyponatremia were significantly lower than those without hyponatremia (p = 0.002).. In this study of a large cohort from a tertiary care hospital in a non-endemic area of TB, 0.07% of patients presenting with hyponatremia, but especially younger patients and patients with high CRP values, were diagnosed with TB. Crucially, patients with moderate to profound hyponatremia had a significantly higher mortality rate and thus required increased medical care.

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Retrospective Studies; Tuberculosis; Vasopressins

Hyponatremia and syndrome of inappropriate antidiuretic hormone (SIADH) is a potentially fatal adverse effect of antidepressants (ADs) and antipsychotics (APs), although its frequency and onset time have not been well documented.. To analyze the frequency and onset time of AD- or AP-induced hyponatremia/SIADH.. We used plural data-mining techniques to search the US Food and Drug Administration Adverse Event Reporting System (FAERS) database for reports on hyponatremia/SIADH induced by psychotropic drugs from January 2004 to June 2020. For each item, we assessed the reporting odds ratio, 95% CI, median onset time, and Weibull distribution parameters.. We identified 36 422 reports related to hyponatremia/SIADH. Signals were detected for all psychotropic drugs that we analyzed, except for clozapine. The median onset time of total AD-induced hyponatremia/SIADH was shorter than that of AP. For all ADs and APs except clozapine, hazards were considered to be the early failure type. In contrast, the hazard of clozapine was considered to be the random failure type. The limitations of this study included several reporting biases and the presence of confounding variables, particularly age.. Most ADs and APs were found to be associated with a risk for hyponatremia/SIADH. In addition, sufficient attention should be paid to signs of hyponatremia/SIADH in the early phase when most ADs and APs are administered. These data are potentially useful for determining AD- or AP-induced hyponatremia/SIADH in the early stage and for preventing its further aggravation into a serious condition.

Topics: Antidepressive Agents; Antipsychotic Agents; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

A 49-year-old man developed severe hyponatremia associated with transient headache and was diagnosed with syndrome of inappropriate antidiuretic hormone secretion (SIADH). Fluid restriction and sodium supplementation corrected the hyponatremia. However, several days later, the patient exhibited hypernatremia with thirst and polyuria. A detailed examination indicated central diabetes insipidus (CDI) with an intrasellar cystic lesion indicative of Rathke's cleft cyst (RCC). A case of RCC exhibiting headache, hyponatremia, and subsequent hypernatremia has been reported. Our case shows that CDI may appear after SIADH in patients with RCC, especially in those with serum sodium levels that unexpectedly increase rapidly beyond the reference range.

Topics: Central Nervous System Cysts; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Vasopressins

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a common problem during the postoperative course after pituitary surgery. Although treatment of this condition is well characterized, prevention strategies are less studied and reported. The authors sought to characterize outcomes and predictive factors of SIADH after implementation of routine postoperative fluid restriction for patients undergoing endoscopic transsphenoidal surgery for pituitary adenoma.. In March 2018, routine postoperative fluid restriction to 1000 ml/day for 7 days was instituted for all patients who underwent surgery for pituitary adenoma. These patients were compared with patients who underwent surgery for pituitary adenoma between March 2016 and March 2018, prior to implementation of routine fluid restriction. Patients with preoperative history of diabetes insipidus (DI) or concern for postsurgical DI were excluded. Patients were followed by neuroendocrinologists and neurosurgeons, and sodium levels were checked between 7 and 10 days postoperatively. SIADH was defined by a serum sodium level less than 136 mmol/L, with or without symptoms within 10 days after surgery. Thirty-day readmission was recorded and reviewed to determine underlying reasons.. In total, 82 patients in the fluid-unrestricted cohort and 135 patients in the fluid-restricted cohort were analyzed. The patients in the fluid-restricted cohort had a significantly lower rate of postoperative SIADH than patients in the fluid-unrestricted cohort (5% vs 15%, adjusted OR [95% CI] 0.1 [0.0-0.6], p = 0.01). Higher BMI was associated with lower rate of postoperative SIADH (adjusted OR [95%] 0.9 [0.9-1.0], p = 0.03), whereas female sex was associated with higher rate of SIADH (adjusted OR [95% CI] 3.1 [1.1-9.8], p = 0.03). There was no difference in the 30-day readmission rates between patients in the fluid-unrestricted and fluid-restricted cohorts (4% vs 7%, adjusted OR [95% CI] 0.5 [0-5.1], p = 0.56). Thirty-day readmission was more likely for patients with history of hypertension (adjusted OR [95% CI] 5.7 [1.3-26.3], p = 0.02) and less likely for White patients (adjusted OR [95% CI] 0.3 [0.1-0.9], p = 0.04).. Routine fluid restriction reduced the rate of SIADH in patients who underwent surgery for pituitary adenoma but was not associated with reduction in 30-day readmission rate.

Topics: Adenoma; Diabetes Insipidus; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Pituitary Neoplasms; Postoperative Complications; Retrospective Studies; Sodium; Vasopressins

Functional pancreatic neuroendocrine tumors (pNETs) rarely produce vasopressin. Here, we reported a case of pNET producing vasopressin in a 78-year-old man with hyponatremia.. The patient presented with anorexia approximately 4 years ago, and the laboratory test results indicated hyponatremia. He was hospitalized 3 times subsequently due to anorexia in the past 4 years, during which laboratory tests consistently indicated severe hyponatremia.. Upon admission, his serum osmolarity, urine osmolarity, urine sodium level, and 24-hour urine sodium level was 277 mOsm/kg H2O, 465 mOsm/kg H2O, 82.5 mmol/L, and 140.25 mmol, respectively. Gallium-68-labeled tetraazacyclododecanetetraacetic acid-Dphel-Tyr3-octreotate positron emission tomography-computed tomography showed a high uptake lesion measuring approximately 1 cm in diameter in the pancreatic body, and the possibility of pNET was considered. Besides, laboratory tests showed that adrenocorticotropic hormone, follicle-stimulating hormone, and luteinizing hormone released by the pituitary was insufficient in the case of low levels of cortisol, estradiol, progesterone, and testosterone. Thus, the diagnosis of the syndrome of inappropriate antidiuresis (SIAD) was considered along with hypopituitarism.. The patient underwent surgery, and pNET was confirmed by pathology examination. The immunohistochemical study showed that the tumor cells were positive for somatostatin receptors 2 and vasopressin.. In the last follow-up 17 months after surgery, the patient was in good condition, taking methylprednisolone 4 mg every other day, and had been free of anorexia or hyponatremia episodes.. This case illustrated the potential ectopic production of vasopressin resulting in SIAD in pNETs, highlighting the adoption of gallium-68-labeled tetraazacyclododecanetetraacetic acid-Dphel-Tyr3-octreotate positron emission tomography-computed tomography and vasopressin immunohistochemical staining in the evaluation of the etiology of SIAD.

Topics: Adrenal Cortex Hormones; Aged; Anorexia; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Neuroendocrine Tumors; Pancreatic Neoplasms; Vasopressins

Recently, chronic hyponatremia, even mild, has shown to be associated with poor quality of life and high mortality. The mechanism by which hyponatremia contributes to those symptoms, however, remains to be elucidated. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a primary cause of hyponatremia. Appropriate animal models are crucial for investigating the pathophysiology of SIADH. A rat model of SIADH has been generally used and mouse models have been rarely used. In this study, we developed a mouse model of chronic SIADH in which stable and sustained hyponatremia occurred after 3-week continuous infusion of the vasopressin V2 receptor agonist 1-desamino-8-D-arginine vasopressin (dDAVP) and liquid diet feeding to produce chronic water loading. Weight gain in chronic SIADH mice at week 2 and 3 after starting dDAVP injection was similar to that of control mice, suggesting that the animals adapted to chronic hyponatremia and grew up normally. AQP2 expression in the kidney, which reflects the renal action of vasopressin, was decreased in dDAVP-infused water-loaded mice as compared with control mice that received the same dDAVP infusion but were fed pelleted chow. These results suggest that "vasopressin escape" occurred, which is an important process for limiting potentially fatal severe hyponatremia. Behavioral analyses using the contextual and cued fear conditioning test and T-maze test demonstrated cognitive impairment, especially working memory impairment, in chronic SIADH mice, which was partially restored after correcting hyponatremia. Our results suggest that vasopressin escape occurred in chronic SIADH mice and that chronic hyponatremia contributed to their memory impairment.

Topics: Animals; Behavior, Animal; Chronic Disease; Disease Models, Animal; Hyponatremia; Inappropriate ADH Syndrome; Male; Memory Disorders; Mice; Mice, Inbred C57BL; Vasopressins

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the most common cause of hyponatraemia in hospital inpatients. We present data on treatment setting, patient characteristics, and outcomes for patients treated with tolvaptan for SIADH across a range of real-world settings in Germany and Spain.. This was a non-interventional, observational, retrospective chart review study. Management was at the discretion of the treating physician, with tolvaptan prescribed according to local clinical practice. Hospital notes and/or medical charts were reviewed from treatment initiation for 6 weeks. Follow-up data were collected when patients were discharged early. Patients were eligible for inclusion if they were ≥ 18 years of age and had been treated with ≥ 2 doses of tolvaptan for one episode of hyponatraemia secondary to SIADH in 2014.. The Full Analysis Set comprised 100 patients from 8 centres. The mean age of patients was 73.9 years. The primary endpoint of the mean increase in serum sodium level from baseline to hospital discharge, or to final available measurement, was 10.3 mmol/L (SD 6.4; 95% CI 9.0, 11.6), from 123.0 mmol/L (SD 6.0) to 133.3 mmol/L (SD 4.9). Seventy-seven patients (77.0%) achieved sodium normalisation within 6 weeks of tolvaptan initiation. Mean daily dose of tolvaptan was 12.7 mg (SD 9.2), and mean treatment duration 28.0 days (SD 16.5). Tolvaptan at off-label doses (< 15 mg/day) was prescribed to 72 patients at some point. A favourable safety and tolerability profile was reported.. Tolvaptan was well tolerated and effectively corrected sodium levels in hospitalised adults with hyponatraemia secondary to SIADH in real-world settings. CLINICALTRIALS.. NCT02545101.

Topics: Adult; Aged; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Germany; Humans; Hyponatremia; Inappropriate ADH Syndrome; Retrospective Studies; Spain; Tolvaptan; Vasopressins

A previously well 21-year-old girl presented to Hospital Teluk Intan, Perak, Malaysia with a short history of fever, vomiting and altered sensorium. She was diagnosed with dengue encephalitis as her dengue NS-1 antigen was positive and her cerebrospinal fluid (CSF) dengue polymerase chain reaction (PCR) was positive with serotype DENV-2. She also had severe hyponatremia due to Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) which caused an episode of seizure. She recovered well with supportive management. SIADH and dengue encephalitis should be considered as one of the differential diagnosis in patients presenting with fever and altered sensorium especially in dengue endemic countries like Malaysia.

Topics: Adult; Dengue; Encephalitis; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins; Young Adult

Syndrome of inappropriate antidiuretic hormone (SIADH) secretion is a recognisable complication of acute porphyria. We report a nine-year-old female patient with hereditary tyrosinaemia type 1 and poor adherence to nitisinone therapy who presented with acute abdominal pain, vomiting and lethargy at Sultan Qaboos University Hospital, Muscat, Oman in 2016. She subsequently developed generalised tonic-clonic seizures attributable to severe hyponatremia that met the diagnostic criteria of SIADH. The acute porphyria screen also appeared positive. The patient responded well to fluid restriction and was discharged home without immediate neurological sequelae. Although acute porphyria is also a recognised complication of uncontrolled tyrosinaemia type 1, to the best of the authors' knowledge, no patient with tyrosinaemia type 1 has been reported to present with SIADH.

Topics: Child; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Oman; Tyrosinemias; Vasopressins

We present a case of severe hyponatraemia due to syndrome of inappropriate antidiuretic hormone (SIADH) in a patient with respiratory syncytial virus (RSV) infection. A retrospective analysis of all patients admitted to our hospital with RSV in the preceding 3-year period revealed hyponatraemia in 41 (28%) cases, of which 13 (8.9%) were moderate or severe. SIADH was explored and confirmed in five (3.4%) patients, raising this as an important, previously unrecognised, complication of RSV infection in adults. Physician awareness of SIADH as a potential complication of RSV will facilitate early diagnosis and treatment of this potentially fatal disorder.

Topics: Adult; Humans; Hyponatremia; Inappropriate ADH Syndrome; Respiratory Syncytial Virus Infections; Retrospective Studies; Vasopressins

Hyponatremia due to elevated arginine vasopressin (AVP) secretion increases mortality in liver failure patients. The mechanisms causing dysregulation of AVP secretion are unknown. Our hypothesis is that inappropriate AVP release associated with liver failure is due to increased brain-derived neurotrophic factor (BDNF) in the supraoptic nucleus (SON). BDNF diminishes GABAA inhibition in SON AVP neurons by increasing intracellular chloride through tyrosine receptor kinase B (TrkB) activation and downregulation of K+/Cl- cotransporter 2 (KCC2). This loss of inhibition could increase AVP secretion. This hypothesis was tested using shRNA against BDNF (shBDNF) in the SON in bile duct ligated (BDL) male rats. All BDL rats had significantly increased liver weight (p < 0.05; 6-9) compared to shams. BDL rats with control -shRNA injections (BDL scrambled [SCR]) developed hyponatremia with increased plasma AVP and copeptin (CPP; all p < 0.05; 6-9) compared to sham groups. This is the first study to show that phosphorylation of TrkB is significantly increased along with significant decrease in phosphorylation of KCC2 in BDL SCR rats compared to the sham rats (p < 0.05;6-8). Knockdown of BDNF in the SON of BDL rats (BDL shBDNF) significantly increased plasma osmolality and hematocrit compared to BDL SCR rats (p < 0.05; 6-9). The BDL shBDNF rats had significant (p < 0.05; 6-9) decreases in plasma AVP and CPP concentration compared to BDL SCR rats. The BDNF knockdown also significantly blocked the increase in TrkB phosphorylation and decrease in KCC2 phosphorylation (p < 0.05; 6-8). The results indicate that BDNF produced in the SON contributes to increased AVP secretion and hyponatremia during liver failure.

Topics: Animals; Brain-Derived Neurotrophic Factor; Disease Models, Animal; Hyponatremia; Liver Failure; Male; Neurons; Rats; Supraoptic Nucleus; Vasopressins

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Lymphoma, Large B-Cell, Diffuse; Vasopressins

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a known cause of hyponatremia, caused by excessive ADH secretion which, in turn, leads to water retention. SIADH has been associated with multiple etiologies, one of which is traumatic brain injury (TBI). Most cases of SIADH after TBI describe a course in which hyponatraemia develops several days to weeks after the trauma and then resolves within a few weeks. We demonstrate a case of SIADH after TBI, which persisted several years after initial presentation, but eventually did resolve spontaneously after five years.

Topics: Brain Injuries, Traumatic; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

Small cell carcinoma (SCC) of the bladder is a rare malignancy, representing less than 1% of bladder cancers diagnosed annually in the USA. In contrast to SCC of the lung, paraneoplastic syndromes are rarely documented in cases of extrapulmonary SCCs, particularly those of genitourinary origin. We present a case of SCC of the bladder presenting with paraneoplastic syndrome of inappropriate antidiuretic hormone, which resolved after treatment with sequential chemoradiation.

Topics: Aged, 80 and over; Carcinoma, Small Cell; Chemoradiotherapy; Cystoscopy; Fluorine Radioisotopes; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Paraneoplastic Syndromes; Positron Emission Tomography Computed Tomography; Treatment Outcome; Urinary Bladder; Urography; Vasopressins

A 57-year-old woman with pre-dialysis chronic kidney disease (CKD) was hospitalized because of fever and fatigue. On admission, increased inflammatory response and pyuria with bacteriuria were observed. Pyelonephritis was successfully treated with antibiotics, whereas her fatigue continued and she developed progressive hypercalcemia and hyponatremia; serum sodium level, 116 mEq/L and corrected serum calcium level, 13.4 mg/dL. Plasma concentrations of adrenocorticotropic hormone and cortisol and serum luteinizing hormone were under the detection level. Although the reaction of other anterior pituitary hormones and the serum antidiuretic hormone (ADH) was preserved, the response of serum luteinizing hormone to administration of luteinizing hormone releasing hormone was impaired. Magnetic resonance imaging showed no structural abnormality in the thalamus, hypothalamus, and pituitary gland. She was diagnosed with adrenal insufficiency caused by partial hypopituitarism in concomitant with pyelonephritis. After starting hydrocortisone replacement, serum levels of sodium and calcium were rapidly normalized. This case highlights the importance of adrenal insufficiency as a differential diagnosis of hypercalcemia in patients with pre-dialysis CKD, especially when hyponatremia was concomitantly observed. Besides, infection should be considered as an important trigger for the development of latent adrenal insufficiency since it could increase the physiological demand of corticosteroid in the body. Also, CKD may enhance the magnitude of hypercalcemia since CKD patients have decreased capacity to increase urinary calcium excretion.

Topics: Acute Disease; Adrenal Insufficiency; Adrenocorticotropic Hormone; Diagnosis, Differential; Dialysis; Female; Humans; Hydrocortisone; Hypercalcemia; Hyponatremia; Hypopituitarism; Luteinizing Hormone; Magnetic Resonance Imaging; Middle Aged; Pyelonephritis; Renal Insufficiency, Chronic; Treatment Outcome; Vasopressins

Topics: Adolescent; Anti-Inflammatory Agents, Non-Steroidal; Cold Temperature; Dental Caries; Etodolac; Female; Humans; Hyponatremia; Neurophysins; Protein Precursors; Renal Elimination; Seizures; Sodium; Toothache; Vasopressins; Water; Water Intoxication; Water-Electrolyte Balance

Although several methods currently exist to determine that a person is hypovolemic, it often remains very challenging to accurately estimate the effective circulating volume or amount of intravascular volume depletion in a non-controlled setting. This depletion of intravascular volume can have many causes and is frequently accompanied by hypotonic hyponatremia as a result of hypovolemia-induced release of arginine vasopressin (AVP) from the posterior pituitary gland. Here, we derive a novel, comprehensible equation that provides a theoretical insight into the complex interrelationship between the degree of isotonic volume depletion and the resultant change in plasma sodium concentration. We believe that the presented model can prove to be a valuable tool for the analysis of fluid and electrolyte imbalances.

Topics: Extracellular Space; Humans; Hyponatremia; Mathematical Concepts; Models, Biological; Neurophysins; Osmotic Pressure; Protein Precursors; Translational Research, Biomedical; Vasopressins

Vasopressin (arginine vasopressin, AVP) plays a crucial role in maintaining body fluid homeostasis. Excessive release of vasopressin can lead to hyponatremia. Changes in cerebral circulation during vasopressin-induced chronic hyponatremia are not elucidated. The present study has been designed to investigate the effect of chronic vasopressin-induced hyponatremia on the regulation of the tone of the middle cerebral artery (MCA) of the rat. Chronic hyponatremia was induced in vivo with the help of vasopressin, released continuously from subcutaneously implanted ALZET mini-osmotic pumps, and a liquid diet. After 3.5 days of chronic hyponatremia, the plasma Na

Topics: Acetylcholine; Acidosis; Animals; Cerebrovascular Circulation; Hyponatremia; Male; Middle Cerebral Artery; Nitric Oxide; Potassium Channels; Rats; Rats, Wistar; Sodium; Vasopressins

Hyponatremia is a common feature of acute illness and associated with increased mortality. This may be explained by a stress-mediated activation of the vasopressin system with an increase in free-water reabsorption.. To investigate whether the association between hyponatremia and mortality could be explained by activation of the vasopressin system.. We prospectively enrolled adult, medical patients seeking emergency care in three centres in Switzerland, France and the United States. We investigated associations between admission plasma sodium and copeptin, a stable portion of the vasopressin-precursor peptide, with 30-day mortality. We performed uni- and multivariate regression analysis.. Of 6962 included patients, 18% had hyponatremia (sodium ≤135 mmol L. This prospective study including medical patients upon emergency room admission found hyponatremia as well as an activation of the vasopressin system to be independently associated with mortality. This suggests that stress- and vasopressin-independent mechanisms are responsible for the association of low sodium levels with mortality.

Topics: Acute Disease; Adult; Aged; Cohort Studies; Correlation of Data; Cross-Cultural Comparison; Emergency Service, Hospital; Female; France; Glycopeptides; Humans; Hyponatremia; Male; Middle Aged; Prospective Studies; Risk; Secretory Rate; Sodium; Switzerland; United States; Vasopressins

Topics: Antidiuretic Hormone Receptor Antagonists; Humans; Hyponatremia; Inappropriate ADH Syndrome; Tolvaptan; Vasopressins

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is defined by euvolemic hyponatremia due to an inappropriate retention of free water under the effect of antidiuretic hormone. It is underdiagnosed despite well-defined criteria. Diagnosis involves a precise evaluation of volemia and the elimination of differential diagnoses. The etiologies are classified into four main groups : tumors, drugs, diseases of the central nervous system and lung diseases. In the case of a newly diagnosed SIADH, investigations depend on the clinical context and should at least include a chest radiograph or a chest CT-scan. Fluid restriction is the recommended first-line treatment for mild or moderate hyponatremia. However, only the etiologic treatment leads to the disappearance of SIADH.. Le syndrome de sécrétion inappropriée d’hormone antidiurétique (SIADH) est défini par une hyponatrémie euvolémique induite par une rétention d’eau libre sous l’effet de l’hormone antidiurétique. Il est sous-diagnostiqué malgré des critères bien définis. Le diagnostic implique une évaluation fine de la volémie et l’élimination des diagnostics différentiels. Les étiologies sont classées en quatre groupes : tumeurs, médicaments, affections neurologiques et affections pulmonaires. La conduite à tenir devant un SIADH sans étiologie évidente est mal codifiée. Elle est orientée par le contexte clinique et doit comprendre au minimum une imagerie thoracique. La restriction hydrique est le traitement recommandé de première ligne en cas d’hyponatrémie légère ou modérée. Toutefois, seul le traitement de l’étiologie permet une disparition du SIADH.

Topics: Diagnosis, Differential; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

Small-molecule inhibitors of heat-shock protein 90 (HSP90) have been under development as chemotherapeutic agents. The adverse events reported from early clinical trials included hyponatremia. Given the limited number of patients enrolled, the number of hyponatremia incidents was remarkable and repeatedly, the event was judged as severe. Inappropriate V2 vasopressin receptor stimulation is an established cause of hyponatremia. We explored the hypothesis that HSP90 inhibition produces hypersensitivity to vasopressin by upregulating V2-receptors.. Experiments were carried out in cell culture using HEK293 cells with heterologous expression of the human V2-receptor and HELA cells with an endogenous V2-receptor complement. We tested the effect of HSP90 inhibition by three structurally unrelated compounds (alvespimycin, luminespib, radicicol) and asserted its specificity in cells depleted of cytosolic HSP90 (by RNA interference). Assays encompassed surface V2-receptor density and vasopressin-stimulated formation of cyclic AMP (cAMP).. The results demonstrate a twofold increase in cell-surface receptor density following pre-incubation with each of the HSP90 inhibitors. The effect had a concentration-dependence consistent with the individual potencies to inhibit HSP90. Similarly, depletion of cytosolic HSP90 increased surface-receptor density and at the same time, reduced the inhibitor effect. Upregulated V2-receptors were fully functional; hence, in culture treated with an HSP90 inhibitor, addition of vasopressin resulted in higher levels of cAMP than in controls.. Since formation of cAMP is the first signalling step in raising water permeability of the collecting duct epithelia, we suggest that V2-receptor upregulation generates hypersensitivity to vasopressin linking HSP90 inhibition to the development of hyponatremia.

Topics: Benzoquinones; Cyclic AMP; Cytosol; HEK293 Cells; HeLa Cells; HSP90 Heat-Shock Proteins; Humans; Hyponatremia; Isoxazoles; Lactams, Macrocyclic; Macrolides; Receptors, Vasopressin; Resorcinols; RNA Interference; Up-Regulation; Vasopressins

Vasopressin is one of the vasopressors used to augment blood pressure in subarachnoid hemorrhage (SAH) patients with clinically significant vasospasm. The purpose of the present study was to determine whether the administration of vasopressin to a population of SAH patients was an independent predictor of developing hyponatremia.. A retrospective review on the health records of 106 patients admitted to the University of Alberta Hospital Neurosciences ICU, Edmonton AB, Canada, with SAH from June 2013 to December 2015 was conducted. Serum sodium changes in patients receiving vasoactive drugs were compared. In addition, independent predictors for hyponatremia (Na < 135 mmol/L) were determined using a multivariate logistic regression model.. Patients treated with vasopressin in addition to other vasoactive drugs had significantly higher sodium changes compared to those treated with other vasoactive drugs (-4.7 ± 6 vs -0.1 ± 2.4 mmol/L, respectively, p value 0.001). Hyponatremia occurred in 14 patients (70 %) treated with vasopressin, 10 patients (44 %) treated with vasoactive drugs other than vasopressin (p value 0.081), and 24 patients (38 %) who did not receive any vasoactive drug (p value 0.013). In multivariate logistic regression analysis, when adjusting for disease severity, age, sex, aneurysm location, and treatment, vasopressin was associated with hyponatremia (OR 3.58, 95 % CI, 1.02-12.5, p value 0.046).. The results of the present study suggest that hyponatremia may be more common in SAH patients treated with exogenous vasopressin compared to those who did not receive it. Serum sodium should be monitored closely when vasopressin is being used in the SAH population. Further studies are needed to confirm the effect of exogenous vasopressin on serum sodium levels in SAH populations.

Topics: Adult; Female; Humans; Hyponatremia; Male; Middle Aged; Retrospective Studies; Subarachnoid Hemorrhage; Vasoconstrictor Agents; Vasopressins

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is an extremely rare cause of hyponatremia post-liver transplantation. A 15-year-old Japanese girl with recurrent cholangitis after Kasai surgery for biliary atresia underwent successful living donor liver transplantation. Peritonitis due to gastrointestinal perforation occurred. Hyponatremia gradually developed but improved after hypertonic sodium treatment. One month later, severe hyponatremia rapidly recurred. We considered the hyponatremia's cause as SIADH. We suspected that tacrolimus was the disease's cause, so we used cyclosporine instead, plus hypertonic sodium plus water intake restriction, which improved the hyponatremia. Symptomatic hyponatremia manifested by SIADH is a rare, serious complication post-liver transplantation.

Topics: Adolescent; Cholangitis; Diagnosis, Differential; Female; Humans; Hyponatremia; Immunosuppressive Agents; Inappropriate ADH Syndrome; Liver Transplantation; Postoperative Complications; Tacrolimus; Vasopressins

Intravenous (IV) fluids are used ubiquitously when children undergo surgical procedures. Until recently, Holliday and Segar's guidelines for calculating maintenance fluids dictated fluid management strategies in postoperative pediatric patients. An increased recognition of hospital-acquired hyponatremia and its associated morbidity has led to a critical re-examination of IV fluid management in this population. Postsurgical patients are at high risk of developing hyponatremia due to the presence of non-osmotic stimuli for antidiuretic hormone release. Recent studies have established that, as they are administered in current practice, hypotonic maintenance fluids are associated with increased rates of hyponatremia. The best available data demonstrate that administration of isotonic fluid reduces hyponatremic risk. In this review, we discuss the collective data available on the subject and offer guidelines for fluid management and therapeutic monitoring.

Topics: Age Factors; Child; Fluid Therapy; Humans; Hyponatremia; Hypotonic Solutions; Infusions, Intravenous; Isotonic Solutions; Neurophysins; Perioperative Care; Postoperative Complications; Protein Precursors; Risk Factors; Treatment Outcome; Vasopressins; Water-Electrolyte Balance

Catecholamines trigger proximal tubular fluid retention and reduce renal excretion of solute-free water. In advanced cirrhosis, non-osmotic hypersecretion of vasopressin (antidiuretic hormone or ADH) is considered the cause of dilutional hyponatraemia, but ADH V2 receptor antagonists are not beneficial in long-term treatment of ascites. To test the hypothesis that water retention in experimental ascitic cirrhosis might depend primarily on adrenergic hyper-function, hormonal status, renal function and tubular free-water reabsorption (TFWR) were assessed in six groups of rats with ascitic cirrhosis: rats with cirrhosis due to 13-week CCl4 (carbon tetrachloride) administration (group G1); cirrhotic rats receiving daily diuretics (0.5 mg/kg furosemide plus 2 mg/kg K(+)-canrenoate) from the 11th to the 13th week of CCl4 (G2), diuretics associated with guanfacine oral prodrug (α2A-adrenergic receptor agonist and sympatholytic agent) at 2 (G3), 7 (G4) or 10 (G5) mg/kg, or with SSP-004240F1 (V2 receptor antagonist) at 1 mg/kg (G6). Natriuresis was lower in G1 than in G2, G4 and G6 (all P<0.05). Guanfacine, added to diuretics (i.e. G3 compared with G2), reduced serum noradrenaline from 423±22 to 211±41 ng/l (P<0.05), plasma renin activity (PRA) from 35±8 to 9±2 ng/ml/h (P<0.05) and TFWR from 45±8 to 20±6 μl/min (P<0.01). TFWR correlated with plasma aldosterone (r=0.51, P<0.01) and urinary potassium excretion (r=0.90, P<0.001). In ascitic cirrhosis, reduced volaemia, use of diuretics (especially furosemide) and adrenergic hyper-function cause tubular retention of water. Suitable doses of sympatholytic agents are effective aquaretics.

Topics: Animals; Ascites; Canrenoic Acid; Diuretics; Furosemide; Guanfacine; Hyponatremia; Liver Cirrhosis, Experimental; Male; Natriuresis; Norepinephrine; Rats; Rats, Wistar; Vasopressins

Hyponatremia is often caused by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Hypersecretion of vasopressin from malignant tumors can be considered a cause of SIADH. Most of these ectopic productions of vasopressin are complications of small cell lung cancer. Cases concomitant with ovarian tumors are very rare, and a specific causative substance from the ovary is often unknown. A 16-year-old woman was diagnosed with an ovarian tumor. She developed hyponatremia that was resistant to medical treatment, but immediately improved after surgical resection of the tumor. Her diagnosis was SIADH caused by an ovarian tumor; however, her serum vasopressin level was normal. It is possible that a vasopressin-like substance causing SIADH was secreted by either nervous system tissue within an immature teratoma or small cell lung cancer. We should be cautious when SIADH is a complication of an ovarian tumor.

Topics: Adolescent; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Ovarian Neoplasms; Teratoma; Vasopressins

During the past 50 years the molecular mechanisms of renal reabsorption of sodium and water have been described and molecules specifically interfering with these mechanisms have been developed (diuretics, vasopressin receptor antagonists). Chronic hyponatremia is caused by relative excess of free water, it occurs within a broad spectrum of diseases associated with hypervolemia (heart failure, liver cirrhosis), normovolemia and hypovolemia and it is a negative prognostic factor for patients with chronic heart failure and cirrhotic ascites. Vaptans (vasopressin antagonists, vasopressin V2-receptor inhibitors) reduce reabsorption of water in the distal nephron, they increase free water excretion and normalize serum concentrations of sodium in normovolemic and hypervolemic conditions associated with hyponatremia. Hyponatremia can be corrected (depending on cause, severity and speed of development) through the reduction of fluid intake, administration of a hypertonic solution NaCl, diuretics, oral administration of urea and by vaptans. The role of vaptans in the treatment of hyponatremia should be defined even better, in Europe vaptans can be used to treat the syndrome of inadequate antidiuretic hormone secretion (SIADH).Key words: hyponatremia - liver cirrhosis - heart failure - syndrome of inadequate secretion ADH - tolvaptan - vasopressin.

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Europe; Heart Failure; Humans; Hyponatremia; Inappropriate ADH Syndrome; Liver Cirrhosis; Receptors, Vasopressin; Sodium; Tolvaptan; Vasopressins

Hyponatraemia is a common, potentially life-threatening, complication of thiazide diuretics. The mechanism of thiazide-induced hyponatraemia is incompletely understood. Previous experiments have suggested a direct effect of thiazide diuretics on the plasma membrane expression of aquaporin (AQP)2.. We examined the effects of a single re-exposure to hydrochlorothiazide (HCTZ) 50 mg on water balance, renal sodium handling and osmoregulation in 15 elderly hypertensive patients with a history of thiazide-induced hyponatraemia and 15 matched hypertensive controls using thiazide diuretics without previous hyponatraemia.. Patients with thiazide-induced hyponatraemia had significantly lower body weight and lower plasma sodium and osmolality at baseline. After HCTZ administration, plasma sodium and osmolality significantly decreased and remained lower in patients compared with controls (P < 0.001). Plasma antidiuretic hormone (ADH) and urine AQP2 were low or suppressed in patients, whereas solute and electrolyte-free water clearance was significantly increased compared with controls. Ad libitum water intake was significantly higher in patients (2543 ± 925 ml) than in controls (1828 ± 624 ml, P < 0.05), whereas urinary sodium excretion did not differ. In contrast, urea excretion remained significantly lower in patients (263 ± 69 mmol per 24 h) compared with controls (333 ± 97 mmol per 24 h, P < 0.05) and predicted the decrease in plasma sodium following HCTZ administration.. Thiazide diuretics are associated with markedly impaired free water excretion at low ADH and AQP2 in elderly patients. The higher water intake and lower urea excretion in patients points to an important role for polydipsia and urea-mediated water excretion in the pathogenesis of thiazide-induced hyponatraemia.

Topics: Aged; Aged, 80 and over; Aquaporin 2; Drinking; Electrolytes; Female; Humans; Hydrochlorothiazide; Hypertension; Hyponatremia; Kidney; Male; Middle Aged; Osmolar Concentration; Sodium; Sodium Chloride Symporter Inhibitors; Urea; Vasopressins; Water-Electrolyte Balance

A 78-year-old woman diagnosed with non-classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency had been under glucocorticoid replacement therapy since the age of 17 years. After several weeks of suffering from gastroenteritis with vomiting, she presented with disturbance of consciousness, hypotension, dehydration, and severe hyponatremia (108 mEq/L) and a markedly increased serum vasopressin concentration (45.5 pg/mL). She regained consciousness after correcting her body-fluid balance with hypertonic saline and intravenous hydrocortisone sodium therapy. Her hyponatremia was likely caused by extra-renal sodium loss and impaired water excretion induced by an increase of serum vasopressin due to volume depletion and glucocorticoid deficiency.

Topics: Adrenal Hyperplasia, Congenital; Adrenal Insufficiency; Aged; Female; Glucocorticoids; Humans; Hyponatremia; Saline Solution, Hypertonic; Sodium; Vasopressins

Neonatal hyponatraemia is common, and related to significant morbidity and mortality. We report a case of a preterm newborn (gestational age of 36 weeks) with hyponatraemia, and with a prenatal diagnosis of cleft lip and palate, with a normal fetal karyotype. On the seventh day of life, a biochemical evaluation for jaundice and mild signs of dehydration showed hyponatraemia of 124 mmol/L. Investigation showed normal adrenal and thyroid functions, plasma hyposmolality (258 mOsm/kg); high urinary sodium (73 mmol/L) and high urinary osmolality (165 mOsm/kg). Despite oral sodium supplementation and fludrocortisone treatment, sodium levels remained between 124 and 130 mmol/L. Cranial ultrasound, brain MRI and renal ultrasound were normal. The diagnosis of hyponatraemia was unpredicted and the investigation was suggestive of reset osmostat, a subtype of the syndrome of inappropriate secretion of antidiuretic hormone, characterised by a subnormal threshold for antidiuretic hormone secretion.

Topics: Anti-Inflammatory Agents; Dehydration; Fludrocortisone; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant, Newborn; Jaundice; Magnetic Resonance Imaging; Male; Osmolar Concentration; Premature Birth; Sodium; Vasopressins

Topics: Addison Disease; Child; Diabetes Mellitus, Type 1; Humans; Hyponatremia; Male; Natriuresis; Polyendocrinopathies, Autoimmune; Rhabdomyolysis; Vasopressins

Topics: Antidiuretic Hormone Receptor Antagonists; Humans; Hyponatremia; Vasopressins

Topics: Antidiuretic Hormone Receptor Antagonists; Humans; Hyponatremia; Vasopressins

The occurrence of electrolyte disorders as hypocalcemia and/or hyponatremia is an uncommon event in preeclampsia, which can be the sign of serious situation, with potentially unfavourable consequences for the mother and her fœtus. Hyponatremia in the setting of preeclampsia is an indicator of severity, and requires the understanding of the etiologic mechanisms to initiate an appropriate treatment. Indeed the often-considered fluid restriction is rarely a treatment option for pregnant women. Hypocalcemia is a complication that must be monitored when a treatment with high doses of intravenous magnesium sulphate is introduced. In this context, hypocalcemia must be sought, with the exclusion of other etiologies as vitamin D deficiency, hypoparathyroidism or renal and extrarenal loss of calcium. A replacement therapy, intravenous or oral according to circumstances, should be considered in case of severe or symptomatic hypocalcemia.

Topics: Adult; Aldosterone; Antihypertensive Agents; Capillary Leak Syndrome; Cesarean Section; Emergencies; Female; Fertilization in Vitro; Fetal Growth Retardation; Humans; Hypocalcemia; Hyponatremia; Infant, Newborn; Infusions, Intravenous; Labetalol; Magnesium Sulfate; Male; Pre-Eclampsia; Pregnancy; Pressoreceptors; Renin-Angiotensin System; Vasopressins

Hyponatraemia, defined as a serum sodium concentration <135 mmol/l, is the most common disorder of body fluid and electrolyte balance encountered in clinical practice. It can lead to a wide spectrum of clinical symptoms, from subtle to severe or even life threatening, and is associated with increased mortality, morbidity and length of hospital stay in patients presenting with a range of conditions. Despite this, the management of patients remains problematic. The prevalence of hyponatraemia in widely different conditions and the fact that hyponatraemia is managed by clinicians with a broad variety of backgrounds have fostered diverse institution- and speciality-based approaches to diagnosis and treatment. To obtain a common and holistic view, the European Society of Intensive Care Medicine (ESICM), the European Society of Endocrinology (ESE) and the European Renal Association - European Dialysis and Transplant Association (ERA-EDTA), represented by European Renal Best Practice (ERBP), have developed the Clinical Practice Guideline on the diagnostic approach and treatment of hyponatraemia as a joint venture of three societies representing specialists with a natural interest in hyponatraemia. In addition to a rigorous approach to methodology and evaluation, we were keen to ensure that the document focused on patient-important outcomes and included utility for clinicians involved in everyday practice.

Topics: Adult; Algorithms; Blood Glucose; Brain Edema; Critical Care; Endocrinology; Evidence-Based Medicine; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infusions, Intravenous; Kidney Diseases; Male; Nephrology; Osmolar Concentration; Saline Solution, Hypertonic; Sodium; Vasopressins

Hyponatraemia, defined as a serum sodium concentration <135 mmol/l, is the most common disorder of body fluid and electrolyte balance encountered in clinical practice. It can lead to a wide spectrum of clinical symptoms, from subtle to severe or even life threatening, and is associated with increased mortality, morbidity and length of hospital stay in patients presenting with a range of conditions. Despite this, the management of patients remains problematic. The prevalence of hyponatraemia in widely different conditions and the fact that hyponatraemia is managed by clinicians with a broad variety of backgrounds have fostered diverse institution- and speciality-based approaches to diagnosis and treatment. To obtain a common and holistic view, the European Society of Intensive Care Medicine (ESICM), the European Society of Endocrinology (ESE) and the European Renal Association - European Dialysis and Transplant Association (ERA-EDTA), represented by European Renal Best Practice (ERBP), have developed the Clinical Practice Guideline on the diagnostic approach and treatment of hyponatraemia as a joint venture of three societies representing specialists with a natural interest in hyponatraemia. In addition to a rigorous approach to methodology and evaluation, we were keen to ensure that the document focused on patient-important outcomes and included utility for clinicians involved in everyday practice.

Topics: Adult; Algorithms; Blood Glucose; Brain Edema; Critical Care; Endocrinology; Evidence-Based Medicine; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infusions, Intravenous; Kidney Diseases; Male; Nephrology; Osmolar Concentration; Saline Solution, Hypertonic; Sodium; Vasopressins

Although the syndrome of inappropriate antidiuretic hormone has connection with various malignant tumors, there are few reports associated with advanced gastric cancer.. We describe the case of a 63-year-old Korean male with inappropriate antidiuretic hormone syndrome due to an ectopic antidiuretic hormone-producing advanced gastric adenocarcinoma manifested with overt serum hypo-osmolar hyponatremia and high urinary sodium concentrations. His adrenal, thyroidal, and renal functioning were normal, and the hyponatremia improved following removal of the tumor. The cancer cells were immunostained and found to be positive for the antidiuretic hormone. To our knowledge, this is the first report of an antidiuretic hormone-secreting advanced gastric adenocarcinoma associated with the syndrome of inappropriate antidiuretic hormone, showing cancer cells immunostained for the antidiuretic hormone.. Although a strong relationship between gastric cancer and the syndrome of inappropriate antidiuretic hormone remains to be established, we suggest that gastric cancer could be included as a differential diagnosis of cancer that is associated with the syndrome of antidiuretic hormone.

Topics: Adenocarcinoma; Humans; Hyponatremia; Immunohistochemistry; Inappropriate ADH Syndrome; Male; Middle Aged; Paraneoplastic Endocrine Syndromes; Stomach Neoplasms; Tomography, X-Ray Computed; Vasopressins

Bile duct ligation (BDL) causes congestive liver failure that initiates hemodynamic changes, resulting in dilutional hyponatremia due to increased water intake and vasopressin release. This project tested the hypothesis that angiotensin signaling at the subfornical organ (SFO) augments drinking behavior in BDL rats. A genetically modified adeno-associated virus containing short hairpin RNA (shRNA) for ANG II receptor subtype 1a (AT1aR) gene was microinjected into the SFO of rats to knock down expression. Two weeks later, BDL or sham surgery was performed. Rats were housed in metabolic chambers for measurement of fluid and food intake and urine output. The rats were euthanized 28 days after BDL surgery for analysis. A group of rats was perfused for immunohistochemistry, and a second group was used for laser-capture microdissection for analysis of SFO AT1aR gene expression. BDL rats showed increased water intake that was attenuated in rats that received SFO microinjection of AT1aR shRNA. Among BDL rats treated with scrambled (control) and AT1aR shRNA, we observed an increased number of vasopressin-positive cells in the supraoptic nucleus that colocalized with ΔFosB staining, suggesting increased vasopressin release in both groups. These results indicate that angiotensin signaling through the SFO contributes to increased water intake, but not dilutional hyponatremia, during congestive liver failure.

Topics: Animals; Behavior, Animal; Bile Ducts; Dependovirus; Disease Models, Animal; Down-Regulation; Drinking Behavior; Gene Knockdown Techniques; Genetic Vectors; Hyponatremia; Ligation; Liver Failure; Male; Proto-Oncogene Proteins c-fos; Rats; Rats, Sprague-Dawley; Receptor, Angiotensin, Type 1; RNA Interference; RNA, Small Interfering; Signal Transduction; Sodium; Subfornical Organ; Transduction, Genetic; Vasopressins

Topics: Cardiac Output, Low; Heart Failure; Humans; Hyponatremia; Vasopressins; Water-Electrolyte Balance

Dysnatremia is a frequent finding in patients with community acquired pneumonia (CAP) and a predictor of mortality. We studied the relation between dysnatremia, comorbidities and CT-pro-AVP and MR-proANP.. We enrolled 2138 patients (60 ± 18 years, 55% male) with CAP from the CAPNETZ database. Pro-atrial natriuretic peptide (proANP), pro-vasopressin (proAVP), serum sodium and CRB-65 score were determined on admission. Patients were followed up for 28 days. Sodium concentration on admission was examined as a function of mortality at 28 days. Hyponatremia (HypoN) was defined as admission serum sodium <136 mmol/L, hypernatremia (HyperN) as admission serum sodium >145 mmol/L.. HypoN was diagnosed in 680 (31.8%) patients, HyperN in 29 (1.4%) patients. Comorbidities were associated with sodium levels, and CT-pro-AVP and MR-proANP were inversely related to sodium levels. Patients with HypoN were older, had a higher CRB-65 score and higher values of CT-proAVP and MR-proANP (all p < 0.05). When examined as a function of sodium values, a U-shaped association was found between sodium levels and 28 day mortality. In multivariate Cox proportional hazards analysis, HypoN and HyperN were independent predictors of 28 day mortality. Sodium levels added to the predictive potential of proAVP and proANP.. HypoN is common at admission among CAP patients and is independently associated with mortality. HyperN is rare at admission among CAP patients but is also independently associated with mortality. The combination of sodium and CT-pro-AVP and MR-proANP levels achieved the highest prediction of mortality.

Topics: Adult; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Biomarkers; Community-Acquired Infections; Comorbidity; Databases, Factual; Female; Germany; Humans; Hypernatremia; Hyponatremia; Male; Middle Aged; Pneumonia; Predictive Value of Tests; Prognosis; Sodium; Vasopressins

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Urea; Vasopressins

Topics: Diagnosis, Differential; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Polydipsia, Psychogenic; Rhabdomyolysis; Vasopressins; Water Intoxication

Apelin and vasopressin levels are regulated in opposite directions to maintain body fluid homeostasis.. We thus assessed plasma apelin to copeptin ratios, with plasma copeptin concentrations as a reliable index of vasopressin secretion, in pathological states combining high levels of vasopressin secretion with hyponatremia.. We carried out a cross-sectional study including 113 healthy subjects, 21 hyponatremic patients with the syndrome of inappropriate antidiuretic hormone (SIADH), and 16 normonatremic and 16 hyponatremic patients with chronic heart failure (CHF) in an academic hospital.. Individual apelin to copeptin ratios were plotted against natremia and compared with those of 10 healthy subjects of a previous study acutely challenged by water loading or hypertonic saline infusion. We calculated the percentage of SIADH/CHF patients whose apelin to copeptin ratio for a given natremia lies outside the 95% prediction limits of the physiological relationship.. In healthy subjects, median (interquartile range) plasma apelin and copeptin concentrations were 254 fmol/mL (225-311) and 4.0 fmol/mL (2.6-6.9), respectively. Sex- and age-adjusted plasma apelin concentrations were 26% higher in SIADH and normonatremic and hyponatremic CHF patients than in healthy subjects. Sex- and age-adjusted plasma copeptin concentration was 75%, 187%, and 207% higher in SIADH and normonatremic and hyponatremic CHF patients, respectively, than in healthy subjects. During an acute osmotic challenge, the plasma apelin to copeptin ratio decreased exponentially with natremia. Apelin to copeptin ratios as a function of natremia were outside the 95% predicted physiological limits for 86% of SIADH patients and 81% of hyponatremic CHF patients.. Inappropriate apelin concentrations and apelin to copeptin ratios as a function of natremia in SIADH and CHF patients suggest that the increase in plasma apelin secretion cannot compensate for the higher levels of vasopressin release and may contribute to the corresponding water metabolism defect.

Topics: Adolescent; Adult; Aged; Apelin; Biomarkers; Cross-Sectional Studies; Female; Glycopeptides; Heart Failure; Humans; Hyponatremia; Inappropriate ADH Syndrome; Intercellular Signaling Peptides and Proteins; Male; Middle Aged; Models, Biological; Neurophysins; Pituitary Gland, Posterior; Protein Precursors; Saline Solution, Hypertonic; Up-Regulation; Vasopressins; Young Adult

Topics: Enalapril; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

Hyponatremia is a serious, but often overlooked, electrolyte imbalance that has been independently associated with a wide range of deleterious changes involving many different body systems. Untreated acute hyponatremia can cause substantial morbidity and mortality as a result of osmotically induced cerebral edema, and excessively rapid correction of chronic hyponatremia can cause severe neurologic impairment and death as a result of osmotic demyelination. The diverse etiologies and comorbidities associated with hyponatremia pose substantial challenges in managing this disorder. In 2007, a panel of experts in hyponatremia convened to develop the Hyponatremia Treatment Guidelines 2007: Expert Panel Recommendations that defined strategies for clinicians caring for patients with hyponatremia. In the 6 years since the publication of that document, the field has seen several notable developments, including new evidence on morbidities and complications associated with hyponatremia, the importance of treating mild to moderate hyponatremia, and the efficacy and safety of vasopressin receptor antagonist therapy for hyponatremic patients. Therefore, additional guidance was deemed necessary and a panel of hyponatremia experts (which included all of the original panel members) was convened to update the previous recommendations for optimal current management of this disorder. The updated expert panel recommendations in this document represent recommended approaches for multiple etiologies of hyponatremia that are based on both consensus opinions of experts in hyponatremia and the most recent published data in this field.

Topics: Adrenal Insufficiency; Antidiuretic Hormone Receptor Antagonists; Clinical Trials as Topic; Diagnosis, Differential; Diuretics; Gastrointestinal Diseases; Genetic Diseases, X-Linked; Humans; Hyponatremia; Hypothyroidism; Hypovolemia; Inappropriate ADH Syndrome; Liver Cirrhosis; Polydipsia; Receptors, Vasopressin; Sodium Chloride; Vasopressins

The aims of this study were to describe the characteristics of hyponatremia in elderly users of antidepressants, to determine the prevalence and risk factors for hyponatremia, and to identify the underlying mechanisms.. Cross-sectional study (March 2007-April 2009) with prospectively collected data. Patients were older than 60 years, used antidepressants, and had a complete geriatric assessment.. Serum sodium and antidiuretic hormone levels, serum osmolality, urine sodium level, and urine osmolality were measured. The prevalence of hyponatremia (serum sodium <135 mM) as an adverse reaction to an antidepressant (AR-AD), defined with Naranjo's algorithm, was calculated. Hyponatremic patients were compared to normonatremic patients with regard to gender, age, weight, history of hyponatremia, hyponatremia-associated medications and disorders, and type and duration of antidepressant use.. Of 358 eligible patients, 345 were included. The prevalence of hyponatremia as an AR-AD was 9.3%. Risk factors were a history of hyponatremia (adjusted OR 11.17, 95%CI 2.56-40.41), weight<60 kg (adjusted OR 3.47, 95%CI 1.19-10.13), and psychosis (adjusted OR 3.62, 95%CI 1.12-11.73). Non-suppressed ADH was found in a minority of hyponatremic patients.. In elderly patients, the prevalence of hyponatremia as adverse reaction to all types of antidepressants was 9%. Patients with previous hyponatremia, weight <60 kg, and psychosis were at risk. Beside SIADH, the nephrogenic syndrome of inappropriate antidiuresis, in which ADH secretion was normal, is postulated as an underlying mechanism. This has consequences for treatment of antidepressant-induced hyponatremia with vasopressin receptor antagonists.

Topics: Aged; Aged, 80 and over; Antidepressive Agents; Cross-Sectional Studies; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Odds Ratio; Prevalence; Prospective Studies; Risk Factors; Sodium; Vasopressins

Multiple sclerosis (MS) is a complex neurodegenerative disease presenting with a diversity of clinical symptoms including palsy and cognitive impairment. We present a 59-year-old woman with a history of secondary progressive MS since 1987, who was referred to our department because of recent onset of confusion and polydipsia. Initial lab tests showed mildly elevated serum sodium levels and low urine osmolality. Under water deprivation, diuresis and low urine osmolality persisted and serum sodium levels rose above 150 mmol/l. Oral desmopressin resulted in normalisation of serum sodium as well as urine osmolarity, confirming a diagnosis of central diabetes insipidus. As drug-induced diabetes could be excluded, pituitary magnetic resonance imaging (MRI) was performed. A demyelinating lesion was detected in the hypothalamus. The patient was started on oral desmopressin treatment (0.2 mg/day). Fluid intake and serum sodium levels have since remained normal. In summary, we report the rare case of a patient presenting with diabetes insipidus due to progressive MS. Diabetes insipidus should be considered in MS patients who develop new onset of polydipsia.

Topics: Atrophy; Cognition Disorders; Confusion; Diabetes Insipidus; Female; Humans; Hyponatremia; Hypothalamus; Magnetic Resonance Imaging; Middle Aged; Multiple Sclerosis, Chronic Progressive; Polydipsia; Sodium; Vasopressins

Binding of vasopressin to its type 2 receptor in renal collecting ducts induces cAMP signaling, transcription and translocation of aquaporin (AQP)2 water channels to the plasma membrane, and water reabsorption from the prourine. Demeclocycline is currently used to treat hyponatremia in patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Demeclocycline's mechanism of action, which is poorly understood, is studied here. In mouse cortical collecting duct (mpkCCD) cells, which exhibit deamino-8-D-arginine vasopressin (dDAVP)-dependent expression of endogenous AQP2, demeclocycline decreased AQP2 abundance and gene transcription but not its protein stability. Demeclocycline did not affect vasopressin type 2 receptor localization but decreased dDAVP-induced cAMP generation and the abundance of adenylate cyclase 3 and 5/6. The addition of exogenous cAMP partially corrected the demeclocycline effect. As in patients, demeclocycline increased urine volume, decreased urine osmolality, and reverted hyponatremia in an SIADH rat model. AQP2 and adenylate cyclase 5/6 abundances were reduced in the inner medulla but increased in the cortex and outer medulla, in the absence of any sign of toxicity. In conclusion, our in vitro and in vivo data indicate that demeclocycline mainly attenuates hyponatremia in SIADH by reducing adenylate cyclase 5/6 expression and, consequently, cAMP generation, AQP2 gene transcription, and AQP2 abundance in the renal inner medulla, coinciding with a reduced vasopressin escape response in other collecting duct segments.

Topics: Adenylyl Cyclases; Animals; Anti-Bacterial Agents; Aquaporin 2; Cells, Cultured; Cyclic AMP; Deamino Arginine Vasopressin; Demeclocycline; Disease Models, Animal; Hyponatremia; In Vitro Techniques; Inappropriate ADH Syndrome; Kidney Medulla; Male; Mice; Minocycline; Rats; Rats, Wistar; Vasopressins

Because of antidiuretic hormone (ADH) disorder on production or function we can observe dysnatremia. In the absence of production by posterior pituitary, central diabetes insipidus (DI) occurs with hypernatremia. There are hereditary autosomal dominant, autosomal recessive or X- linked forms. When ADH is secreted but there is an alteration on his receptor AVPR2, it is a nephrogenic diabetes insipidus in acquired or hereditary form. We can make difference on AVP levels and/or on desmopressine response which is negative in nephrogenic forms. Hyponatremia occurs when there is an excess of ADH production: it is a euvolemic hypoosmolar hyponatremia. The most frequent etiology is SIADH (syndrome of inappropriate secretion of ADH), a diagnostic of exclusion which is made after eliminating corticotropin deficiency and hypothyroidism. In case of brain injury the differential diagnosis of cerebral salt wasting (CSW) syndrome has to be discussed, because its treatment is perfusion of isotonic saline whereas in SIADH, the treatment consists in administration of hypertonic saline if hyponatremia is acute and/or severe. If not, fluid restriction demeclocycline or vaptans (antagonists of V2 receptors) can be used in some European countries. Four types of SIADH exist; 10 % of cases represent not SIADH but SIAD (syndrome of inappropriate antidiuresis) due to a constitutive activation of vasopressin receptor that produces water excess. c 2013 Published by Elsevier Masson SAS.

Topics: Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diagnosis, Differential; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Pituitary Diseases; Pituitary Gland, Posterior; Receptors, Vasopressin; Sodium Chloride; Vasopressins; Water-Electrolyte Imbalance

Surgical manipulation of the pituitary stalk, neurohypophysis or the hypothalamus may disturb control of the plasma sodium level. The factors that might predict the risk of postoperative sodium imbalance are not clear, and were investigated in this study.. A retrospective survey of 129 surgical records for the occurrence of plasma sodium levels outside the normal range, following transsphenoidal procedures. Median patient age was 49 (range 20-78) years, 65 female. 73 of the operated lesions were non-functioning pituitary adenomas. Patients were considered to have impaired plasma sodium balance if the range of 135-145 mmol/L was not maintained.. Of all 129 surgical cases, 68 (53%) experienced an imbalance in sodium levels. Severe sodium imbalance (≥ 149 or ≤ 131 mmol/L) was observed in 28 patients (22%). 13 showed hypernatraemia (median day 1), and 15 hyponatraemia (median day 6). Tumour size was associated with an increased incidence of sodium imbalance, particularly in patients younger than 49 years; surgery resulted in sodium imbalance in 38% of young patients operated on for tumours < 22 mm and in 76% of young patients, operated on for tumours ≥ 22 mm. Overall, tumour size increased with patients' age, and tumour size was less predictive for sodium disturbances in elderly patients. Median time in hospital was 5 days for patients without sodium imbalance, 6 days for patients with hypernatraemia and 11 days for patients with hyponatraemia.. Following pituitary surgery, patients with large tumours, in particular those of young age, are at higher risk for losing control of their plasma sodium level. Increased ADH secretion (hyponatraemia), but not transient diabetes insipidus was associated with a prolonged hospital stay. Postoperative follow-up of patients with sellar tumours should include careful monitoring of plasma sodium levels within the first two postoperative weeks and clear patients' instructions.

Topics: Adenoma; Adult; Aged; Analysis of Variance; Diabetes Insipidus, Neurogenic; Female; Homeostasis; Humans; Hypernatremia; Hyponatremia; Male; Middle Aged; Pituitary Neoplasms; Postoperative Complications; Retrospective Studies; Sella Turcica; Sodium; Tumor Burden; Vasopressins; Young Adult

Gitelman syndrome (GS) is a renal tubular disorder of the thiazide-sensitive sodium chloride cotransporter, which is located in the distal tubule of the loop of Henle. We present a rare case of GS complicated by severe hyponatraemia and hypophosphataemia. A 17-year-old boy was admitted to our institution with fever and lethargy. The workup revealed typical features of GS, i.e. hypokalaemia, hypomagnesaemia and metabolic alkalosis. In this report, we discuss the differential diagnoses and rationale for accepting GS as the most likely diagnosis. This case was complicated by severe hyponatraemia (115 mmol/L) and hypophosphataemia (0.32 mmol/L). We concluded that the syndrome of inappropriate secretion of antidiuretic hormones could not be ruled out and that respiratory alkalosis was the most likely aetiology of hypophosphataemia. This case report also generates an interesting discussion on water and electrolyte metabolism.

Topics: Adolescent; Alkalosis, Respiratory; Electrolytes; Fever; Gitelman Syndrome; Humans; Hyponatremia; Hypophosphatemia; Lethargy; Male; Vasopressins

Carbamazepine (CBZ) is a drug widely used in the therapy of epilepsy and mood disorders. One frequently observed side effect is hyponatraemia. The role of vasopressin in hyponatraemic action of CBZ is discussed controversially. In this study, we tested the influence of CBZ on water and salt homoeostasis in rat under different hydration states and under vasopressin 2 receptor (V2R) antagonism by satavaptan to elucidate the renal and vasopressin independent action of CBZ.. CBZ-treated rats were investigated on metabolic cages after (i) 6 day with ad libitum fluid intake, (ii) moderate water load and (iii) water restriction. The effect of satavaptan was tested in clearance experiments under continuous saline infusion in anaesthetized rats after CBZ pretreatment.. Compared to controls, CBZ induced a higher urinary flow rate which was most pronounced (20-fold) after water load and significantly elevated (2-fold) after 10-h water restriction. In addition, CBZ consistently increased renal sodium loss but failed to decrease plasma sodium concentration. In the presence of satavaptan, urinary flow and natriuresis were further increased by CBZ, while there was no differential effect on urea excretion and anion gap.. At the investigated dose (50 mg/kg body weight), CBZ did not induce hyponatraemia or antidiuresis in the rat. However, depending on the hydration state, it induced an increased water and electrolyte loss. Its enhanced influence on urinary flow and natriuresis in the presence of satavaptan suggests additional renal targets for CBZ, independent of vasopressin signalling.

Topics: Animals; Anticonvulsants; Antidiuretic Hormone Receptor Antagonists; Carbamazepine; Dehydration; Diuresis; Female; Hyponatremia; Kidney; Morpholines; Natriuresis; Rats; Rats, Wistar; Receptors, Vasopressin; Spiro Compounds; Vasopressins; Water-Electrolyte Balance

Bile duct ligation (BDL), a model of hepatic cirrhosis, is associated with dilutional hyponatremia and inappropriate vasopressin release. ΔFosB staining was significantly increased in vasopressin and oxytocin magnocellular neurosecretory cells in the supraoptic nucleus (SON) of BDL rats. We tested the role of SON ΔFosB in fluid retention following BDL by injecting the SON (n = 10) with 400 nl of an adeno-associated virus (AAV) vector expressing ΔJunD (a dominant negative construct for ΔFosB) plus green fluorescent protein (GFP) (AAV-GFP-ΔJunD). Controls were either noninjected or injected with an AAV vector expressing only GFP. Three weeks after BDL or sham ligation surgery, rats were individually housed in metabolism cages for 1 wk. Average daily water intake was significantly elevated in all BDL rats compared with sham ligated controls. Average daily urine output was significantly greater in AAV-GFP-ΔJunD-treated BDL rats compared with all other groups. Daily average urine sodium concentration was significantly lower in AAV-GFP-ΔJunD-treated BDL rats than the other groups, although average daily sodium excretion was not different among the groups. SON expression of ΔJunD produced a diuresis in BDL rats that may be related to decreased circulating levels of vasopressin or oxytocin. These findings support the view that ΔFosB expression in SON magnocellular secretory cells contribute to dilutional hyponatremia in BDL rats.

Topics: Animals; Cholestasis; Disease Models, Animal; Green Fluorescent Proteins; Hyponatremia; Ligation; Liver Cirrhosis; Male; Oxytocin; Proto-Oncogene Proteins c-fos; Rats; Rats, Sprague-Dawley; Supraoptic Nucleus; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Alcoholism; Beer; Emergency Nursing; Emergency Service, Hospital; Humans; Hyponatremia; Male; Myelinolysis, Central Pontine; Nursing Assessment; Vasopressins

Conivaptan is a nonspecific arginine vasopressin receptor antagonist that has been used as therapy in adults who have hypervolemic hyponatremia due to congestive heart failure. Its use in children with congestive heart failure has not been reported. We describe the use of conivaptan in a 4-month-old infant girl with severe hypervolemic hyponatremia and heart failure. A therapeutic weight-based dose was extrapolated from the adult dose. Conivaptan therapy was administered for 48 hours, after which the patient recovered from her hyponatremia without untoward effects. Arginine vasopressin receptor antagonists such as conivaptan may be useful as therapy for hyponatremia associated with heart failure. Further studies are required before conivaptan can be recommended for routine use in children.

Topics: Benzazepines; Female; Heart Failure; Hormone Antagonists; Humans; Hyponatremia; Infant; Neurophysins; Protein Precursors; Severity of Illness Index; Treatment Outcome; Vasopressins

Topics: Child; Fluid Therapy; Hospitalization; Humans; Hypernatremia; Hyponatremia; Hypotonic Solutions; Infusions, Intravenous; Isotonic Solutions; Risk; Vasopressins

Topics: Amitriptyline; Carbamazepine; Comorbidity; Demeclocycline; Diabetic Neuropathies; Diuretics; Furosemide; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Saline Solution, Hypertonic; Spain; Urea; Vasopressins

Topics: Benzazepines; Clinical Trials as Topic; Drug Resistance; Humans; Hyponatremia; Tolvaptan; Vasopressins

Topics: Antidiuretic Hormone Receptor Antagonists; Heart Failure; Humans; Hyponatremia; Morpholines; Sodium; Spiro Compounds; Vasopressins

The Asian variant of intravascular large B cell lymphoma is a special type of intravascular lymphoma with hemophagocytic syndrome and hypercytokinemia including interleukin-6, which stimulates antidiuretic hormone synthesis in the hypothalamus. We present here that the syndrome of inappropriate antidiuretic hormone secretion frequently occurs in patients with the Asian variant of intravascular large B cell lymphoma. The syndrome of inappropriate antidiuretic hormone secretion was found in eight of 118 (6.8%) lymphoma patients at the first diagnosis. Although there were six (5.1%) among 118 lymphoma patients with the Asian variant of intravascular large B cell lymphoma, four of the six patients (66.7%) developed the syndrome of inappropriate antidiuretic hormone secretion. In four patients with the Asian variant of intravascular large B cell lymphoma with the syndrome of inappropriate antidiuretic hormone secretion, elevated serum interleukin-6 and low sodium levels were almost normalized after chemotherapy. The Asian variant of intravascular large B cell lymphoma patients frequently develop the syndrome of inappropriate antidiuretic hormone secretion, and interleukin-6 might play a role in the occurrence of this disease. We should pay attention to hyponatremia caused by the syndrome of inappropriate antidiuretic hormone secretion in patients with the Asian variant of intravascular large B cell lymphoma.

Topics: Adult; Aged; Aged, 80 and over; Asia; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Interleukin-6; Lymphoma, Large B-Cell, Diffuse; Male; Middle Aged; Sodium; Syndrome; Vasopressins; Young Adult

Topics: Critical Care; Humans; Hyponatremia; Inappropriate ADH Syndrome; Osmolar Concentration; Urea; Vasopressins; Water-Electrolyte Balance

Topics: Humans; Hyponatremia; Treatment Outcome; Vasopressins

To evaluate changes in both the N-terminal (arginine vasopressin; AVP) and C-terminal (copeptin) fragments of the vasopressin prohormone before, during, and after an ultramarathon race and to assess vasopressin and copeptin concentrations in runners with and without hyponatremia.. Observational study.. Three trials (2 sodium balance and 1 hyponatremia treatment) in 2 separate approximately 160-km footraces [Western States Endurance Run (WSER) and Javelina Jundred (JJ100)].. Six hyponatremic and 20 normonatremic runners; 19 finishers with 7 completing 100 km.. Plasma AVP ([AVP]p), copeptin ([copeptin]p), sodium ([Na]p), and protein (%plasma volume change; %PV) concentrations.. In the WSER Sodium Trial, a 3-fold prerace to postrace increase in both [AVP]p (0.7 ± 0.4 to 2.7 ± 1.9 pg/mL; P < 0.05) and [copeptin]p (10.3 ± 12.5 to 28.2 ± 16.3 pmol/L; nonsignificant) occurred, despite a 2 mEq/L decrease in [Na]p (138.7 ± 2.3 to 136.7 ± 1.6 mEq/L; NS). A significant correlation was noted between [AVP]p and [copeptin]p postrace (r = 0.82; P < 0.05). In the WSER Treatment Trial, despite the presence of hyponatremia pretreatment versus posttreatment ([Na]p = 130.3 vs 133.5 mEq/L, respectively), both [AVP]p (3.2 vs 2.1 pg/mL) and [copeptin]p (22.5 vs 24.9 pmol/L) were well above the detectable levels. A significant correlation was noted between [AVP]p and [copeptin]p 60 minutes after treatment (r = 0.94; P < 0.05). In the JJ100 Sodium Trial, significant correlations were found between [copeptin]p change and %PV change (r = -0.34; P < 0.05) and between [AVP]p change and [Na]p change (r = 0.39; P < 0.05) but not vice-versa.. [Copeptin]p seems to be a reliable surrogate of stimulated [AVP]p during exercise. Nonosmotic vasopressin stimulation occurs during ultradistance running. [Copeptin]p may better reflect chronic (%PV) vasopressin secretion under conditions of endurance exercise.

Topics: Adult; Athletes; Blood Proteins; Blood Volume; Female; Glycopeptides; Humans; Hyponatremia; Male; Middle Aged; Physical Endurance; Running; Sodium; Vasopressins

Topics: Anticonvulsants; Antimanic Agents; Carbamazepine; Diabetes Insipidus, Nephrogenic; Humans; Hypernatremia; Hyponatremia; Lithium Carbonate; Oxcarbazepine; Risk Factors; Valproic Acid; Vasopressins

Exercise-associated hyponatremia (EAH) is a well know electrolyte disorder in endurance athletes. Although fluid overload is the most like etiology, recent studies, however, argued whether EAH is a disorder of vasopressin secretion. The aims of the present study were to investigate (i) the prevalence of EAH in male ultra-marathoners and (ii) whether fluid intake, aldosterone or vasopressin, as measured by copeptin, were associated with post-race serum sodium concentration ([Na+]). In 50 male ultra-marathoners in a 100 km ultra-marathon, serum [Na+], aldosterone, copeptin, serum and urine osmolality, and body mass were measured pre- and post-race. Fluid intake, renal function parameters and urine excretion were measured. No athlete developed EAH. Copeptin and aldosterone increased; a significant correlation was found between the change in copeptin and the change in serum [Na+], no correlation was found between aldosterone and serum [Na+]. Serum [Na+] increased by 1.6%; body mass decreased by 1.9 kg. The change in serum [Na+] and body mass correlated significantly and negatively. The fluid intake of ~ 0.58 l/h was positively related to the change in body mass and negatively to both post-race serum [Na+] and the change in serum [Na+]. We conclude that serum [Na+] was maintained by both the mechanisms of fluid intake and the hormonal regulation of vasopressin.

Topics: Aldosterone; Athletes; Drinking; Electrolytes; Humans; Hyponatremia; Male; Middle Aged; Running; Sodium; Vasopressins

Topics: Humans; Hyponatremia; Vasopressins

Because boys are four times more likely than girls to develop autism, the role of male hormones (androgens) has received considerable scrutiny. Some researchers implicate arginine vasopressin, an androgen-dependent hormone from the pituitary gland that elicits male behavior. Elevated vasopressin is also the most common cause of low blood sodium (hyponatremia)--most serious in the brains of children. Hyponatremia causes astrocytes to swell, then release the amino acids taurine and glutamine and their water to compensate. Taurin--the brain osmolyte/inhibitory neurotransmitter that suppresses vasopressin--was the amino acid most wasted or depleted in urine of autistic children. Glutamine is a critical metabolic fuel in brain neurons, astrocytes, endothelial cells, and the intestines, especially during hypoglycemia. Because glutamine is not thought to cross the blood-brain barrier significantly, the implications of low blood glutamine in these children are not recognized. Yet children with high brain glutamine from urea cycle disorders are rarely diagnosed with autistic disorders. Other common events in autistic children that release vasopressin are gastrointestinal inflammation, hypoglycemia, and stress. Signs of hyponatremia in these children are salt cravings reported online and anecdotally, deep yellow urine revealing concentration, and relief of autistic behavior by fluid/salt diets. Several interventions offer promise: (a) taurine to suppress vasopressin and replenish astrocytes; (b) glutamine as fuel for intestines and brain; (c) arginine to spare glutamine, detoxify ammonia, and increase brain blood flow; and (d) oral rehydration salts to compensate dilutional hyponatremia. This hypothesis appears eminently testable: Does your child crave salt? Is his urine deep yellow?

Topics: Astrocytes; Autistic Disorder; Brain; Female; Glutamine; Humans; Hyponatremia; Male; Models, Biological; Sodium, Dietary; Taurine; Vasopressins

A 60-year-old female underwent right upper lobectomy of the lung and lymph node dissection under a diagnosis of cancer in the upper lobe of the right lung. Pathological examination showed stage IIIA adenocarcinoma with mediastinal lymph node metastasis. One month after the operation, adjuvant chemotherapy with carboplatin (CBDCA) and paclitaxel (PTX) was initiated. Four days after the chemotherapy, hyponatremia progressed, and central nervous system disorder developed. A diagnosis of syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was made. She recovered after fluid intake restriction and electrolyte correction. SIADH was considered to be due to the adverse effects of anticancer drugs. In postoperative adjuvant chemotherapy, attention should be paid to the serum Na level.

Topics: Adenocarcinoma; Adenocarcinoma of Lung; Animals; Antineoplastic Agents; Antineoplastic Agents, Phytogenic; Antineoplastic Combined Chemotherapy Protocols; Carboplatin; Carcinoma, Non-Small-Cell Lung; Combined Modality Therapy; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lung; Lung Neoplasms; Lymphatic Metastasis; Middle Aged; Paclitaxel; Vasopressins

To explore pathological mechanisms of central hyponatremia and its treatment.. Synchronous assay was made for changes of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), endogenous digitalis-like substance (EDLS), antidiuretic hormone (ADH) in blood, and Na(+) concentrations in blood and urine, and plasma- and urine-osmolality in 68 patients with acute craniocerebral injury (ACI).. Of the 68 patients with ACI, 27 were found to have hyponatremia, and such illness was mostly concentrated on severe cases.. The central hyponatremia in patients with ACI may be related to the increase in the secretion of EDLS and ADH as the result of damaged functions of the hypothalamic-hypophysial system, and it seems that the decrease in blood ANP and BNP has no direct effect on Na(+) concentrations in blood. Inappropriate secretion of antidiuretic hormone syndrome and cerebral salt-wasting syndrome are the two main reasons for hyponatremia in patients with craniocerebral injury. The pathological mechanism, diagnostic standards, as well as treatment methods for the two, however, are not just the same. Intravenous injection of extrinsic thyrotropin-releasing hormone might inhibit dilutional hyponatremia arising from the increase in ADH secretion by patients with ACI.

Topics: Adolescent; Adult; Atrial Natriuretic Factor; Cardenolides; Case-Control Studies; Child; Child, Preschool; Craniocerebral Trauma; Female; Glasgow Coma Scale; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Male; Middle Aged; Natriuretic Peptide, Brain; Neurophysins; Protein Precursors; Saponins; Vasopressins; Young Adult

Topics: Humans; Hyponatremia; Liver Cirrhosis; Prognosis; Severity of Illness Index; Vasopressins

Hyponatremia is among the most common biochemical abnormalities in hospital inpatients. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is one of several causes of hyponatremia, particularly in patients with pulmonary diseases. The mechanism of SIADH associated with pulmonary infection is, however, poorly understood. We report an unusual case of hyponatremia in a man with pulmonary TB and central diabetes insipidus with biochemical evidence of ectopic antidiuretic hormone production as a possible mechanism causing hyponatremia.

Topics: Antidiuretic Agents; Deamino Arginine Vasopressin; Follow-Up Studies; Humans; Hyponatremia; Male; Middle Aged; Sodium; Tuberculosis, Pulmonary; Vasopressins

A 74-year-old man was diagnosed with nephrotic syndrome due to focal segmental glomerulosclerosis, and steroid therapy was initiated. Subsequently, he was affected by deep mycosis, and hence, voriconazole (VRCZ) was administered. On the 16th day, he was transferred to our hospital because of somnolence and malaise. His systolic blood pressure was approximately 80 mmHg, and he showed decreased skin turgor, indicating volume depletion. Laboratory analysis revealed hyponatremia and liver dysfunction. Discontinuation of VRCZ and drip infusion of normal saline improved the consciousness disorder, hyponatremia, and liver dysfunction. The levels of antidiuretic hormone (ADH) and plasma renin activity were elevated. This patient showed high excreted urine sodium, despite volume depletion and low serum osmolality. Therefore, this patient was diagnosed with salt-losing nephropathy (SLN). SLN should be considered for treatment of VRCZ-associated hyponatremia, together with syndrome of inappropriate secretion of ADH.

Topics: Aged; Antifungal Agents; Biomarkers; Chemical and Drug Induced Liver Injury; Fluid Therapy; Humans; Hyponatremia; Kidney Diseases; Liver; Male; Neurophysins; Protein Precursors; Pyrimidines; Renin; Sodium; Sodium Chloride; Time Factors; Treatment Outcome; Triazoles; Vasopressins; Voriconazole; Water-Electrolyte Balance

Nephrogenic syndrome of inappropriate antidiuresis (NSIAD), the X-linked disease resulting from activating mutation of the vasopressin V2 receptor gene (AVPR2), is a recently described condition causative of episodes of hyponatremia in boys and male and female adults.. The objective of the study was the pathophysiological characterization of NSIAD.. A family with NSIAD was identified and investigated for hyponatremic episodes and degrees of urine dilution defects. For the first time, the impact of the mutated V2R on aquaporin 2 (AQP2) excretion is reported.. The study was conducted at a referral center.. Five patients of seven carriers (two young brothers and their mother and her two sisters) were investigated together with age-matched controls.. There were no interventions.. In NSIAD patients, urinary AQP2 excretion occurred independently of concomitant vasopressin excretion and strongly correlated with urine osmolality, confirming direct AQP2 involvement in urine concentration. Water loading was followed by a very slow and incomplete elimination in the asymptomatic hemizygous boy with no suppression of AQP2 excretion and a delayed elimination in the heterozygous women because of an incomplete suppression of AQP2, and it induced hyponatremia in all NSIAD patients. Two hemizygous carriers presented with severe hyponatremia-induced seizures, and the repetition in one of them led to mental retardation.. Hyponatremia was a constant and characteristic aspect of the abnormal response to even mild water-loading tests in an asymptomatic hemizygous child as well as heterozygous adults. We confirm the phenotypic variability of NSIAD, a disease that should be regarded in pediatric intensive care units in presence of severe and/or recurrent hyponatremia, and also in adults, because carriers are prone to hyponatremia.

Topics: Adult; Aquaporin 2; Case-Control Studies; Child, Preschool; DNA Mutational Analysis; Family; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Male; Pedigree; Receptors, Vasopressin; Vasopressins

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Chronic Disease; Heart Failure; Humans; Hyponatremia; Sodium; Tolvaptan; Vasopressins

Although hyponatremia occurs in most patients with severe malaria, its pathogenesis, prognostic significance, and optimal management have not been established. Clinical and biochemical data were prospectively collected from 171 consecutive Bangladeshi adults with severe malaria. On admission, 57% of patients were hyponatremic. Plasma sodium and Glasgow Coma Score were inversely related (r(s) = -0.36, P < 0.0001). Plasma antidiuretic hormone concentrations were similar in hyponatremic and normonatremic patients (median, range: 6.1, 2.3-85.3 versus 32.7, 3.0-56.4 pmol/L; P = 0.19). Mortality was lower in hyponatremic than normonatremic patients (31.6% versus 51.4%; odds ratio [95% confidence interval]: 0.44 [0.23-0.82]; P = 0.01 by univariate analysis). Plasma sodium normalized with crystalloid rehydration from (median, range) 127 (123-140) mmol/L on admission to 136 (128-149) mmol/L at 24 hours (P = 0.01). Hyponatremia in adults with severe malaria is common and associated with preserved consciousness and decreased mortality. It likely reflects continued oral hypotonic fluid intake in the setting of hypovolemia and requires no therapy beyond rehydration.

Topics: Acetylcysteine; Adolescent; Adult; Aged; Bangladesh; Female; Glasgow Coma Scale; Humans; Hyponatremia; Hypovolemia; Malaria; Male; Middle Aged; Seasons; Sodium; Vasopressins; Young Adult

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Heart Failure; Humans; Hyponatremia; Tolvaptan; Treatment Outcome; Vasopressins

Topics: Clinical Competence; Humans; Hyponatremia; Proton Pump Inhibitors; Risk Factors; Sodium; Vasopressins

We describe a rare case of thymic neuroblastoma with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). A 60-year-old male patient was admitted to our hospital for further examination and treatment of anterior mediastinal tumor found at a regular health check-up. On examination there was hyponatremia, decrease in plasma osmolarity and elevation of plasma antidiuretic hormone (ADH) level. Thus, he underwent total thymectomy under the diagnosis of thymoma with SIADH. The tumor was located in the right lobe of the thymus and the final diagnosis was thymic neuroblastoma. To our knowledge, this is the first reported case of thymic neuroblastoma in which production of ADH by tumor cells is demonstrated immunohistochemically. This case highlights the need to consider functional activity of thymic neuroblastoma and complete resection of the tumor is warranted for treatment.

Topics: Biomarkers; Biopsy; Humans; Hyponatremia; Immunohistochemistry; Inappropriate ADH Syndrome; Magnetic Resonance Imaging; Male; Middle Aged; Neuroblastoma; Osmolar Concentration; Thymectomy; Thymus Neoplasms; Tomography, X-Ray Computed; Treatment Outcome; Up-Regulation; Vasopressins

Dehydration increases vasopressin (antidiuretic hormone) secretion from the posterior pituitary gland to reduce water loss in the urine. Vasopressin secretion is determined by action potential firing in vasopressin neurones, which can exhibit continuous, phasic (alternating periods of activity and silence), or irregular activity. Autocrine kappa-opioid inhibition contributes to the generation of activity patterning of vasopressin neurones under basal conditions and so we used in vivo extracellular single unit recording to test the hypothesis that changes in autocrine kappa-opioid inhibition drive changes in activity patterning of vasopressin neurones during dehydration. Dehydration increased the firing rate of rat vasopressin neurones displaying continuous activity (from 7.1 +/- 0.5 to 9.0 +/- 0.6 spikes s(1)) and phasic activity (from 4.2 +/- 0.7 to 7.8 +/- 0.9 spikes s(1)), but not those displaying irregular activity. The dehydration-induced increase in phasic activity was via an increase in intraburst firing rate. The selective -opioid receptor antagonist nor-binaltorphimine increased the firing rate of phasic neurones in non-dehydrated rats (from 3.4 +/- 0.8 to 5.3 +/- 0.6 spikes s(1)) and dehydrated rats (from 6.4 +/- 0.5 to 9.1 +/- 1.2 spikes s(1)), indicating that kappa-opioid feedback inhibition of phasic bursts is maintained during dehydration. In a separate series of experiments, prodynorphin mRNA expression was increased in vasopressin neurones of hyperosmotic rats, compared to hypo-osmotic rats. Hence, it appears that dynorphin expression in vasopressin neurones undergoes dynamic changes in proportion to the required secretion of vasopressin so that, even under stimulated conditions, autocrine feedback inhibition of vasopressin neurones prevents over-excitation.

Topics: Action Potentials; Animals; Cholecystokinin; Dehydration; Electrophysiology; Enkephalins; Female; Hypernatremia; Hyponatremia; Immunohistochemistry; In Situ Hybridization; Naltrexone; Narcotic Antagonists; Neurons; Oxytocin; Protein Precursors; Rats; Rats, Sprague-Dawley; Receptors, Opioid, kappa; RNA, Messenger; Vasopressins

To study any possible relation between hyponatremia following brain injury and the presence of cerebral salt-wasting syndrome (CSWS) or the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), and if vasopressin, brain natriuretic peptide (BNP) and aldosterone have a role in its mechanism.. Patients with brain injury admitted to the intensive care unit were included and had their BNP, aldosterone and vasopressin levels dosed on day 7.. Twenty six adult patients were included in the study. Nine (34.6%) had hyponatremia and presented with a negative water balance and higher values of urinary sodium, serum potassium and diuresis than patients with normonatremia. The serum levels of BNP, aldosterone, and vasopressin were normal and no relation was observed between plasma sodium and BNP, aldosterone or vasopressin.. The most likely cause of hyponatremia was CSWS and there was no correlation between BNP, aldosterone and vasopressin with serum sodium level.

Topics: Adolescent; Adult; Aldosterone; Brain Diseases, Metabolic; Brain Injuries; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Natriuretic Peptide, Brain; Vasopressins; Young Adult

Topics: Algorithms; Humans; Hyponatremia; Shock, Septic; Vasoconstrictor Agents; Vasopressins

Impaired urinary dilution leading to water retention and hyponatremia may occur in patients with cardiac failure, cirrhosis, pregnancy, hypothyroidism, glucocorticoid and mineralocorticoid deficiency. The mechanisms for these defects predominantly involve the non-osmotic stimulation of arginine vasopressin release with upregulation of aquaporin 2 water channel expression and trafficking to the apical membrane of the principal cells of the collecting duct. These perturbations are reversed by V2 vasopressin receptor antagonists. In contrast, urinary concentration defects leading to polyuria are vasopressin-resistant. They may involve several factors, such as impaired counter-current concentration secondary to downregulation of Na-K-2Cl co-transporter. Vasopressin-resistant downregulation of aquaporin 2 expression has also been described as a factor in impaired urinary concentration.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Aquaporin 2; Arginine Vasopressin; Blood Volume; Female; Heart Failure; Homeostasis; Humans; Hyponatremia; Liver Cirrhosis; Models, Biological; Polyuria; Pregnancy; Pregnancy Complications; Pressoreceptors; Sodium-Potassium-Chloride Symporters; Urine; Vasopressins; Water-Electrolyte Balance

A 3-year-old girl presented with osmotic demyelination syndrome after undergoing uneventful neuroendoscopic cystostomy for a growing cystic suprasellar craniopharyngioma following microscopic subtotal resection 1 year previously. Endocrinopathy had well been controlled by hormone replacement therapy and administration of 1-amino-8-d-arginine-vasopressin with serum sodium concentration within the normal range. She presented generalized seizure and fever on postoperative day 7, with hyponatremia beginning on postoperative day 4 and deteriorating despite frequent correction. The serum sodium concentration began to fluctuate on the same day, in the range 111-164 mEq/l, which lasted for 2 weeks, refractory for intense management. Her body temperature also fluctuated between hypo- and hyperthermia not correlated with serum inflammatory markers. Her conscious disturbance progressively deteriorated with spastic paraparesis. T(2)-weighted magnetic resonance (MR) imaging taken on postoperative day 19 revealed hyperintense areas in the pons, external capsule, bilateral thalami, and basal nuclei, which had not been recognized before, suggesting osmotic demyelination syndrome causing central pontine and extrapontine myelinolysis. MR imaging taken on postoperative days 230 and 360 showed some diminished lesions but others persisted and resulted in a cavity. The patient's depressed conscious level did not improve. Suprasellar craniopharyngioma with long-standing hypothalamic dysfunction may be associated with severe osmotic demyelination syndrome even after less invasive surgery, so serum sodium derangement after surgery should be promptly corrected even if only subtle signs are present.

Topics: Brain; Child, Preschool; Consciousness Disorders; Craniopharyngioma; Disease Progression; Female; Fever; Hormone Replacement Therapy; Humans; Hyponatremia; Hypothalamus; Magnetic Resonance Imaging; Myelinolysis, Central Pontine; Nerve Fibers, Myelinated; Neurosurgical Procedures; Pons; Postoperative Complications; Vasopressins; Water-Electrolyte Balance

Hyponatraemia is the most common electrolyte balance disorder occurring in hospitalized patients. The disease results frequently from inappropriate secretion of vasopressin (SIADH). It has been evidenced that the brain consequences of hyponatraemia are more dramatic in young females than in men or postmenopausal women. Since both vasopressin and oestrogen have been reported to inhibit ion fluxes essential for the adaptation of the brain to the lowering of serum sodium concentration, we sought to study the effect of acute and chronic hyponatraemia or hyponatraemia associated with vasopressin on brain morphology in male and female rats. Hyponatraemia was induced with vasopressin (AVP) or with desmopressin (dDAVP) in 12 male and 12 female adult Wistar rats for either 3 hours (acute) or 3.5 days (chronic). The brains of the animals with diagnosed hyponatraemia were fixed in 10% formalin and, following the standard procedure, stained with haematoxylin and eosin. Acute hyponatraemia resulted in white matter oedema with no obvious differences between genders or between groups with AVP- or dDAVP-induced hyponatraemia. Although in chronic hyponatraemia most neurons and astrocytic nuclei appeared to be normal, some neurons were swollen or ischaemic ("dark" neurons) and astrocytes showed a weak reaction. The most spectacular differences between males and females were found in the appearance of blood vessels. Swollen endothelial cells were observed more frequently in female than in male brains and in AVP- than in dDAVP-induced hyponatraemia. The widened Virchow-Robin spaces indicated perivascular oedema and blood-brain barrier damage. The results point to limited vascular adaptation to AVP-associated hyponatraemia in female gender.

Topics: Animals; Brain; Female; Hyponatremia; Male; Rats; Rats, Wistar; Sex Factors; Vasopressins

Schizophrenia, many believe, reflects an enhanced vulnerability to psychological stress. Controlled exposure to stressors, however, has produced inconclusive results, particularly with regards to neurohormones. Some of the variability may be attributable to the nature and psychological significance of the stimulus and failure to control physiologic confounds. In addition, it is possible that the heterogeneity of schizophrenia is an important factor. In a carefully designed study and in a controlled setting, we measured the neuroendocrine response of eight polydipsic hyponatremic (PHS), seven polydipsic normonatremic (PNS), and nine nonpolydipsic normonatremic (NNS) (ie normal water balance) schizophrenic in-patients as well as 12 healthy controls (HC) to two different stressors: one of which appears to influence neuroendocrine secretion through its psychological (cold pressor) and the other (upright posture) through its systemic actions. Subjects in the three psychiatric groups were stabilized and acclimated to the research setting, and all received saline to normalize plasma osmolality. Following the cold pressor, plasma adrenocorticotropin and cortisol levels showed a more prolonged rise in PHS patients relative to PNS patients. NNS patients, in contrast, exhibited blunted responses relative to both of the polydipsic groups and the HC. Peak vasopressin responses were also greater in PHS and blunted in NNS patients. Responses to the postural stimulus were similar across patient groups. These findings provide a mechanism for life threatening water intoxication in schizophrenia; help to reconcile conflicting findings of stress responsiveness in schizophrenia; and potentially identify a discrete patient subset with enhanced vulnerability to psychological stress.

Topics: Adult; Cold Temperature; Drinking; Endocrine System Diseases; Female; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Male; Middle Aged; Neurosecretory Systems; Schizophrenia; Stress, Psychological; Thirst; Vasopressins; Water Intoxication; Water-Electrolyte Imbalance

Water intoxication is a rare cause of coma. The leading causes of excessive hydration are endurance exercise, drug abuse, iatrogenic, cerebral salt wasting, or psychiatric conditions. Self-induced water intoxication in an otherwise healthy person is exceedingly rare.. Single patient case report and review of the literature.. We describe a previously fit and healthy 13-year-old girl who was admitted to the Accident and Emergency department in a comatose state following an unwitnessed seizure. On examination she had a fluctuating Glasgow Coma Score, bilateral mydriatic pupils that responded poorly to light, and an upgoing right plantar. Blood pressure, pulse rate, and oximetry, as well as body mass index, were normal. Routine blood examination revealed hyponatremia, hypochloremia, and a low hematocrit. Water intoxication was suspected and confirmed by reduced urine sodium, serum, and urine osmolality. The computed tomographic brain scan, lumbar puncture opening pressure, and cerebrospinal fluid examination were all normal. She regained consciousness and was fully orientated within 24 hours following intravenous NaCl administration. In this case, thirst without any other apparent pathology led to voluntary water intoxication.. Our case illustrates the classic picture of self-induced water intoxication in a previously fit and healthy patient.

Topics: Adult; Coma; Female; Humans; Hyponatremia; Vasopressins; Water

Symptoms of hyponatremia and diuresis due to cerebral salt wasting syndrome (CSWS) are often observed after aneurysmal subarachnoid hemorrhage (SAH). Inadequately treated CSWS is known to work as a trigger of symptomatic vasospasm in SAH patients. Therefore, it is indispensable to detect and treat CSWS as early as possible in ICU. A 36-year-old man with SAH was admitted to our ICU. His urine volume increased excessively 3 days after ICU admission, and it reached a peak (39,250 ml x day(-1)) on the 6th day in ICU. Since infusion volume was controlled with regard to daily urinary output, hyponatremia was not noticeable and excessive urine volume stood out conspicuously. Though vasopressin and desmopressin were administered, the symptoms of natriuresis and hyponatremia were aggravated, associated with hyper secretion of natriuretic peptides (ANP 160 pg x dl(-1), BNP 172 pg x dl(-1)). Recent studies revealed that hyponatremia and hypovolemia following SAH might be caused by exaggerated secretion of natriuretic peptides. Experimental studies showed that the administration of vasopressin and desmopressin cause excessive secretion of natriuretic peptides under the circumstance of volume expansion in rats. We infer that the administration of vasopressin and desmopressin to our patient deterionated natriuresis in CSWS as in the previous experimental findings.

Topics: Adult; Animals; Atrial Natriuretic Factor; Brain Diseases; Contraindications; Humans; Hyponatremia; Hypovolemia; Male; Natriuresis; Rats; Subarachnoid Hemorrhage; Syndrome; Urination Disorders; Vasopressins

Topics: Cardiovascular Diseases; Humans; Hyponatremia; Vasoconstrictor Agents; Vasopressins

We reported a 92-year-old woman with hyponatremia (117 mmol/l) occurring three days after the introduction of tramadol. Diagnosis of inappropriate antidiuretic hormone secretion was based on blood and urinary analysis and dosage of antidiuretic hormone. Natremia became normal after tramadol cessation and fluid restriction. Natremia must be measured when neurological abnormality occurs with tramadol treatment.

Topics: Aged, 80 and over; Analgesics, Opioid; Female; Humans; Hyponatremia; Muscle, Skeletal; Pain; Tramadol; Vasopressins

Topics: Fluid Therapy; Humans; Hyponatremia; Interleukin-6; Physical Endurance; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Dogs; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins; Water-Electrolyte Imbalance

A 66-year-old woman was admitted to our hospital because of vomiting and appetite loss. For the 2 days prior to admission, she had a cold, which had developed into acute viral bronchitis on admission. Because laboratory data on admission showed hyponatremia, intravenous infusion of Ringer's lactate solution was started. However, generalized seizures appeared, and she developed a coma on the day of admission. Her plasma antidiuretic hormone (ADH) level was high in the context of a low serum osmolality on the second hospital day. The infusion rate was increased, and the patient's consciousness level returned to normal. However, her normalized serum Na level declined again as she drank much water to reduce throat discomfort. As the throat discomfort caused by the throat inflammation improved with azulene gargling, her water intake was reduced, and the serum Na concentration returned to normal. Thus, polydipsia caused by a throat inflammation partially contributed to hyponatremia in this patient. We note that increased ADH secretion has been reported in adults with acute respiratory infection. Therefore, we concluded that polydipsia caused by the throat inflammation, plus increased ADH secretion, resulted in hyponatremia in this patient. We should pay attention to the behavior of drinking extra fluid in patients with acute respiratory infections.

Topics: Aged; Bronchitis; Drinking Behavior; Female; Humans; Hyponatremia; Pharyngitis; Seizures; Vasopressins; Water Intoxication

Although hyponatremia is a common, usually mild, and relatively asymptomatic disorder of electrolytes, acute severe hyponatremia can cause substantial morbidity and mortality, particularly in patients with concomitant disease. In addition, overly rapid correction of chronic hyponatremia can cause severe neurologic deficits and death, and optimal treatment strategies for such cases are not established. An expert panel assessed the potential contributions of aquaretic nonpeptide small-molecule arginine vasopressin receptor (AVPR) antagonists to hyponatremia therapies. This review presents their conclusions, including identification of appropriate treatment populations and possible future indications for aquaretic AVPR antagonists.

Topics: Antidiuretic Hormone Receptor Antagonists; Humans; Hyponatremia; Vasopressins

We report the development of recurrent hyponatremia after intrathecal methotrexate that was not associated with elevated levels of antidiuretic hormone. We speculate that a central nervous system natriuretic peptide may be involved in the pathogenesis of the naturesis following intrathecal methotrexate.

Topics: Aged; Antimetabolites, Antineoplastic; Female; Humans; Hyponatremia; Injections, Spinal; Methotrexate; Natriuretic Peptides; Recurrence; Vasopressins

A 71-year old man with failed back syndrome was admitted to hospital with oliguria that had occurred 4 days after his dose of paroxetine had been increased to 40 mg x day(-1). Laboratory data on admission revealed hyponatremia (124 mmol x l(-1)), low serum osmolarity (267 mOsm x l(-1)) with a normal level of serum antidiuretic hormone (1.7 pg x ml(-1)), and concentrated urine (430 mOsm x l(-1)). He was diagnosed as having syndrome of inappropriate secretion of antidiuretic hormone, associated with paroxetine; this drug was discontinued immediately after admission. The hyponatremia was treated with saline infusion, water restriction, and furosemide; serum sodium level returned to normal on hospital day 5. Paroxetine is being increasingly used for depression and chronic pain management because of its favorable side-effect profile; however, we should be alert to hyponatremia in patients on paroxetine by carrying out periodic monitoring of serum electrolytes, especially in elderly patients.

Topics: Aged; Antidepressive Agents, Second-Generation; Chronic Disease; Depressive Disorder; Electrolytes; Humans; Hyponatremia; Inappropriate ADH Syndrome; Intervertebral Disc Displacement; Male; Pain; Paroxetine; Sodium; Spinal Stenosis; Vasopressins

To observe the changes of plasma renin activity, antidiuretic hormone and brain natriuretic peptide in chronic heart failure (CHF) and their correlation with hyponatremia.. Plasma levels of PRA, ADH, and BNP were measured by radioimmunology in 76 CHF patients. Forty-one out of 76 CHF patients with hyponatremia and 35 CHF patients without hyponatremia were identified by serum sodium. The rates of rehospitalization within 3 months were compared in two groups.. Levels of plasma renin activity, ALD, and BNP in CHF patients with hyponatremia were notably higher than those in patients without hyponatremia classified by New York Heart Association (NYHA) grade II - IV: PRA [(2.7 +/- 1.0) ng.ml(-1).h(-1) vs. (1.8 +/- 0.7) ng.ml(-1).h(-1), (4.3 +/- 1.2) ng.ml(-1).h(-1) vs. (3.0 +/- 0.9) ng.ml(-1).h(-1), (5.6 +/- 1.3) ng.ml(-1).h(-1) vs. (3.5 +/- 1.1) ng.ml(-1).h(-1), respectively, P < 0.05], ADH [(59.7 +/- 17.4) ng/L vs. (48.6 +/- 15.3) ng/L, (68.4 +/- 17.6) ng/L vs. (56.3 +/- 19.2) ng/L, (75.3 +/- 20.0) ng/L vs. (51.4 +/- 16.2) ng/L, respectively, P < 0.05] and BNP [(276.4 +/- 75.2) ng/L vs. (185.3 +/- 55.3) ng/L, (380.1 +/- 113.6) ng/L vs. (258.5 +/- 62.1) ng/L, (564.0 +/- 125.2) ng/L vs. (405.3 +/- 102.9) ng/L, respectively, P < 0.05]. In the simple regression analyses, hyponatremia was negative correlated with PRA, ADH and BNP (r = -0.31, P < 0.05; r = -0.28, P < 0.05, r = -0.80, P < 0.01). The rate of rehospitalization within 3 months in hyponatremia group was higher than that in control group.. There is relation of hyponatremia to the changes of plasma renin activity, antidiuretic hormone and brain natriuretic peptide in chronic heart failure. Hyponatremia may accelerate the excretion of plasma PRA, ADH and BNP in chronic heart failure. Neuroendocrine activation in patients of congestive heart failure with hyponatremia is higher than that of normal natremia group.

Topics: Aged; Aged, 80 and over; Female; Heart Failure; Humans; Hyponatremia; Male; Middle Aged; Natriuretic Peptide, Brain; Renin; Sodium; Vasopressins

Two children with complete congenital anterior hypopituitarism developed hyponatremia; inappropriate secretion of antidiuretic hormone was documented despite adequate hormonal replacement therapy. These cases show that congenital hypopituitarism can be associated with SIADH in children later than the neonatal period, despite adequate replacement therapy.

Topics: Adolescent; Child, Preschool; Female; Fluid Therapy; Hormone Replacement Therapy; Humans; Hyponatremia; Hypopituitarism; Inappropriate ADH Syndrome; Magnetic Resonance Imaging; Male; Pituitary Gland, Anterior; Treatment Outcome; Vasopressins

Topics: Extracellular Fluid; Fluid Therapy; Humans; Hyponatremia; Hypotonic Solutions; Isotonic Solutions; Vasopressins

Disorders of sodium imbalance are commonly encountered in clinical practice and can have a substantial impact on the prognosis of the patient. These disorders are more common in the elderly. Sodium disorders can cause serious neurologic symptoms and even death, particularly among hospitalized patients. The identification of sodium abnormalities and appropriate clinical intervention are critical for improving patient outcomes. Early recognition of hyponatremia and hypernatremia can provide a clue to an underlying disorder. In this update, we have summarized age-related homeostatic changes that impair sodium balance, medications that alter salt and water handling, and the recognition and management of sodium disorders in elderly patients.

Topics: Age Factors; Aged; Benzothiadiazines; Diuretics; Education, Medical, Continuing; Humans; Hypernatremia; Hyponatremia; Prognosis; Sodium; Sodium Chloride Symporter Inhibitors; Vasopressins; Water-Electrolyte Balance

Yamanouchi is developing conivaptan, a diuretic and active vasopressin V1a and V2 antagonist, which has an aquaretic effect, for the potential treatment of hyponatremia and heart failure. In January 2004, Yamanouchi submitted an NDA in the US for injectable conivaptan for the treatment of hyponatremia and, in December 2004, the FDA issued approval, although additional safety data were requested.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Clinical Trials as Topic; Clinical Trials, Phase III as Topic; Diuretics; Edema; Heart Failure; Humans; Hyponatremia; Molecular Structure; Structure-Activity Relationship; Vasopressins

Nonosmotic antidiuretic hormone (ADH) activity can cause severe hyponatremia during involuntary fluid administration. We looked for evidence of this before and during intravenous (IV) fluid administration in children treated for gastroenteritis.. In this prospective observational study, plasma ADH, electrolytes, osmolality, and glucose were measured in 52 subjects before (T0) and 4 hours after (T4) starting 0.45% saline + 2.5% dextrose and subsequently when indicated. Hormonal markers of stress were measured at T0. Urine samples were collected to measure electrolytes and osmolality.. The nonosmotic stimuli of ADH secretion that we identified were vomiting (50 of 52), dehydration (median: 5%; range: 3-8%), hypoglycemia (2 of 52), and raised hormonal markers of stress (mean +/- SD: cortisol, 1094 +/- 589 nmol/L; reverse triiodothyronine, 792 +/- 293 pmol/L). At T0, half the children were hyponatremic (plasma sodium concentration of < 135 mmol/L; n = 27). The median plasma ADH concentration at T0 was significantly elevated (median: 7.4 pg/mL; range: < 1.9-85.6 pg/mL). ADH was high in both hyponatremic and normonatremic children and remained high at T4 in 33 of the 52 children, 22 of whom were concurrently hyponatremic. At T4, mean plasma sodium concentration was unchanged in the hyponatremic children but was 2.6 mmol/L (+/-2.0) lower in those who were initially normonatremic. Urine tonicity was high compared with 0.45% saline in 16 of 19 children at baseline and in 20 of 37 children after 3 to 12 hours of IV fluids.. Nonosmotic stimuli of ADH secretion are frequent in children with gastroenteritis. Their persistence during IV-fluid administration predisposes to dilutional hyponatremia. The use of hypotonic saline for deficit replacement needs to be reassessed.

Topics: Child; Child, Preschool; Female; Fluid Therapy; Gastroenteritis; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Male; Prospective Studies; Vasopressins

Managing children with diabetes insipidus (DI) in the perioperative period is complicated and frequently associated with electrolyte imbalance compounded by over- or underhydration. In this study the authors developed and prospectively evaluated a multidisciplinary approach to the perioperative management of DI with a comparison to 19 historical control children. Eighteen children either with preoperative DI or undergoing neurosurgical operations associated with a high risk for developing postoperative DI were identified and managed using a standardized protocol. In all patients in whom DI occurred during or after surgery, a continuous intravenous infusion of aqueous vasopressin was initiated and titrated until antidiuresis was established. Intravenous fluids were given as normal saline and restricted to two thirds of the estimated maintenance rate plus amounts necessary to replace blood losses and maintain hemodynamic stability. In all children managed in this fashion, perioperative serum sodium concentrations were generally maintained between 130 and 150 mEq/L, and no adverse consequences of this therapy developed. In the 24-hour period evaluated, the mean change in serum sodium concentrations between the historical controls was 17.6 +/- 9.2 mEq/L versus 8.36 +/- 6.43 mEq/L in those children managed by the protocol. Hyponatremia occurred less frequently in the children managed with this protocol compared with historical controls.

Topics: Adolescent; Child; Child, Preschool; Clinical Protocols; Deamino Arginine Vasopressin; Diabetes Insipidus; Female; Humans; Hyponatremia; Hypotonic Solutions; Infusions, Intravenous; Male; Neurosurgical Procedures; Perioperative Care; Postoperative Complications; Prospective Studies; Renal Agents; Seizures; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Aquaporin 4; Aquaporins; Astrocytes; Cells, Cultured; Child; Humans; Hyponatremia; Isotonic Solutions; Pediatrics; Rats; Rehydration Solutions; Severity of Illness Index; Vasopressins

Older depressed patients are at high risk for development of hyponatremia after initiation of the selective serotonin reuptake inhibitor paroxetine, despite clinical monitoring and preventive management. The purposes of this study were to determine the incidence and etiology of paroxetine-induced hyponatremia in older patients and to identify patient characteristics that may account for variability in susceptibility to this adverse event.. This prospective, longitudinal study was conducted in a university-based ambulatory psychiatric research clinic from August 1999 through September 2001. Patients included 75 men and women aged 63 through 90 years (mean +/- SD age, 75.3 +/- 6.0 years) who received a diagnosis of a current Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, major depressive episode and were prescribed paroxetine. We monitored plasma sodium levels before initiating paroxetine therapy and after 1, 2, 4, 6, and 12 weeks of treatment. In a subset of individuals, we measured levels of antidiuretic hormone, glucose, serum urea nitrogen, and creatinine. Hyponatremia was defined as a plasma sodium level of less than 135 mEq/L after initiation of paroxetine therapy.. Hyponatremia developed in 9 (12%) of the 75 patients after initiation of paroxetine treatment. Mean +/- SD time to development of hyponatremia was 9.3 +/- 4.7 days (median, 9 days; range, 1-14 days; n = 8). In the multivariate regression, lower body mass index and lower baseline plasma sodium level (<138 mEq/L) were significant risk factors for the development of hyponatremia in these patients.. Hyponatremia is an under recognized and potentially serious complication of paroxetine treatment in older patients. Our results provide a foundation for understanding the etiology and risk factors associated with paroxetine-induced hyponatremia.

Topics: Aged; Aged, 80 and over; Antidepressive Agents, Second-Generation; Biomarkers; Blood Glucose; Blood Urea Nitrogen; Creatinine; Dose-Response Relationship, Drug; Female; Humans; Hyponatremia; Incidence; Male; Middle Aged; Natriuresis; Osmolar Concentration; Paroxetine; Pennsylvania; Prospective Studies; Regression Analysis; Risk Factors; Selective Serotonin Reuptake Inhibitors; Severity of Illness Index; Sodium; Statistics as Topic; Treatment Failure; Vasopressins

Topics: Acute Disease; Child; Energy Metabolism; Fluid Therapy; Humans; Hyponatremia; Isotonic Solutions; Sodium Chloride; Urination; Vasopressins; Water-Electrolyte Balance

Inappropriate antidiuretic hormone secretion syndrome is rare in patients with gynecologic tumors.. A 22-year-old woman presented with inappropriate antidiuretic hormone secretion symptoms during the 2 months preceding the diagnosis of an immature ovarian teratoma. Vasopressin levels in serum and in the urine were very low. Restriction of water intake and surgical removal of the teratoma resulted in the definitive correction of the hyponatremia. This observation suggests that immature teratoma cells can produce a vasopressin-like factor, and the syndrome may be a sign of an ovarian malignancy.. Pelvic organs should be examined when the more common causes of inappropriate antidiuretic hormone secretion syndrome have been ruled out.

Topics: Adult; Antineoplastic Combined Chemotherapy Protocols; Drinking; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Ovarian Neoplasms; Teratoma; Vasopressins

Managing children with diabetes insipidus (DI) in the perioperative period is complicated and frequently associated with electrolyte imbalance compounded by over- or underhydration. In this study the authors developed and prospectively evaluated a multidisciplinary approach to the perioperative management of DI with a comparison to 19 historical control children. Eighteen children either with preoperative DI or undergoing neurosurgical operations associated with a high risk for developing postoperative DI were identified and managed using a standardized protocol. In all patients in whom DI occurred during or after surgery, a continuous intravenous infusion of aqueous vasopressin was initiated and titrated until antidiuresis was established. Intravenous fluids were given as normal saline and restricted to two thirds of the estimated maintenance rate plus amounts necessary to replace blood losses and maintain hemodynamic stability. In all children managed in this fashion, perioperative serum sodium concentrations were generally maintained between 130 and 150 mEq/L, and no adverse consequences of this therapy developed. In the 24-hour period evaluated, the mean change in serum sodium concentrations between the historical controls was 17.6 +/- 9.2 mEq/L versus 8.36 +/- 6.43 mEq/L in those children managed by the protocol. Hyponatremia occurred less frequently in the children managed with this protocol compared with historical controls.

Topics: Adolescent; Child; Child, Preschool; Clinical Protocols; Deamino Arginine Vasopressin; Diabetes Insipidus; Female; Humans; Hyponatremia; Hypotonic Solutions; Infusions, Intravenous; Male; Neurosurgical Procedures; Perioperative Care; Postoperative Complications; Prospective Studies; Renal Agents; Seizures; Sodium; Vasopressins; Water-Electrolyte Balance

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by hyponatremia and the plasma hypoosmolality induced by water retention attributable to persistent antidiuretic hormone (ADH) release. It has been reported that SIADH may occur due to various factors in patients with malignant tumor. We report a case of hypopharyngeal cancer complicated by SIADH following chemotherapy. A 72-year-old woman with hypopharyngeal cancer was treated by oral administration of S-1 and intravenous administration of low-dose cisplatin following radiation therapy. General fatigue and coma occurred during the third course of this chemotherapy, using S-1 and low-dose cisplatin. We believed that she had SIADH because of the results of examinations including hyponatremia, serum hypoosmolality and increasing serum ADH level. We treated her by fluid restriction and intravenous administration of hypertonic saline and furosemide, and she recovered. Unfortunately, her hypopharyngeal cancer gradually progressed and she died of acute pneumonia three months later.

Topics: Aged; Antimetabolites, Antineoplastic; Antineoplastic Agents; Carcinoma, Squamous Cell; Cisplatin; Drug Combinations; Fatal Outcome; Female; Humans; Hyponatremia; Hypopharyngeal Neoplasms; Inappropriate ADH Syndrome; Osmolar Concentration; Oxonic Acid; Pyridines; Radiotherapy, Adjuvant; Tegafur; Vasopressins

We describe a novel missense mutant of arginine vasopressin (AVP)-dependent neurohypophyseal diabetes insipidus in an autosomal dominant family. A 54-year-old woman was admitted to our hospital because of thyroidectomy for thyroid cancer. After thyroidectomy she was found to have hypernatremia and polyuria and polydipsia both of which had been present from childhood. She had no obstructive hydronephrosis. Her father, father's younger sister and her third son also had polyuria and polydipsia. Basal plasma AVP concentration at normal plasma osmolality was normal but did not respond to increased plasma osmolality despite hyperosmolality during infusion of hypertonic saline infusion, indicating that plasma AVP secretion was impaired. Sodium concentration in urine and urine osmolality were low and increased after nasal administration of DDAVP. There was a diminished but bright signal of pituitary posterior gland on magnetic resonance T1 weighted image. Molecular genetic analysis demonstrated that the patient and her son had a single heterozygous missense mutation (G-->A) at nucleotide 1829 in 1 AVP allele, yielding an abnormal AVP precursor with lacking Glu-47 in its neurophysin II moiety. The abnormal AVP precursor may be related to the impaired AVP secretion.

Topics: Adult; Base Sequence; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Female; Humans; Hyponatremia; Male; Middle Aged; Molecular Sequence Data; Mutation, Missense; Neurophysins; Pedigree; Polyuria; Protein Precursors; Sequence Analysis, DNA; Vasopressins

The vasopressin (VP) magnocellular neurosecretory cells (MNCs) in the supraoptic and paraventricular (PVN) nuclei are regulated by estrogen and exhibit robust expression of estrogen receptor (ER)-beta. In contrast, only approximately 7.5% of oxytocin (OT) MNCs express ER-beta. We examined the osmotic regulation of ER-beta mRNA expression in MNCs using quantitative in situ hybridization histochemistry. Hyper-osmolality induced via 2% hypertonic saline ingestion significantly decreased, whereas sustained hypo-osmolality induced via d-d-arginine VP and liquid diet increased ER-beta mRNA expression in MNCs (p < 0.05). Thus, the expression of ER-beta mRNA correlated inversely with changes in plasma osmolality. Because hyper-osmolality is a potent stimulus for VP and OT release, this suggests an inhibitory role for ER-beta in MNCs. Immunocytochemistry demonstrated that the decrease in ER-beta mRNA was translated into depletion of receptor protein content in hyper-osmotic animals. Numerous MNCs were positive for ER-beta in control animals, but they were virtually devoid of ER-beta-immunoreactivity (IR) in hyper-osmotic animals. The osmotically induced decrease in ER-beta expression was selective for MNCs because ER-beta-IR remained unaltered in PVN parvocellular neurons. Plasma estradiol and testosterone were not correlated with ER-beta mRNA expression after osmotic manipulation, suggesting that ER-beta expression was not driven by ligand availability. Expression of FOS-IR in MNCs with attenuated ER-beta-IR, and the absence of FOS-IR in parvocellular neurons that retain ER-beta-IR suggest a role for neuronal activation in the regulation of ER-beta expression in MNCs. Thus, osmotic modulation of ER-beta expression in MNCs may augment or attenuate an inhibitory effect of gonadal steroids on VP release.

Topics: Animals; Blood Volume; Body Weight; Estrogen Receptor beta; Hematocrit; Hormones; Hypernatremia; Hyponatremia; Male; Neurons; Osmolar Concentration; Osmotic Pressure; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Rats, Sprague-Dawley; Receptors, Estrogen; Sodium Chloride; Supraoptic Nucleus; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

A patient with a history of schizophrenia was brought to the emergency department with extensive self-inflicted soft tissue injuries. Primary polydipsia was evident on admission, because he had a maximally dilute urine, a urine flow rate of 10 ml/min, and hyponatraemia (100 mmol/l). During an imaginary consultation with Professor McCance in which he applied basic principles of integrative physiology and a deductive analysis in quantitative terms, other reasons for the polyuric state were considered. Moreover, based on the very low value for the concentration of urea in plasma (< 0.7 mmol/l, BUN 1 mg /dl), the goals of therapy to prevent osmotic demyelination became evident. Applying this simple approach, a more comprehensive and accurate differential diagnosis, and a plan for therapy to avoid serious complications was compiled.

Topics: Adult; Diabetes Insipidus; Diagnosis, Differential; Diuresis; Humans; Hyponatremia; Male; Polyuria; Renal Agents; Schizophrenia; Urea; Vasopressins

Hypopituitarism and hyponatremia, especially when severe, are infrequent findings particularly when the cause of hypopituitarism at presentation is unknown and untreated. Interestingly, hyponatremia is usually seen in elderly patients with hypopituitarism due to various causes. We present a case with unrecognized and untreated hypopituitarism due to a large aneurysm of the internal carotid artery in the sellar region causing the syndrome of inappropriate secretion of antidiuretic hormone (SIADH).

Topics: Aneurysm; Carotid Artery, Internal; Female; Humans; Hyponatremia; Hypopituitarism; Inappropriate ADH Syndrome; Magnetic Resonance Angiography; Magnetic Resonance Imaging; Middle Aged; Radiography; Vasopressins

Topics: Cathartics; Colonoscopy; Humans; Hyponatremia; Phosphates; Polyethylene Glycols; Seizures; Vasopressins

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Renal Agents; Vasopressins

To study the physiological mechanisms of plasma hypoosmolality in patients with pneumonia and on this basis to elaborate principles of therapy for this condition.. 52 individuals of different age, including 26 patients with pneumonia, were examined. Osmolality, the concentrations of ions of sodium, potassium, magnesium, and creatinine were measured in the serum.. The patients with pneumonia were found to have osmolality, hyponatremia in combination with severe hypodiuresis, high urinary osmotic pressure and intensive reabsorption of osmotically free water in the kidney, which leads to blood dilution. As hypoosmolality usually causes higher diuresis and decreased urinary osmolality; hypodiuresis with high urinary osmolality in pneumonia is indicative of effective renal performance and its altered regulation evidently due to the hypersecretion of vasopressin or to the decreased formation of a number of autacoids in the kidney.. Blood hypoosmolality and hyponatremia in the examined patients result from inadequate blood osmolality and high urinary osmotic concentrating. The principles of this condition in pneumonia are discussed and aquaretics are proposed for use as pathogenetic therapy.

Topics: Acute Disease; Adolescent; Adult; Convalescence; Female; Humans; Hyponatremia; Male; Middle Aged; Osmolar Concentration; Pneumonia; Vasopressins

Hyponatremia as the presenting manifestation of empty sella syndrome is rare. There is little clinical experience in the management of this problem and its possible therapeutic complications. We herein report on a 44-year-old woman with a past history of massive postpartum hemorrhage who was admitted because of hyponatremia and disturbed consciousness. Initial biochemical data suggested the effects of antidiuretic hormone, but fluid restriction alone offered limited benefit. Later, hormonal levels indicated hypopituitarism. Magnetic resonance imaging and cisternography led to a diagnosis of empty sella. Although glucocorticoid substitution was initiated and the clinical condition initially improved, possible myelinolysis subsequently became a complication. With early recognition and immediate replacement of hypotonic fluid, the patient completely recovered. We report this case to illustrate the fact that glucocorticoid substitution and concurrent fluid restriction can probably lead to myelinolysis in empty sella syndrome patients. We suggest that the serum sodium level should be frequently monitored and that much more attention should be paid to the neurologic signs when substituting glucocorticoids in these patients, even though the increment in the serum sodium level is acceptable. Once possible myelinolysis develops, early recognition is critical, and the immediate replacement of hypotonic fluid is suggested.

Topics: Adult; Empty Sella Syndrome; Female; Humans; Hyponatremia; Myelinolysis, Central Pontine; Vasopressins

Hyponatremia can result from a wide range of causes. While hyponatremia is known to occur in patients with hypopituitarism, severe hyponatremia occurring as the presenting feature of hypopituitarism is very rare. We present two cases in which severe hyponatremia developed with weakness, light-headedness and seizure. The hyponatremia in these 2 cases mimicked the laboratory diagnostic criteria of a syndrome of inappropriate secretion of antidiuretic hormone (SIADH). However, the hormone studies displayed hypopituitarism. Hyponatremia was completely corrected after administering a supplement of prednisolone and L-thyroxine. Computerized tomography of the brain revealed an adenoma of the pituitary gland. These two cases illustrate that severe hyponatremia may be the presenting feature of clinically non-functional pituitary adenoma with hypopituitarism, which should be kept in mind in the differential diagnosis of hyponatremia mimicking SIADH.

Topics: Adenoma; Aged; Anti-Inflammatory Agents; Diagnosis, Differential; Drug Therapy, Combination; Humans; Hyponatremia; Male; Middle Aged; Pituitary Neoplasms; Prednisolone; Thyroid Hormones; Thyroxine; Vasopressins

To determine the potential role of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in the pathogenesis of cerebral salt wasting.. Clinical case report.. Regional pediatric intensive care unit.. A 3-yr-old boy with a cerebral infarct secondary to traumatic carotid artery dissection who developed hyponatremia associated with weight loss and excessive renal sodium excretion on the sixth day after hospitalization.. Plasma concentrations of ANP, BNP, antidiuretic hormone, and renin were determined serially and compared with concentrations measured in a group of eight healthy children undergoing elective surgical procedures. Compared with controls, ANP and BNP plasma concentrations on the eighth day after hospitalization were increased 1.9-fold and 7.7-fold, respectively. Thereafter, the course of ANP and BNP paralleled that of sodium and H2O excretion and remained elevated until the 14th (BNP) and 16th (ANP) days after hospitalization. Serum antidiuretic hormone and renin concentrations were within normal ranges during the entire observation period.. Cerebral salt wasting is associated with elevated plasma concentrations of ANP and BNP. Natriuretic peptides may play a role in the pathogenesis of this syndrome.

Topics: Atrial Natriuretic Factor; Carotid Artery, Internal, Dissection; Cerebral Infarction; Child; Child, Preschool; Humans; Hyperpituitarism; Hyponatremia; Male; Natriuretic Peptide, Brain; Renin; Vasopressins

We report a pregnant woman presenting with seizure secondary to hyponatremia by inappropriate antidiuretic hormone secretion. Aetiology was unknown urinary and lung tuberculosis. This case report presents diagnosis strategy of inappropriate antidiuretic hormone secretion and the arguments for its aetiology.

Topics: Adult; Female; Humans; Hyponatremia; Pregnancy; Pregnancy Complications; Seizures; Tuberculosis, Pulmonary; Tuberculosis, Urogenital; Vasopressins

Life-threatening and fatal hyponatraemic complications following ecstasy use have previously been documented.. To define clinical features of hyponatraemia following the ingestion of 3,4-methylenedioxymethamphetamine (MDMA, 'ecstasy').. Retrospective case series.. All enquiries to the London centre of the National Poisons Information Service (NPIS) between December 1993 and March 1996 were screened for cases of MDMA use associated with hyponatraemia (serum sodium <130 mmol/l). History of fluid consumption, presenting features and subsequent clinical course were recorded.. Seventeen patients, aged 15-26 years, were identified. Serum sodium levels ranged between 107 mmol/l and 128 mmol/l. In six patients, biochemical results were consistent with inappropriate secretion of antidiuretic hormone (SIADH). Analytical confirmation of MDMA ingestion was obtained in 10 patients. Ten patients were known to have ingested a large amount of non-alcoholic or alcoholic fluid. The clinical pattern was remarkably uniform, with initial vomiting and disturbed behaviour, followed in 11 patients by seizures. Drowsiness, a mute state and disorientation were observed for up to 3 days. Two patients died; 14 made a complete recovery.. MDMA can cause life-threatening hyponatraemic encephalopathy when accompanied by excessive fluid ingestion. The mechanism involves inappropriate secretion of antidiuretic hormone.

Topics: Adolescent; Adult; Alcohol Drinking; Amphetamine-Related Disorders; Drinking; Female; Hallucinogens; Humans; Hyponatremia; Male; N-Methyl-3,4-methylenedioxyamphetamine; Retrospective Studies; Vasopressins

The magnocellular neurones of the hypothalamo-neurohypophysial system (HNS) play a vital role in the maintenance of body homeostasis by regulating oxytocin (OT) and vasopressin (VP) secretion from the posterior pituitary. During hyperosmolality, OT and VP mRNA levels are known to increase by approximately two-fold, whereas during chronic hypoosmolality, OT and VP mRNA levels decrease to approximately 10-20% of basal levels. In these studies, we evaluated changes in cell size associated with these physiological conditions. Cell and nuclear sizes of neurones in the supraoptic nucleus (SON), the nucleus of the lateral olfactory tract (LOT) and the medial habenular nucleus (MHB) were measured from neurones identified by in situ hybridization histochemistry for beta(III)-tubulin mRNA, and measurements were made from OT and AVP magnocellular neurones in the SON after phenotypic identification by immunohistochemistry. Under hypoosmolar conditions, the cell and nuclear sizes of OT and VP magnocellular neurones decreased to approximately 60% of basal values, whereas cell and nuclear sizes of OT and VP neurones in hyperosmolar rats increased to approximately 170% of basal values. In contrast, neither hyperosmolality, nor hypoosmolality significantly affected cell and nuclear sizes in the LOT and MHB. These results confirm previous studies that showed that magnocellular neurones increase cell size in response to hyperosmolar conditions and, for the first time, demonstrate a marked decrease in cell size in the SON in response to chronic hypoosmolar conditions. These dramatic changes in cell and nuclear size directly parallel changes in OT and VP gene expression in the magnocellular neurones of the SON and, consequently, are consistent with the pronounced bidirectional changes in gene expression and cellular activity found during these osmotic perturbations. Our results therefore support the concept of global alterations in the synthetic activity of magnocellular OT and AVP neurones in response to extracellular osmolality.

Topics: Animals; Cell Size; Gene Expression; Habenula; Hyponatremia; Hypothalamus, Anterior; In Situ Hybridization; Male; Neurons; Olfactory Pathways; Osmolar Concentration; Oxytocin; Rats; Rats, Sprague-Dawley; RNA, Messenger; Transcription, Genetic; Vasopressins; Water-Electrolyte Balance

Topics: Aged; Aged, 80 and over; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Renal Agents; Self Medication; Vasopressins

Five patients with well-controlled, long-standing, central diabetes insipidus had acute development of dehydration, hyponatremia, and inappropriate natriuresis in the setting of polyuria resistant to exogenous antidiuretic hormone. Hyponatremia and dehydration worsened with fluid restriction or use of exogenous antidiuretic hormone. We discuss the challenges in diagnosis and management of probable salt wasting in children with central diabetes insipidus.

Topics: Adolescent; Adult; Child; Child, Preschool; Diabetes Insipidus, Neurogenic; Female; Humans; Hyponatremia; Male; Polyuria; Sodium Chloride; Vasopressins

Hyponatremia is a well known complication of traumatic and nontraumatic cerebral injury, often related to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Nonetheless, it also can be associated with a different entity, the syndrome of cerebral salt wasting (CSW). The authors report the case of a 4.5-year-old boy presenting with major head injury who at day 6 after admission had generalized tonic-clonic seizures caused by severe acute hyponatremia (serum sodium level, 119 mmol/L) and signs of dehydration. Despite initial isotonic rehydration, hyponatremia persisted because of excessive renal salt losses and concomitant enormous water losses, necessitating increasing amounts of sodium, up to 160 mmol/kg/d, and large amounts of intravenous fluids, up to 27 L/d. Highly increased levels of atrial natriuretic peptide (ANP) confirmed the diagnosis of CSW. The occurrence of a CSW has to be recognized early in the clinical course for adequate treatment and remains one of the important differential diagnosis of SIADH in hyponatremic states in patients with cerebral disorders, especially after head injury.

Topics: Acute Disease; Adrenocorticotropic Hormone; Aldosterone; Atrial Natriuretic Factor; Brain; Brain Injuries; Child, Preschool; Humans; Hydrocortisone; Hyponatremia; Male; Sodium; Vasopressins

How does a neuron, challenged by an increase in synaptic input, display a response that is independent of the initial level of activity? Here we show that both oxytocin and vasopressin cells in the supraoptic nucleus of normal rats respond to intravenous infusions of hypertonic saline with gradual, linear increases in discharge rate. In hyponatremic rats, oxytocin and vasopressin cells also responded linearly to intravenous infusions of hypertonic saline but with much lower slopes. The linearity of response was surprising, given both the expected nonlinearity of neuronal behavior and the nonlinearity of the oxytocin secretory response to such infusions. We show that a simple computational model can reproduce these responses well, but only if it is assumed that hypertonic infusions coactivate excitatory and inhibitory synaptic inputs. This hypothesis was tested first by applying the GABA(A) antagonist bicuculline to the dendritic zone of the supraoptic nucleus by microdialysis. During local blockade of GABA inputs, the response of oxytocin cells to hypertonic infusion was greatly enhanced. We then went on to directly measure GABA release in the supraoptic nucleus during hypertonic infusion, confirming the predicted rise. Together, the results suggest that hypertonic infusions lead to coactivation of excitatory and inhibitory inputs and that this coactivation may confer appropriate characteristics on the output behavior of oxytocin cells. The nonlinearity of oxytocin secretion that accompanies the linear increase in oxytocin cell firing rate reflects frequency-facilitation of stimulus-secretion coupling at the neurohypophysis.

Topics: Animals; Bicuculline; Computer Simulation; Deamino Arginine Vasopressin; Electrophysiology; Excitatory Postsynaptic Potentials; GABA Antagonists; gamma-Aminobutyric Acid; Hyponatremia; Infusions, Intravenous; Male; Microdialysis; Models, Neurological; Neural Inhibition; Neurons; Osmolar Concentration; Oxytocin; Rats; Rats, Sprague-Dawley; Rats, Wistar; Saline Solution, Hypertonic; Sodium; Stimulation, Chemical; Supraoptic Nucleus; Vasopressins

Topics: Aged; Aging; Humans; Hyponatremia; Inappropriate ADH Syndrome; Middle Aged; Renal Agents; Vasopressins

Hyponatremia after cranial vault remodeling has been noted in a pediatric patient population. If left untreated, the patients may develop a clinical hypoosmotic condition that can lead to cerebral edema, increased intracranial pressure, and eventually, to central nervous system and circulatory compromise. The hyponatremia has traditionally been attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH); however, in our patients the treatment has been resuscitation with normal saline as opposed to fluid restriction (the accepted treatment of SIADH), thus placing the diagnosis of SIADH in question. Patients who developed hyponatremia after intracranial injury or surgery were, until recently, grouped together as having SIADH. However, there are diagnosis and treatment differences between SIADH and another distinct but poorly understood disorder that is designated cerebral salt wasting syndrome (CSW). CSW is associated with increased urine output and increased urine sodium concentration and volume contraction, and it is frequently seen after a central nervous system trauma. We therefore developed a prospective study to evaluate the cause of the sodium imbalance.Ten consecutive pediatric patients who underwent intracranial surgery for various craniosynostotic disorders were postoperatively monitored in the pediatric intensive care unit for hemodynamic, respiratory, and fluid management. The first four patients were evaluated for electrolyte changes and overall fluid balance to determine the consistency with which these changes occurred. The remaining six patients had daily (including preoperative) measurement of serum electrolytes, urine electrolytes, urine osmolarity, serum antidiuretic hormone (ADH), aldosterone, and atrial natriuretic hormone (ANH). All patients received normal saline intravenous replacement fluid in the postoperative period. All of the patients developed a transient hyponatremia postoperatively, despite normal saline resuscitation. Serum sodium levels as low as 128 to 133 mEq per liter (normal, 137 to 145 mEq per liter) were documented in the patients. All patients had increased urine outputs through the fourth postoperative day (>1 cc/kg/h). The six patients who were measured had an increased ANH level, with a peak value as high as 277 pg/ml (normal, 25 to 77 pg/ml). ADH levels were low or normal in all but one patient, who had a marked increase in ADH and ANH. Aldosterone levels were variable. On the basis of t

Topics: Aldosterone; Atrial Natriuretic Factor; Child, Preschool; Craniosynostoses; Electrolytes; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Infusions, Intravenous; Male; Postoperative Complications; Prospective Studies; Resuscitation; Skull; Sodium; Sodium Chloride; Vasopressins

We observed severe overhydration in an 18-month-old Japanese girl with primary polydipsia. The secretion of antidiuretic hormone (ADH) was decreased, and urinary excretion of aquaporin-2, a vasopressin-sensitive water channel protein, was suppressed under basal conditions, but the response of aquaporin-2 to ADH was essentially preserved. These findings suggest that the water channel itself was intact and that overhydration resulting from polydipsia was responsible for the decreased ADH secretion and suppression of the water channel protein.

Topics: Aquaporin 2; Aquaporin 6; Aquaporins; Child; Dehydration; Drinking Behavior; Female; Humans; Hyponatremia; Magnetic Resonance Imaging; Osmolar Concentration; Saline Solution, Hypertonic; Seizures; Vasopressins

1. Many polydipsic schizophrenics exhibit enhanced antidiuretic hormone (ADH) activity and thus are hyponatremic and suffer life-threatening water intoxication. Excess cortisol inhibits ADH, while cortisol insufficiency produces impairments in water balance resembling those seen in hyponatremic schizophrenics. Furthermore, hyponatremia normally upregulates cortisol receptors on the neurons which synthesize ADH, which should make them more sensitive to the effects of cortisol. 2. The author treated a hyponatremic schizophrenic, whose water imbalance was unresponsive to standard clinical interventions including clozapine, with a 4-week open trial of 60 mg cortisol daily, followed by a three week taper. 3. Mean serum sodium levels appeared to increase modestly from 114.3 to 118.5 mEq/l while the patient received adjunctive cortisol (P < .06). 4. While a modest effect was seen, the results do not suggest that adjunctive cortisol will reverse hyponatremia, and instead support other data indicating that these patients exhibit a central resistance to glucocorticoid actions.

Topics: Adult; Anti-Inflammatory Agents; Drinking Behavior; Humans; Hydrocortisone; Hyponatremia; Male; Schizophrenia; Sodium; Vasopressins; Water Intoxication; Water-Electrolyte Balance

We report an unusual case of inappropriate antidiuresis with undetectable vasopressin in an elderly man presenting with confusion due to severe hyponatremia. Further investigations led to the diagnosis of non-functional pituitary macroadenoma. The patient had normal thyroid and adrenal function. The abnormal water balance resolved promptly after transsphenoidal removal of the tumor, confirmed by a repeat water loading test. We conclude that inappropriate antidiuresis in the absence of excess vasopressin secretion may implicate mass effect from an underlying pituitary tumor.

Topics: Adenoma; Aged; Confusion; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Pituitary Neoplasms; Vasopressins

Topics: Acute Disease; Aquaporins; Brain Edema; Chronic Disease; Humans; Hyponatremia; Hypovolemia; Vasopressins; Water-Electrolyte Imbalance

A case of isolated ACTH deficiency who developed autoimmune-mediated hypothyroidism and still showed impaired water diuresis during glucocorticoid replacement therapy is reported. A 45-year-old woman was initially admitted for nausea, vomiting, and general malaise. Her serum sodium and plasma osmolality, ACTH and cortisol values were low, but her urine osmolality was high. Other pituitary hormone levels, thyroid hormone levels, and a computed tomogram of the pituitary gland were normal. The patient was treated with hydrocortisone and followed in the outpatient clinic; however, she was lost to follow up 18 months after admission. Three years later she presented with hypoglycemia and hyponatremia. Her serum or plasma ACTH, FT3, FT4, cortisol levels were low and her serum TSH level was high. Pituitary stimulation tests revealed a blunted response of ACTH to CRH and an exaggerated response of TSH to TRH. Plasma ADH was inappropriately high, and a water-loading test revealed impaired water diuresis and poor suppression of ADH. Although ADH was suppressed, impaired water diuresis was observed in the water loading test after hydrocortisone supplementation. Thyroxine supplementation completely normalized the water diuresis. Her outpatient clinic medical records revealed a gradual increase in TSH levels during follow up, indicating that she had developed hypothyroidism during glucocorticoid replacement therapy. The hyponatremia on the first admission was due to glucocorticoid deficiency, whereas the hyponatremia on the second admission was due to combined deficiencies of glucocorticoid and thyroid hormones.

Topics: Adrenal Insufficiency; Adrenocorticotropic Hormone; Autoimmune Diseases; Blood; Diuresis; Female; Hormone Replacement Therapy; Humans; Hydrocortisone; Hyponatremia; Hypothyroidism; Middle Aged; Osmolar Concentration; Thyrotropin; Thyroxine; Triiodothyronine; Urine; Vasopressins

Little is known regarding the effect of chronic changes in neuronal activity on the extent of collateral sprouting by identified CNS neurons. We have investigated the relationship between activity and sprouting in oxytocin (OT) and vasopressin (VP) neurons of the hypothalamic magnocellular neurosecretory system (MNS). Uninjured MNS neurons undergo a robust collateral-sprouting response that restores the axon population of the neural lobe (NL) after a lesion of the contralateral MNS (). Simultaneously, lesioned rats develop chronic urinary hyperosmolality indicative of heightened neurosecretory activity. We therefore tested the hypothesis that sprouting MNS neurons are hyperactive by measuring changes in cell and nuclear diameters, OT and VP mRNA pools, and axonal cytochrome oxidase activity (COX). Each of these measures was significantly elevated during the period of most rapid axonal growth between 1 and 4 weeks after the lesion, confirming that both OT and VP neurons are hyperactive while undergoing collateral sprouting. In a second study the hypothesis that chronic inhibition of neuronal activity would interfere with the sprouting response was tested. Chronic hyponatremia (CH) was induced 3 d before the hypothalamic lesion and sustained for 4 weeks to suppress neurosecretory activity. CH abolished the lesion-induced increases in OT and VP mRNA pools and virtually eliminated measurable COX activity in MNS terminals. Counts of the total number of axon profiles in the NL revealed that CH also prevented axonal sprouting from occurring. These results are consistent with the hypothesis that increased neuronal activity is required for denervation-induced collateral sprouting to occur in the MNS.

Topics: Animals; Axons; Axotomy; Central Nervous System; Electron Transport Complex IV; Functional Laterality; Histocytochemistry; Hypertrophy; Hyponatremia; Hypothalamo-Hypophyseal System; In Situ Hybridization; Male; Microscopy, Electron; Nerve Regeneration; Neurons; Oxytocin; Paraventricular Hypothalamic Nucleus; Peptides; Pituitary Gland; Rats; Rats, Sprague-Dawley; RNA, Messenger; Supraoptic Nucleus; Time Factors; Vasopressins

Topics: Antipsychotic Agents; Humans; Hyponatremia; Piperazines; Vasopressins

A 79-year-old woman suffering from urinary incontinence and unsteady gait was diagnosed as having idiopathic normal pressure hydrocephalus (NPH) with hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The concentration of antidiuretic hormone was high while the plasma osmolality was low in the presence of concentrated urine during the episodes of hyponatremia. Magnetic resonance imaging (MRI) of the head showed enlargement of the third and lateral ventricles. After ventriculoperitoneal shunt surgery, the symptoms of NPH and hyponatremia improved. It may be possibly explained that mechanical pressure on the hypothalamus from the third ventricle is responsible for hyponatremia.

Topics: Aged; Cerebral Ventricles; Female; Follow-Up Studies; Humans; Hydrocephalus, Normal Pressure; Hyponatremia; Inappropriate ADH Syndrome; Magnetic Resonance Imaging; Myelography; Radionuclide Imaging; Sodium; Vasopressins; Ventriculoperitoneal Shunt

We experienced four cases with hyponatremia due to SIADH, which seems to be related to inflammation. The plasma Na concentration decreased when the patients had fever and increased plasma CRP level. In such conditions, plasma vasopressin concentration (PAVP) and the plasma interleukin-6 (IL-6) concentration were increased. There was significant correlation between them. The animal experiments were carried out to investigate the role of interleukin in the development of SIADH. Intravenous administrations of IL-1 beta increased AVP, atrial natriuretic hormone (ANH) and ACTH. The changes in AVP and ACTH were abolished by the pretreatment with an intravenous administration of indomatacin. Moreover, the intracerebroventricular administration (ICV) of IL-1 beta also increased AVP, atrial natriuretic hormone (ANH) and ACTH. The pretreatment of indomatacin attenuated the changes in AVP and ACTH. The intravenous administration of IL-1 beta increased the urinary sodium excretion. The pretreatement of HS142-1, an ANH antagonist, abolished the increase in urinary sodium excretion induced by IL-1 beta. These results suggested that the interleukin play an important role in the development of SIADH associated with inflammation.

Topics: Adrenocorticotropic Hormone; Adult; Aged; Aged, 80 and over; Animals; Atrial Natriuretic Factor; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Inflammation; Interleukin-1; Interleukin-6; Male; Rats; Rats, Sprague-Dawley; Vasopressins

Topics: Adrenal Insufficiency; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Inappropriate ADH Syndrome; Pituitary-Adrenal System; Practice Guidelines as Topic; Vasopressins

A 60-year-old woman was admitted with severe hyponatremia. Basal values of adrenocorticotropic hormone (ACTH), thyroid hormone and cortisol were normal on admission. Impairment of water diuresis was observed by water loading test. Initially, we diagnosed her condition as the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). By provocation test, we finally confirmed that the hyponatremia was caused by hypothalamic adrenal insufficiency. The basal values of ACTH and cortisol might not be sufficient to exclude the possibility of adrenal insufficiency. Therefore, it is necessary to evaluate adrenal function by provocation test or to re-evaluate it after recovery from hyponatremia.

Topics: Adrenal Insufficiency; Adrenocorticotropic Hormone; Female; Humans; Hydrocortisone; Hyponatremia; Hypothalamo-Hypophyseal System; Inappropriate ADH Syndrome; Middle Aged; Pituitary-Adrenal System; Thyrotropin; Vasopressins

Hyponatremia is commonly seen in patients with severe and moderate head injury, but it is rarely reported in those with mild head injury. The authors report a patient with mild head injury who presented with data typical of inappropriate secretion of antidiuretic hormone (SIADH), but showed no clinical deterioration. Though the clinical significance of this condition is unclear, the true incidence of this pathology might well be found to be higher than expected, should it receive more clinical and/or serological attention. Continuing clinical assessment will be needed to determine the significance of this condition in relation to that in patients with SIADH following the various causes reported previously.

Topics: Aged; Craniocerebral Trauma; Female; Humans; Hyponatremia; Syndrome; Vasopressins

Topics: Child; Humans; Hyponatremia; Intraoperative Complications; Risk Factors; Vasopressins

Pharmacology of conivaptan hydrochloride (YM087) was investigated in in vitro and in vivo studies. In radioligand binding study, YM087 showed high affinity for both V1A and V2 receptors in animal and human species. Affinity of YM087 for V1A and V2 receptors was comparable to that of vasopressin (AVP). In functional antagonistic activity study, YM087 concentration-dependently inhibited AVP-induced intracellular Ca2+ elevation via human V1A receptors and AVP-stimulated cAMP accumulation via human V2 receptors. Intravenous administration of YM087 dose-dependently inhibited AVP-induced pressor responses and produced a dose-dependent aquaresis in rats and dogs. Oral administration of YM087 showed a potent and long-lasting antagonistic activity on V1A and V2 receptors. YM087 was effective in dogs with heart failure and in heart failure rats with hyponatremia and edema. These results reveal that YM087 is the first orally active V1A/V2 receptor antagonist and suggest that YM087 may be useful in the treatment of congestive heart failure and hyponatremia.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Calcium; Cyclic AMP; Dogs; Female; Heart Failure; Humans; Hyponatremia; In Vitro Techniques; Male; Radioligand Assay; Rats; Vasopressins

Hyponatremia is an uncommon but widely reported complication of selective serotonin uptake inhibitors (SSRIs), and most of the case reports involve elderly patients. The presentation is usually that of SIADH, but the underlying mechanism leading to the syndrome is poorly understood. Since the use of SSRIs is becoming more popular among elderly depressed patients and because of the potentially serious consequence of hyponatremia, psychiatrists should be alert to the development of the complication and familiarize themselves with its diagnosis and treatment. We report two elderly patients who were identified to have hyponatremia after the commencement of paroxetine. This illustrates the need for monitoring of plasma sodium level if a patient's clinical condition deteriorates. Other factors possibly related to the hyponatremia are discussed and a review of the diagnosis and management of SSRI-related hyponatremia is included.

Topics: Aged; Depressive Disorder; Female; Humans; Hyponatremia; Paroxetine; Selective Serotonin Reuptake Inhibitors; Sodium; Vasopressins

Topics: Extracellular Space; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant, Newborn; Infant, Very Low Birth Weight; Intensive Care Units, Neonatal; Lung Diseases; Pressoreceptors; Sodium-Potassium-Exchanging ATPase; Vasopressins

A 66-year-old hypertensive male with acute intracerebral hemorrhage developed acute hyponatremic coma 3 days after the addition of enalapril and a combination of amiloride and a thiazide diuretic to his hypotensive regimen. The patient recovered consciousness and serum sodium normalized 2 days after fluid restriction and withdrawal of both medications. Three weeks later, upon inadvertent reinstitution of enalapril and indapamide, severe hyponatremic encephalopathy promptly recurred; recovery was again rapid following fluid restriction and withdrawal of both medications. This temporal relationship establishes the thiazide diuretic or the angiotensin converting enzyme inhibitor or both as the cause of the profound symptomatic hyponatremia in this patient. Results of simultaneous serum and urine osmolality assays on several occasions were consistent with a decrease in free water clearance, a result of either increased antidiuretic hormone (ADH) secretion or potentiation of its peripheral action, and thiazide-induced natriuresis. The use of a thiazide diuretic in the presence of either of these aberrations of ADH homeostasis most likely explains the profound and rapid development of hyponatremia. Drug-induced disturbances in serum osmolality are a potentially reversible cause of deterioration of the mental state in a patient with an acute cerebrovascular accident.

Topics: Aged; Amiloride; Benzothiadiazines; Central Nervous System; Cerebral Hemorrhage; Coma; Diuretics; Enalapril; Humans; Hypertension; Hyponatremia; Indapamide; Male; Osmolar Concentration; Sodium; Sodium Chloride Symporter Inhibitors; Vasopressins; Water

We evaluated the causal role of glucocorticoid deficiency in the hyponatremia that developed in a 57-year-old Japanese man with hypothyroidism following the performance of a total thyroidectomy for laryngeal cancer. The plasma concentration of vasopressin (1.78 pg/ml) was not suppressed in the presence of hyponatremia (125 mEq/l). The urinary excretion of sodium was increased, and the plasma renin activity and plasma aldosterone concentration were suppressed. The infusion of hypertonic saline increased the plasma osmolality, but not the plasma concentration of vasopressin. An oral water load (20 ml/kg of body weight) did not suppress the plasma vasopressin level or induce diuresis. Pretreatment with hydrocortisone normalized the response of plasma vasopressin to the water load was well as the diuretic response during the hypothyroid state. The urinary excretion of 17-hydroxycorticosteroids was below normal in the hypothyroid state in the face of normal serum cortisol concentration. The correction of the hypothyroidism returned these abnormalities to normal. A disturbed metabolism of glucocorticoid may have been responsible for the hyponatremia and disturbance in plasma vasopressin regulation observed in this hypothyroid patient.

Topics: Diuresis; Glucocorticoids; Humans; Hydrocortisone; Hyponatremia; Hypothyroidism; Laryngeal Neoplasms; Male; Middle Aged; Postoperative Complications; Thyroidectomy; Vasopressins

Hyponatremia after subarachnoid hemorrhage (SAH) is commonly associated with diuresis and natriuresis, but the causes are still controversial. We investigated whether brain natriuretic peptide (BNP) was related to such hyponatremia.. Plasma BNP concentrations were measured by immunoradiometric assay in 18 patients at 0 to 2 days (period 1), 7 to 9 days (period 2), and > 14 days (period 3) after SAH. Plasma concentrations of antidiuretic hormone (ADH), atrial natriuretic peptide (ANP), and noradrenaline were also measured during period 2.. The 11 patients with hyponatremia (serum sodium concentration of < 135 mEq/L) had much higher plasma BNP concentrations during each period than did healthy controls (P < 0.05), whereas the 7 patients with normonatremia did not show statistically higher values. In the patients with hyponatremia, the plasma BNP concentration during period 2 was statistically higher than that during periods 1 and 3 (P < 0.05). The plasma noradrenaline concentration during period 2 was higher in patients with hyponatremia than in those with normonatremia (P < 0.05), whereas the plasma concentrations of ADH and ANP during period 2 were not statistically different between the hyponatremic and normonatremic patients.. We conclude that BNP may be related to hyponatremia associated with natriuresis following SAH. The increase of noradrenaline may promote the secretion of BNP.

Topics: Acute Disease; Aged; Female; Humans; Hyponatremia; Male; Middle Aged; Natriuretic Peptide, Brain; Nerve Tissue Proteins; Norepinephrine; Radioimmunoassay; Sodium; Subarachnoid Hemorrhage; Vasopressins

Polydipsia-hyponatremia is a poorly understood disorder that causes considerable mortality and morbidity. Hyponatremia in polydipsia-hyponatremia has been attributed to disturbances in antidiuretic hormone (ADH) function. Improvements in polydipsia-hyponatremia during clozapine treatment offered the chance to see if levels of ADH and other hormones associated with osmoregulation changed with improvement in biochemical and clinical measures of polydipsia-hyponatremia.. In this preliminary, longitudinal study, we studied 2 male schizophrenic patients (DSM-III-R) who had polydipsia-hyponatremia. Measures were (1) biochemical and clinical: serum sodium and osmolality, urine osmolality and specific gravity, normalized diurnal weight gain, and estimated urine volume and (2) endocrine: ADH, angiotensin II, atrial natriuretic peptide, and prolactin. Measures were collected during 2 months of baseline (typical neuroleptic) and 6 months of clozapine treatment.. Single-case statistical procedures showed significant changes in sodium levels (a.m. and p.m.), estimated urine volume, and a.m. urine specific gravity in both patients and significantly decreased diurnal weight gain in 1 patient. Both serum and urine osmolality showed improvement, but values did not reach statistical significance. Low baseline ADH levels persisted through 6 months of clozapine treatment and showed no changes in the context of improvements in serum sodium and osmolality. No significant changes were seen in levels of angiotensin II and atrial natriuretic peptide.. Given the limitations of this study, there is some evidence to suggest that the improvements in serum sodium and osmolality during clozapine treatment of polydipsia-hyponatremia may not be related to serum levels of ADH, although altered ADH receptor function cannot be ruled out. These data need to be extended in larger samples.

Topics: Adult; Angiotensin II; Atrial Natriuretic Factor; Circadian Rhythm; Clozapine; Humans; Hyponatremia; Longitudinal Studies; Male; Middle Aged; Osmolar Concentration; Prolactin; Schizophrenia; Sodium; Urine; Vasopressins; Water Intoxication

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with neuropsychiatric lupus (NP-SLE) is rare. We report a case of SIADH associated with the new onset of SLE in an 88-yr-old female. The unique features of this case include the extreme age of onset of SLE presenting with neuropsychiatric manifestations and positive antiribosomal P antibody titres. Both the NP manifestations of SLE and SIADH were highly correlated with the SLE disease activity. This case illustrates a novel presentation of NP-SLE with SIADH which may develop due to antibody-mediated hypothalamic dysfunction.

Topics: Aged; Aged, 80 and over; Aldosterone; Antibodies, Antinuclear; Brain; Complement C3; Complement C4; Depressive Disorder; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lupus Erythematosus, Systemic; Magnetic Resonance Imaging; Protozoan Proteins; Renin; Ribosomal Proteins; Vasopressins

A 72-year-old man was hospitalized with asymptomatic hyponatremia. Despite hyponatremia, urinary sodium excretion with urine osmolality exceeding plasma osmolality persisted. Plasma vasopressin levels were high and independent of plasma osmolality during hypertonic saline infusion. Computed tomography of the chest showed enlarged mediastinal and right hilar lymph nodes. Microscopically, a specimen of lymph nodes obtained by biopsy represented vasopressin-producing small cell lung carcinoma. Chemotherapy plus irradiation improved the hyponatremia. Thus, careful evaluation is necessary to determine the cause of hyponatremia disorders in elderly patients.

Topics: Aged; Antineoplastic Combined Chemotherapy Protocols; Biomarkers, Tumor; Biopsy; Bronchoscopy; Carcinoma, Small Cell; Follow-Up Studies; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lung Neoplasms; Magnetic Resonance Imaging; Male; Osmosis; Radiotherapy, Adjuvant; Sodium; Tomography, X-Ray Computed; Vasopressins

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant, Newborn; Vasopressins; Water-Electrolyte Balance

Neurohypophyseal function was studied by hypertonic saline infusion with plasma vasopressin measurement in 3 patients with adrenal insufficiency before and after cortisol replacement. Although each patient had different causes of adrenal insufficiency, all showed impaired water excretion before replacement. The first patient with isolated adrenocorticotropin deficiency had marked hyponatremia and inappropriate vasopressin secretion which was normalized after replacement, indicating vasopressin hypersecretion during hypoadrenocorticism. The second patient had combined anterior and posterior pituitary deficiency due to postpartum hypopituitarism and showed completely absent vasopressin secretion, with her polyuria being masked before cortisol replacement, suggesting a vasopressin-independent intrarenal mechanism of antidiuresis. The third patient with panhypopituitarism due to a pituitary tumor also had preexisting diabetes insipidus with defective vasopressin secretion. In this case, however, plasma vasopressin was found to be elevated when adrenal insufficiency and hyponatremia subsequently developed. Together, these results indicate that vasopressin hypersecretion does occur during adrenal insufficiency, but that the accompanying urinary diluting defect may be attributable either to vasopressin-dependent or to vasopressin-independent mechanisms.

Topics: Adrenal Insufficiency; Adrenocorticotropic Hormone; Adult; Aged; Diabetes Insipidus; Female; Humans; Hydrocortisone; Hyponatremia; Hypopituitarism; Male; Pituitary Neoplasms; Polyuria; Vasopressins; Water-Electrolyte Balance

Fluoxetine is widely prescribed for depressed patients. Hyponatremia secondary to inappropriate secretion of antidiuretic hormone has been reported in a few cases associated with routine use of fluoxetine, especially in elderly patients. The mechanism has been postulated to be linked to the inappropriate secretion of antidiuretic hormone. Serum concentrations of antidiuretic hormone and fluoxetine have not been reported in previously published reports.. We report two new cases of severe and reversible hyponatremia associated with routine use of fluoxetine therapy in two elderly women. Fluoxetine-induced inappropriate secretion of antidiuretic hormone was confirmed by elevated serum concentrations of antidiuretic hormone and fluoxetine.

Topics: Aged; Aged, 80 and over; Antidepressive Agents, Second-Generation; Contraindications; Female; Fluoxetine; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

For unclear reasons, life-threatening water intoxication often coincides with acute psychosis in polydipsic schizophrenic patients with chronic hyponatremia. In contrast, most polydipsic schizophrenic patients are normonatremic and never manifest hyponatremia. To explore whether the effect of acute psychosis on water balance differs in these 2 schizophrenic subgroups, we compared their responses to drug-induced psychotic exacerbations.. Matched polydipsic schizophrenic patients with (n = 6) and without (n = 8) hyponatremia were identified based on past and current indexes of fluid intake and hydration. A transient psychotic exacerbation was induced with an infusion of the psychotomimetic methylphenidate hydrochloride (0.5 mg/kg of body weight over a 60-second period). Antidiuretic hormone levels, subjective desire for water, and factors known to influence water balance were measured at 15-minute intervals for 2 hours.. Except for the expected differences in plasma osmolality and sodium, basal measures were similar in the 2 groups. Following methylphenidate administration, antidiuretic hormone levels increased more in the hyponatremic patients (P < .02), despite their consistently lower plasma osmolality (P < .007). No known or putative antidiuretic hormone stimulus could account for this finding. Only basal positive psychotic symptoms (P < .09) and plasma sodium (P < .18) were even marginally associated with the peak antidiuretic hormone responses, but neither factor could explain the difference in the response by the 2 groups.. Psychotic exacerbations are associated with enhanced antidiuretic hormone secretion, for unknown reasons, in schizophrenic patients with hyponatremia and polydipsia, thereby placing them at increased risk of life-threatening water intoxication.

Topics: Acute Disease; Adult; Arginine Vasopressin; Blood Pressure; Drinking; Female; Heart Rate; Humans; Hydrocortisone; Hyponatremia; Inappropriate ADH Syndrome; Male; Methylphenidate; Osmolar Concentration; Psychiatric Status Rating Scales; Schizophrenia; Schizophrenic Psychology; Sodium; Thirst; Vasopressins; Water Intoxication

We describe a 78-year-old female patient with severe hyponatremia owing to inappropriate antidiuresis. Despite hyponatremia, the urinary sodium excretion persisted with urine osmolality exceeding plasma osmolality. Although a water load decreased plasma sodium concentration and osmolality, the patient excreted only 40% of the water load after 4 h without decreased urine sodium concentrations and osmolality. The plasma vasopressin levels relative to plasma osmolality were not inappropriately elevated. Intravenous administration of the selective nonpeptide vasopressin V2 antagonist OPC-31260 decreased sodium concentration and osmolality in urine to lower values than in plasma. Concomitantly, the urine volume excretion increased markedly. In addition, restriction of water or administration of demeclocycline improved plasma sodium and plasma vasopressin levels relative to plasma osmolality to be normal. The findings indicate that the inappropriate antidiuresis in this patient was related to hyperfunction of the arginine vasopressin V2 receptor in the kidney which is not due to inappropriately secreted vasopressin.

Topics: Aged; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Injections, Intravenous; Sodium; Vasopressins

Vasopressin (AVP) secretion is principally under osmotic regulation, which is altered by nonosmotic stimuli. It is known that the manner of osmotic regulation of AVP secretion in hypoosmolar state of man consists of four types. The types have (A) random changes in plasma AVP without relation of plasma osmolality; (B) plasma AVP secretion correlated closely to plasma osmolality with a low osmotic threshold for AVP release; (C) nonsuppressible AVP secretion with normal osmotic release of AVP; (D) no abnormalities in AVP secretion. In this study, we found an entirely different type of AVP secretion from the above types in six patients with hyponatremia resulting from various causes during infusion of 5% hypertonic saline. To clarify the mechanism underlying the AVP secretion, we analyzed the interaction between osmotic and nonosmotic stimuli of AVP secretion in these patients. Despite hyponatremia, plasma AVP levels in all patients were not suppressed, which was attributed at least in part to the presence of nonosmotic stimuli for AVP release. These stimuli include nausea, hypotension, blood volume contraction, glucocorticoid deficiency or their combinations. Hypertonic saline infusion increased both serum sodium concentrations and plasma osmolality, although to subnormal levels, and concomitantly, alleviated some of the nonosmotic stimuli for AVP release formerly present in these patients. However, plasma AVP concentrations decreased rapidly during the infusion and reached the nadir in all patients. This phenomenon may be due to alleviation of nonosmotic stimuli for AVP release. Thus, the findings indicate that the potentiating effect of nonosmotic stimuli for AVP secretion may modify the osmotic regulation of AVP secretion in hypoosmolar state, resulting in the type of AVP secretion in this study.

Topics: Aged; Aged, 80 and over; Female; Humans; Hyponatremia; Infusions, Intravenous; Male; Middle Aged; Osmolar Concentration; Saline Solution, Hypertonic; Vasopressins

Topics: Aged; Benzothiadiazines; Diuretics; Drinking; Female; Humans; Hyponatremia; Promethazine; Sodium Chloride Symporter Inhibitors; Vasopressins

The antidiuretic hormone (vasopressin) is involved, either directly or indirectly, in the pathogenesis of almost all forms of hyponatremia. This means that blockage of the ADH effect at the renal ADH receptor represents a rational approach in the treatment of hyponatremia, in particular in difficult-to-treat and symptomatic forms. Recently, orally absorbable, non-peptidergic competitive ADH antagonists (aquaretics) have been introduced, which bind with high affinity to renal ADH receptor subtypes. Initial investigations in humans show that the substance is well tolerated. Numerous studies on patients with hyponatremia of varying genesis have since been started. It is to be expected that the availability of this new dass of substances will result in marked improvements in the treatment of acute and chronic forms of hyponatremia.

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Male; Vasopressins

Hyponatremia after pituitary surgery is presumed to be due to antidiuresis; however, detailed prospective investigations of water balance that would define its pathophysiology and true incidence have not been established. In this prospective study, the authors documented water balance in patients for 10 days after surgery, monitored any sodium dysregulation, further characterized the pathophysiology of hyponatremia, and correlated the degree of intraoperative stalk and posterior pituitary damage with water balance dysfunction. Ninety-two patients who underwent transsphenoidal pituitary surgery were studied. To evaluate posterior pituitary damage, a questionnaire was completed immediately after surgery in 61 patients. To examine the osmotic regulation of vasopressin secretion in normonatremic patients, water loads were administered 7 days after surgery. Patients were categorized on the basis of postoperative plasma sodium patterns. After pituitary surgery, 25% of the patients developed spontaneous isolated hyponatremia (Day 7 +/- 0.4). Twenty percent of the patients developed diabetes insipidus and 46% remained normonatremic. Plasma arginine vasopressin (AVP) was not suppressed in hyponatremic patients during hypoosmolality or in two-thirds of the normonatremic patients after water-load testing. Only one-third of the normonatremic patients excreted the water load and suppressed AVP normally. Hyponatremic patients were more natriuretic, had lower dietary sodium intake, and had similar fluid intake and cortisol and atrial natriuretic peptide (ANP) levels compared with normonatremic patients. Normnonatremia, hyponatremia, and diabetes insipidus were associated with increasing degrees of surgical manipulation of the posterior lobe and pituitary stalk during surgery. The pathophysiology of hyponatremia after transsphenoidal surgery is complex. It is initiated by pituitary damage that produces AVP secretion and dysfunctional osmoregulation in most surgically treated patients. Additional events that act together to promote the clinical expression of hyponatremia include nonatrial natriuretic peptide-related excess natriuresis, inappropriately normal fluid intake and thirst, as well as low dietary sodium intake. Patients should be monitored closely for plasma sodium, plentiful dietary sodium replacement, mild fluid restriction, and attention to symptoms of hyponatremia during the first 2 weeks after transsphenoidal surgery.

Topics: Adult; Arginine Vasopressin; Atrial Natriuretic Factor; Child; Diabetes Insipidus; Diuresis; Female; Fluid Therapy; Humans; Hydrocortisone; Hyponatremia; Incidence; Intraoperative Complications; Male; Natriuresis; Pituitary Diseases; Pituitary Gland; Pituitary Gland, Posterior; Postoperative Complications; Prospective Studies; Renal Agents; Sodium; Sodium, Dietary; Sphenoid Bone; Thirst; Vasopressins; Water; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Topics: Hallucinogens; Humans; Hyponatremia; N-Methyl-3,4-methylenedioxyamphetamine; Vasopressins; Water Intoxication

The purpose of this report is to determine the mechanisms that lead to hyponatremia when isotonic saline was the only fluid infused into rats given antidiuretic hormone (ADH), and what might minimize the degree of this hyponatremia. Normal rats were deprived of food and water for the 24-hr study period. They received an infusion of isotonic saline to expand their extracellular fluid (ECF) volume with and without exogenous ADH administration (N = 8 in each of the four groups). Similar studies were also carried out in 32 rats fed a low electrolyte diet for 72 hr before the experiment. An additional control group was fed the low electrolyte diet supplemented with sodium (Na), potassium (K), and chloride (Cl). Hyponatremia developed over 24 hr in rats fed their usual diet if treated with ADH and isotonic saline (fall, 13 +/- 2 mM, P < 0.01). The hyponatremia was caused by negative balance for Na + K salts. Hyponatremia did not develop after the saline + ADH treatment if rats were pretreated for 3 days with a low electrolyte diet. Two factors were required to develop this hyponatremia--generation of electrolyte-free water as a result of the excretion of a large quantity of Na + K salts at a high concentration in the urine, and prevention of the excretion of this electrolyte-free water by ADH. Increasing the avidity for Na reabsorption by the kidney prevented this type of hyponatremia from developing.

Topics: Animals; Hyponatremia; Isotonic Solutions; Male; Rats; Rats, Wistar; Renal Agents; Sodium Chloride; Sodium Chloride, Dietary; Vasopressins; Water-Electrolyte Imbalance

Axonal injury to hypothalamic magnocellular vasopressin (AVP) and oxytocin (OT) neurons causes degeneration of a substantial subpopulation of these neurons. In this study, we investigated the influence of osmolality on this injury-induced cell death. Normonatremic, chronically hypernatremic, and chronically hyponatremic rats received pituitary stalk compression (SC), which causes degeneration of AVP and OT terminals in the neurohypophysis. Twenty-one days after SC, rats were perfused and hypothalami were serially sectioned and alternately stained for AVP-neurophysin and OT-neurophysin immunoreactivities. Normonatremic and hypernatremic rats exhibited a triphasic pattern of water intake after SC, with peak intakes 3 times higher than those exhibited by sham-operated normonatremic rats. In contrast, hyponatremic SC rats exhibited peak water intakes of 600 ml/24 hr, approximately 9-10 times the water intakes of sham-operated normonatremic rats. In normonatremic rats, SC caused degeneration of 65% of the AVP neuron population in the SON and 73% in the PVN, but only 31% of the OT neuron population in the SON and 35% in the PVN. Similar results were found in hypernatremic rats after SC. However, in hyponatremic rats SC caused degeneration of 97% of the AVP neuron population in the SON and 93% in the PVN, and 90% of the OT neuron population in the SON and 84% in the PVN. Our results, therefore, demonstrate that injury-induced degeneration of magnocellular AVP and OT neurons is markedly exacerbated by chronic hypo-osmolar conditions, but neuronal survival is not enhanced by chronic hyperosmolar conditions.

Topics: Animals; Axons; Cell Count; Cell Death; Cell Survival; Deamino Arginine Vasopressin; Drinking; Hypernatremia; Hyponatremia; Male; Nerve Degeneration; Neurons; Oxytocin; Rats; Rats, Sprague-Dawley; Sodium; Sodium Chloride; Time Factors; Vasopressins

Topics: 3,4-Methylenedioxyamphetamine; Adult; Coma; Hallucinogens; Humans; Hyponatremia; Male; Serotonin Agents; Vasopressins

A neonate with cleft lip and palate and hypopituitarism had persistent hyponatremia despite treatment with hydrocortisone, L-thyroxine, and growth hormone. Serum sodium concentration and urinary osmolality increased and decreased appropriately and concurrently with alterations in sodium and water intake. The ability to regulate serum concentrations of antidiuretic hormone at subnormal serum sodium concentrations indicated a reset osmostat.

Topics: Cleft Lip; Cleft Palate; Female; Humans; Hyponatremia; Hypopituitarism; Infant, Newborn; Vasopressins; Water-Electrolyte Balance

To determine whether polydipsia is responsible for the altered water excretion in the subset of polydipsic schizophrenic patients who develop hyponatremia, the regulation of antidiuretic function was assessed in polydipsic schizophrenic patients with hyponatremia (n = 5), polydipsic schizophrenic patients without hyponatremia (n = 5), nonpolydipsic schizophrenic patients (n = 6), and normal controls (n = 8). The severity and duration of polyuria were similar in the two polydipsic groups. After oral water loading, maximal free water clearance was similar across all four groups. Free water clearance diminished, however, at lower plasma osmolalities in the hyponatremic polydipsics (P < 0.02) and at higher plasma osmolalities in the normonatremic polydipsics (P < 0.05) relative to that in the nonpolydipsic schizophrenics and normal subjects. The increase in plasma vasopressin after osmotic stimulation with hypertonic saline was slightly, but significantly (P < 0.02), blunted in both polydipsic groups. Hyponatremia occurs in some polydipsic schizophrenics because the relationship between free water clearance to plasma osmolality/sodium is shifted to the left. Polydipsia per se is not responsible for this still unexplained shift.

Topics: Adult; Blood Glucose; Blood Pressure; Creatinine; Female; Humans; Hyponatremia; Male; Middle Aged; Polyuria; Schizophrenia; Schizophrenic Psychology; Sodium; Thirst; Urea; Urine; Vasopressins

Topics: Adult; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Porphobilinogen; Porphyria, Acute Intermittent; Transaminases; Vasopressins

Hyponatremia following subarachnoid hemorrhage (SAH) occurs due to the inappropriate secretion of antidiuretic hormone (SIADH). However, this condition is also sometimes associated with certain dehydration states.. To clarify the pathogenesis, daily values of urine volume, water balance, and sodium balance (Na Bal) were correlated with plasma levels of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), and plasma renin activity (PRA) in 31 cases of SAH.. Na Bal was markedly negative on days 2 and 3. Cumulative Na Bal showed continuous negative values until day 10 following SAH. ANP values showed a consistent elevation, while ADH showed only an initial surge. PRA, as the gross indicator of circulatory volume, showed a lack of suppression, indicating no increase in the circulatory volume.. Hyponatremia following SAH therefore appears to be the result of increased natriuresis, due to the inappropriate elevation of ANP rather than SIADH. In this situation, water restriction should not be recommended, since the circulatory volume is decreased.

Topics: Adult; Aged; Aneurysm, Ruptured; Atrial Natriuretic Factor; Body Water; Dehydration; Female; Humans; Hyponatremia; Intracranial Aneurysm; Male; Middle Aged; Natriuresis; Renin; Subarachnoid Hemorrhage; Vasopressins

A prospective observational study of the pathophysiology of sodium and water disorders in patients with pituitary region tumours after surgical excision was carried out in 20 patients. Serial pre-operative and post-operative fluid and sodium balance, plasma and urine elctrolyte biochemistry and their derived parameters, and circulating hormones associated with fluid balance, atrial natriureic peptide (ANP) and antidiuretic hormone (ADH) were documented to correlate with the patients' clinical conditions. Ten out of these twenty cases developed diabetes insipidus (DI) requiring ADH replacement therapy, although in the majority (6 cases), this way only a transient event. Of the nine patients who developed hyponatraemia, six had symptoms such as impaired consciousness and convulsions. Four patients developed alternating hypoatraemia and hypernatraemia, which constituted a difficult group, where appropriate sodium and fluid management, and ADH replacement therapy were based upon twice daily plasma and urine biochemistry and their derived parameters. Whilst DI in this group of patients was the result of a low circulating ADH level, hyponatraemia was not associated with an exaggerated ADH activity (6.0 +/- 2.3 vs 7.4 +/- 2.3 pmol/ml, mean +/- SEM). Rather, hyponatraemia was strongly associated with an elevated circulating ANP concentration (82.4 +/- 10.5 vs 30.0 +/- 3.1 pmol/ml, mean +/- SEM, p < 0.001), resulting in salt wasting and hypovolaemia.

Topics: Adolescent; Adult; Aged; Atrial Natriuretic Factor; Child; Creatinine; Deamino Arginine Vasopressin; Female; Humans; Hyponatremia; Male; Middle Aged; Pituitary Neoplasms; Postoperative Complications; Prospective Studies; Sodium; Urea; Vasopressins; Water; Water-Electrolyte Balance

Both central diabetes insipidus (DI) and a high rate of excretion of sodium (Na) and chloride (Cl) contributed to the development of polyuria and dysnatremia in two patients during the acute postoperative period after neurosurgery. To minimize difficulties in diagnosis and projections for therapy, two available (but not often used) clinical tools were helpful. First, the osmole excretion rate early on revealed the co-existence of central DI and an osmotic diuresis. The osmoles excreted were largely Na salts; after antidiuretic hormone acted, this electrolyte diuresis caused the urine flow rate to be much higher than otherwise anticipated. Interestingly, part of this saline diuresis occurred when the extracellular fluid volume was contracted. The tool to explain the basis for the dysnatremias was a tonicity balance. Hypernatremia, which developed before treatment of central DI, was primarily a result of a positive balance for Na rather than a large negative balance for water. Moreover, hyponatremia that developed once antidiuretic hormone acted was primarily a result of a negative balance for Na; the urine volume was large and its Na concentration was hypertonic. To prevent a further decline in the plasma Na concentration, either the Na concentration in the urine should be decreased by provision of urea or a loop diuretic while replacing all unwanted water and electrolyte losses; alternatively, the fluid infused should have a similar Na concentration and volume as the urine (infuse hypertonic saline).

Topics: Adult; Deamino Arginine Vasopressin; Diabetes Insipidus; Diuresis; Female; Humans; Hypernatremia; Hyponatremia; Male; Natriuresis; Osmosis; Postoperative Complications; Sodium; Vasopressins

Topics: Aldosterone; Creatinine; Humans; Hyponatremia; Kidney Transplantation; Kidney Tubules, Distal; Prednisolone; Renin; Sodium; Tacrolimus; Time Factors; Vasopressins

Topics: Adolescent; Chlorides; Craniopharyngioma; Humans; Hyponatremia; Hypopituitarism; Male; Neoplasm Recurrence, Local; Pituitary Neoplasms; Postoperative Complications; Sodium; Syndrome; Vasopressins

Children and menstruant women are far more likely than men to develop metabolic brain damage from hyponatremia. We evaluated brain adaptation and mortality from hyponatremia in male and female rats of three different age groups. With acute hyponatremia, the mortality was 84% in prepubertal rats vs. 15% in adults and 0% in elderly rats. With chronic hyponatremia, mortality was 13% in adult males vs. 62% in females. Testosterone pretreatment significantly decreased mortality (from 62 to 9% in adult females, and from 100% to zero in prepubertal rats), but estrogen significantly increased mortality (from 13 to 44% in adult males). With acute hyponatremia in adult rats, brain sodium was significantly decreased (-17%), but in prepubertal rats it was actually increased (+ 37%). Cerebral perfusion during chronic hyponatremia was significantly impaired in adult females vs. males or controls (P < 0.01). Neither vasopressin administration nor chronic hyponatremia induced with desmopressin resulted in any mortality or decrement of cerebral perfusion. Thus age, gender, and the cerebral effects of vasopressin are major determinants of mortality in experimental metabolic encephalopathy.

Topics: Adaptation, Physiological; Aging; Animals; Brain; Brain Diseases; Chronic Disease; Estrogens; Female; Hormones; Hyponatremia; Male; Rats; Sex Characteristics; Sexual Maturation; Survival Analysis; Testosterone; Vasopressins

Topics: Adult; Bradycardia; Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Humans; Hyponatremia; Pregnancy; Pregnancy Complications, Cardiovascular; Vasopressins

A retrospective analysis was performed to study the fluid and sodium status of patients undergoing transsphenoidal surgery (TS) for Cushing's disease. We evaluated the time of onset, duration, and relative incidence of isolated hyponatremia and identified possible factors associated with it. Of 58 patients that underwent TS over 1 yr, 52 without postoperative diabetes insipidus or volume depletion were studied. Isolated hyponatremia after TS for Cushing's disease occurred in 21%, and symptomatic hyponatremia (plasma sodium, < or = 125 mmol/L) with new onset headache, nausea, and emesis occurred in 7.0% of all operated. These later patients escaped monitoring and intervention for 24 h. The development of hyponatremia began early in the postoperative period and progressed slowly over 7 days. Maximum antidiuresis occurred on postoperative day 7. Vasopressin levels measured in two patients while hypoosmolar suggested that unregulated vasopressin release contributed to the hyponatremia. Cortisol levels, glucocorticoid replacement, and pituitary adenoma size were similar in normonatremic and hyponatremic patients. Patients combining a history of an estrogenic milieu and documented posterior pituitary trauma at surgery experienced lower nadir plasma sodium. All hyponatremic patients were fluid restricted, and none developed progressive neurological symptoms, morbidity, or mortality. We speculate that the mild degree and slow rate of development of hyponatremia and/or active monitoring and intervention contributed to the good outcome.

Topics: Adolescent; Adult; Cushing Syndrome; Female; Humans; Hyponatremia; Incidence; Male; Pituitary Gland; Postoperative Complications; Retrospective Studies; Sodium; Sphenoid Bone; Time Factors; Vasopressins

An old women was in an 8-year-period 9 times admitted to the hospital because of severe mental disturbances. The average serum sodium concentration was 126.25 +/- 2.43 mmol/l at the admissions; it increased to 139.44 +/- 1.40 mmol/l after intravenous infusion of hypertonic solutions accompanied with the disappearance of the mental disturbances. The patient was usually chronically hyponatremic due to the increased water intake and the insufficient water excretion. The latter was induced by the augmented vasopressin levels. The remarkable feature of the syndrome of inappropriate antidiuretic hormone secretion was its association with lowered blood level of atrial natriuretic factor accompanied by sodium, and volume depletion. Discontinuation of the exaggerated water intake resulted in the elimination of the permanent hyponatremia; no episode of water intoxication occurred during the last 3 and 1/2 years.

Topics: Aged; Atrial Natriuretic Factor; Cognition Disorders; Drinking Behavior; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins; Water Intoxication

Topics: Animals; Atrial Natriuretic Factor; Brain; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney Failure, Chronic; Vasopressins; Water-Electrolyte Balance

Chlorpropamide (CPM) has been reported to produce impaired water excretion due to the enhancement of renal vasopressin (ADH) action and/or due to centrally enhanced ADH release, but it is still unknown whether CPM gives rise to ADH release with a subsequent hyponatremia in diabetes mellitus (DM), which, in turn, causes an impairment of the central nervous system. In 3 patients with DM, who developed hyponatremia during the treatment with CPM, an acute water load (WL) was carried out in the presence and absence of the drug, and plasma ADH was determined with plasma and urine osmolalities. Moreover, in 2 cases, MRI scans of the brain were taken. In all the patients, acute WL tests failed to suppress completely ADH release in response to changes in plasma osmolality in the presence of CPM, which, in turn, resulted in the impaired water excretion. In the absence of CPM, an acute WL normally suppressed plasma ADH leading to the diuresis. MRI scans illustrated the presence of central pontine myelinolysis. It is likely that CPM might stimulate ADH release in DM with a subsequent hyponatremia and brain damages.

Topics: Aged; Chlorpropamide; Demyelinating Diseases; Diabetes Complications; Diabetes Mellitus; Female; Humans; Hypoglycemic Agents; Hyponatremia; Magnetic Resonance Imaging; Male; Middle Aged; Osmolar Concentration; Pons; Vasopressins

Death following pediatric tonsillectomy is very rare. If deaths occur, they are most commonly due to bleeding or aspiration. In this presentation, we would like to illustrate another potentially lethal complication following the pediatric tonsillectomy, iatrogenic hyponatremia. We have encountered 3 patients who have developed post-operative hyponatremia. This has resulted in 2 deaths. The third patient was successfully treated and developed no permanent sequela. We will discuss the etiology and pathophysiology of post-operative hyponatremia including guidelines for administering fluid and electrolytes intra-operatively and post-operatively. We expect that fatal post-operative hyponatremia can be avoided in the pediatric tonsillectomy patients.

Topics: Child; Electrolytes; Female; Humans; Hyponatremia; Male; Osmolar Concentration; Tonsillectomy; Vasopressins

Topics: Aged; Blood Volume; Female; Humans; Hyponatremia; Kidney Concentrating Ability; Osmolar Concentration; Vasopressins; Water Deprivation

Overhydration can contribute to fatal complications of falciparum malaria, even though renal function may be normal. In this context, the role of inappropriate secretion of antidiuretic hormone (ADH) has been controversial. Therefore, we have analyzed ADH serum concentrations together with serum osmolality and sodium levels in serum and urine of 17 consecutively studied patients with severe falciparum malaria. Serum sodium levels were low in 13 of 17 patients upon admission and returned to normal levels during antiparasitic therapy. Urine sodium levels were low in seven of 13 patients before treatment and increased during therapy. Urine sodium concentrations were high, however, in the remaining six patients. Serum osmolality was lower in these six patients than in the other seven hyponatremic patients (P < 0.002). In relation to serum osmolality, ADH levels were inappropriately high in these six patients, which confirms the presence of inappropriate secretion of ADH. Serum creatinine levels were not higher in these six patients than in those without inappropriate secretion of ADH. Inappropriate secretion of ADH seemed to be a major cause of hyponatremia, since other factors that could lead to this condition were not found in these six patients. In conclusion, we have shown, that human falciparum malaria can be associated with inappropriate secretion of ADH.

Topics: Adult; Creatinine; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Malaria, Falciparum; Male; Middle Aged; Osmolar Concentration; Potassium; Sodium; Thyroxine; Tumor Necrosis Factor-alpha; Vasopressins

We describe a 71 year old man with a neurodegenerative condition who developed chronic inappropriate antidiuretic hormone secretion and hypothermia resulting in recurrent episodes of impaired consciousness. This combination of abnormalities is attributable to hypothalamic disease and has not to our knowledge been previously reported with clearly documented antidiuretic hormone excess.

Topics: Aged; Chronic Disease; Demyelinating Diseases; Humans; Hyponatremia; Hypothermia; Male; Vasopressins; Water Intoxication

A 70-year-old woman was admitted because of disturbance of her consciousness. Physical examinations and laboratory data suggested hypothyroidism. Primary hypothyroidism was subsequently confirmed with endocrinological examinations. Antidiuretic hormone (ADH) levels were elevated despite severe hyponatremia. On admission, urinary sodium concentration was 10mEq/l. The patient was treated with saline intravenously; serum sodium level increased from 120 to 125mEq/l and urinary sodium concentration increased from 10 to 54mEq/l. Mental confusion developed and serum sodium level dropped with urinary sodium concentration above 20mEq/l when thyroid replacement was started with the cessation of saline infusion. The patient's state of consciousness, elevated ADH levels, decreased serum sodium level and urinary sodium concentration were improved by thyroid replacement together with hydrocortisone therapy. Effects of acute water loading were abnormal with the administration of iodothyronine (T3) alone but were normalized with the administration of hydrocortisone together with T3. On discharge she was treated with the oral administration of levothyroxine alone. Pituitary hormones were normal. These results suggest that the patient was in a state of hypoadrenocorticism. Impaired water excretion in a state of hypoadrenocorticism due to hypothyroidism may give rise to an inappropriate secretion of ADH thereby resulting in hyponatremia, which in turn leads to hypotonic dehydration induced by water intoxication.

Topics: Adrenal Cortex; Adrenal Insufficiency; Aged; Dehydration; Female; Humans; Hyponatremia; Hypothyroidism; Vasopressins; Water Intoxication

The present case was a 44-year-old man who had been diagnosed as having noninsulin-dependent diabetes mellitus 2 years before admission. He gradually showed severe neuropathy and emaciation because of poor control of his blood glucose levels. He was admitted to our hospital because of disturbance of consciousness with hyponatremia. The endocrinological findings including thyroid and adrenal functions revealed no abnormalities. Insufficiency of water diuresis was noted in the water loading test. Severe orthostatic hypotension was noted during the standing up test, and an excessive response in the plasma ADH level was also noted. These findings demonstrated that excessive ADH secretion occurred to compensate for the fall in blood pressure because of the breakdown of homeostatic regulation in blood pressure due to diabetic neuropathy. It is suggested that hyponatremia seemed to be subsequently induced by hypersecretion of ADH.

Topics: Adult; Blood Pressure; Diabetes Mellitus, Type 2; Diabetic Neuropathies; Diuresis; Emaciation; Humans; Hyponatremia; Hypotension, Orthostatic; Male; Osmotic Pressure; Saline Solution, Hypertonic; Vasopressins

Topics: Diabetes Insipidus; Heart Failure; Humans; Hyponatremia; Kidney; Kidney Concentrating Ability; Male; Middle Aged; Vasopressins; Water-Electrolyte Balance

The relationship between plasma atrial natriuretic peptide (ANP) and antidiuretic hormone (ADH) both of which show high values after subarachnoid hemorrhage and cerebral vasospasm was studied. The subjects were 23 patients who were admitted because of aneurysmal subarachnoid hemorrhage during three years from March, 1989 to March, 1992 and in whom plasma ANP and ADH levels could be determined over time. Cerebral vasospasm was evaluated by the finding of cerebral angiography, clinical symptoms, and presence or not of low density areas on CT. Hyponatremia was defined as the serum sodium level of 130 mEq/l or less for two days or more. Angiographical vasospasm was found in 17 patients (85%), symptomatic vasospasm in 15 patients (65.2%), low density areas on CT in 9 patients (40.9%) and hyponatremia in 8 patients (34.8%). Symptomatic vasospasm was noted in 7 of the 8 patients (87.5%) with hyponatremia, low density areas on CT in 4 patients (50%), the detection rate being high. The plasma ANP and ADH levels were 76.7 +/- 32.1 pg/ml and 2.2 +/- 0.7 pg/ml respectively in the patients with symptomatic vasospasm against 38.3 +/- 21.3 pg/ml and 2.4 +/- 0.6 pg/ml respectively without symptomatic vasospasm, the plasma ANP level being significantly high in the patients with symptomatic vasospasm (p < 0.01). The plasma ANP and ADH were 71.2 +/- 33.8 pg/ml and 2.0 +/- 1.1 pg/ml respectively in the patients with low density areas on CT against 51.2 +/- 31.3 pg/ml and 1.8 +/- 0.5 pg/ml respectively without low density areas on CT.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Atrial Natriuretic Factor; Humans; Hyponatremia; Intracranial Aneurysm; Ischemic Attack, Transient; Rupture, Spontaneous; Subarachnoid Hemorrhage; Vasopressins

The present study was undertaken to determine whether the non-peptide V2 antidiuretic hormone (ADH) antagonist 5-dimethylamino-1[4-(2- methylbenzoylamino)benzoyl]-2,3,4,5-tetrahydro-1H-benzazepine (OPC-31260) normalized hyponatremia in rats with an experimental syndrome of inappropriate secretion of ADH (SIADH). Rats were administered V2 agonist 1-deamino-8-D-arginine vasopressin (dDAVP) subcutaneously at a rate of 5 ng/hr using an osmotic minipump and a 40 ml/day liquid diet. Serum sodium levels (SNa) and serum osmolality (SOsm) markedly decreased to 119 mEq/liter and 249 mOsm/kg H2O, respectively, 48 hours after the start of dDAVP administration. Hyponatremia persisted in a similar magnitude during the observation period of 14 days. On days 7 to 13 OPC-31260, administered 5 mg/kg per day orally, promptly raised SNa and SOsm to 134 mEq/liter and 282 mOsm/kg H2O in half a day, respectively, followed by the normalization of SNa and SOsm during the rest of the observation period. The cease of administration of OPC-31260 again decreased SNa and SOsm in rats receiving dDAVP. In contrast, SNa and SOsm were within the normal values in rats receiving 0.15 M NaCl, a vehicle for dDAVP, in the presence or absence of OPC-31260. The administration of OPC-31260 promptly caused marked water diuresis on day 7 in the hyponatremic rats receiving dDAVP, namely 5 mg/kg OPC-31260 markedly increased urinary volume and decreased UOsm. These results indicate that there is dilutional hyponatremia in rats receiving dDAVP and 40 ml/day liquid diets, and that OPC-31260 is an effective therapeutic for hyponatremia associated with dDAVP-induced SIADH.

Topics: Animals; Benzazepines; Deamino Arginine Vasopressin; Hyponatremia; Inappropriate ADH Syndrome; Male; Osmolar Concentration; Rats; Rats, Sprague-Dawley; Sodium; Vasopressins

Topics: Animals; Benzazepines; Cells, Cultured; Hyponatremia; Inappropriate ADH Syndrome; Kidney Tubules, Collecting; Muscle, Smooth, Vascular; Piperidines; Quinolones; Rats; Rats, Brattleboro; Rats, Sprague-Dawley; Vasopressins

The defense of brain volume during hyponatremia cannot be explained by the losses of brain sodium and potassium. We have examined the brain losses of organic osmolytes in rats after 24 h of severe hyponatremia induced by the administration of vasopressin and 5% dextrose in water. Normonatremic controls and animals with intermediate plasma sodium concentration ([Na]) were produced in vasopressin-treated animals by the administration of isocaloric gavages containing varying amounts of NaCl and free water. The animals were killed at 24 h by decapitation, and one brain hemisphere was quickly frozen in liquid nitrogen for organic osmolyte determinations. When compared with controls (plasma [Na] = 139 +/- 1.5 mM), hyponatremic animals (plasma [Na] = 96 +/- 1 mM) had significantly reduced brain contents for sodium, potassium, chloride, glutamate, myo-inositol, N-acetylaspartate, aspartate, creatine, taurine, gamma-aminobutyric acid, and phosphoethanolamine. Plasma [Na] was highly correlated (P < 0.001) with the brain contents for sodium, potassium, and organic osmolytes. Whereas the observed increase in brain water during hyponatremia was only 4.8%, by calculation, brain swelling without brain organic osmolyte losses would have been 11%, an amount that jeopardizes survival.

Topics: Acute Disease; Amino Acids; Animals; Brain; Creatine; Deamino Arginine Vasopressin; Hyponatremia; Inositol; Male; Rats; Rats, Sprague-Dawley; Vasopressins

A 51-year-old Japanese man was referred for the evaluation of persistent hyponatremia. The serum sodium level remained around 120 mmol/l despite mild water restriction. His past history included chronic alcoholism, myocardial infarction and lumbar disc herniation. Carbamazepine (200 mg, b.i.d.) has been used for more than 8 years for low back pain. Serum sodium returned to normal after carbamazepine was stopped, and rechallenge produced acute symptomatic hyponatremia (117 mmol/l) on day 2 after a total dose of 600 mg. Hepatic, renal and endocrine function were within normal limits, and the response to a water load (20 ml/kg) was also normal. Partial central diabetes insipidus was diagnosed by his response to water restriction and nasal desmopressin administration. Polyuria and hypernatremia were not evident in this case, probably due to a combination of low solute intake and low, but not deficient, levels of plasma ADH. This case demonstrates that carbamazepine may cause acute hyponatremia even in central diabetes insipidus, probably by sensitizing the distal renal tubules.

Topics: Carbamazepine; Diabetes Insipidus; Humans; Hyponatremia; Male; Middle Aged; Vasopressins; Water-Electrolyte Balance

Topics: Antipsychotic Agents; Combined Modality Therapy; Electroconvulsive Therapy; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Middle Aged; Schizophrenia; Schizophrenic Psychology; Vasopressins

The syndrome of inadequate secretion of antidiuretic hormone (SIADH) following treatment with a tricyclic antidepressant is demonstrated using the example of a 70 year-old man admitted for weakness and cognitive disturbances. Because of incontinence he had been periodically treated since 1989 with imipramine (Tofranil) by his family doctor. On admission he was seriously hyponatriemic and had low plasmatic osmolality, significantly lower than urinary osmolality. Creatinine, urea and uric acid in serum were also below normal values. Like other drugs tricyclic antidepressants can rarely induce an increased release of ADH by direct hypothalamic stimuli. In this patient imipramine was terminated and within a few days of reduced fluid intake and substitution of sodium a sustained clinical improvement and normalisation of laboratory parameters was noted. The patient was discharged to his home after three weeks.

Topics: Aged; Humans; Hyponatremia; Imipramine; Inappropriate ADH Syndrome; Male; Osmolar Concentration; Vasopressins

Seventeen unselected, consecutive patients with intracranial disease and accompanying hyponatraemia were studied. All would previously have been diagnosed as having the syndrome of inappropriate antidiuretic hormone (ADH) secretion on the basis of spot plasma/urinary electrolyte testing with the application to them of existing standard laboratory criteria. Timed urinary collections and matching plasma samples were available in all but three cases for the derivation of creatinine, osmotic and free-water clearances, tubular reabsorbed water, and fractional water and sodium excretions. In a number of patients the plasma renin, aldosterone and ADH levels were also assayed. On the basis of the overall findings, 13 patients were diagnosed as in fact having a salt-wasting state whilst in only four patients was the diagnosis of inappropriate ADH secretion (SIADH) substantiated. It is suggested that obtaining simple derived parameters of sodium and water homeostasis can add significantly in differentiating between these quite opposite syndromes.

Topics: Aged; Aldosterone; Brain Diseases; Female; Homeostasis; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Postoperative Complications; Renin; Vasopressins; Water-Electrolyte Balance

For intracranial diseases, plasma atrial natriuretic peptide (ANP), antidiuretic hormone (ADH) and aldosterone were determined and their effects on the development of hyponatremia with central origin were studied. The subjects were 71 cases of intracranial diseases which were admitted to our hospital during a period of 1 year from March, 1989 to March, 1990. The diseases were broken down to subarachnoid hemorrhage 26 cases, hypertensive intracerebral hemorrhage 19 cases, head injury 12 cases, cerebral infarction 11 cases and 3 other cases. Serum-urine electrolytes, plasma ANP and ADH were determined in the acute stage on Day 1 to 4, in the hyponatremia stage on Day 5 to 14 and in the chronic stage on Day 15 downward. Hyponatremia was defined as the serum sodium level of 130 mEq/l or less. Cases evidently having other causes such as heart failure and renal insufficiency were excluded. In the normal control group of persons who were admitted to our hospital for a close checkup (n = 20), plasma ANP was 26.5 +/- 11.6 pg/ml (10-50); levels of 50 pg/ml or more were regarded as abnormally high. 1) Hyponatremia was found in 18 cases (25.4%), subarachnoid hemorrhage in 7 cases, hypertensive intracerebral hemorrhage in 4 cases, head injury in 5 cases and others in 2 cases. 2) The time of onset of hyponatremia was on the 8.3 hospital day. The duration was 7.2 days. The minimum serum sodium level was 124.6 mEq/l. 3) There was no significant change in the plasma aldosterone level at each stage.2+ Predicting development of hyponatremia from plasma ADH and ANP levels in the acute stage is difficult. Inadequate secretion of ANP rather than ADH appeared to be an important factor for the development of hyponatremia, but the plasma ANP level was not always abnormally high, so involvement of other sodium diuretic factors should also be kept in mind.

Topics: Adult; Aged; Aged, 80 and over; Aldosterone; Atrial Natriuretic Factor; Brain Diseases; Female; Humans; Hyponatremia; Male; Middle Aged; Vasopressins

A five-year-old girl with known sickle cell disease presented with severe hyponatremia and findings compatible with syndrome of inappropriate secretion of antidiuretic hormone (SIADH). She was found to have lead levels in the Class III category. By exclusion, we postulated that the SIADH was in some way related to the high lead levels, since this was the only abnormality the patient exhibited. The toxic lead levels and the elevated vasopressin levels rapidly responded to dimercaprol and calcium EDTA chelation therapy.

Topics: Anemia, Sickle Cell; Chelation Therapy; Child, Preschool; Dimercaprol; Edetic Acid; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lead; Lead Poisoning; Vasopressins

We found symptomatic hyponatremia in four elderly patients in which serum sodium (Na) levels ranged from 101 to 122 mEq/l. All 4 patients had low levels of plasma adrenocorticotropic hormone (ACTH), serum cortisol, and urinary excretion of 17-OHCS, and poor responses of ACTH to exogenous insulin and antidiuretic hormone (ADH). Other pituitary hormones were all normal. They were therefore diagnosed as having isolated ACTH deficiency. Plasma ADH was relatively high despite hypoosmolality which was associated with the hyponatremia. Water loading test revealed impaired water excretion and poor suppression of plasma ADH. Replacement with 20-30 mg hydrocortisone completely restored the serum Na level and restored the plasma ADH level to the normal range in all 4 patients. Other factors such as decreased glomerular filtration, enhanced urinary Na loss and decreased Na intake were also included. These results indicate that there is marked hyponatremia and that in the presence of hypoosmolality the sustained secretion of ADH is the key factor in causing the impaired water excretion and hyponatremia in isolated ACTH deficiency.

Topics: Adrenocorticotropic Hormone; Aged; Humans; Hyponatremia; Male; Middle Aged; Vasopressins

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Central Nervous System Diseases; Child; Child, Preschool; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Kallikreins; Male; Middle Aged; Sex Factors; Uric Acid; Vasopressins

We determined serum atrial natriuretic peptide (ANP) and anti-diuretic hormone (ADH) on a time course basis in cases of subarachnoid hemorrhage and studied their influence on the development of hyponatremia. Twenty six cases of subarachnoid hemorrhage were admitted to our hospital in the past 1 year, and by the site of ruptured aneurysms, there were Acom 6 cases, ICA 6 cases, MCA 5 cases and VA BA 4 cases. Serum ANP and ADH levels were determined in the acute phase on Day 1-4, in the hyponatremia phase on Day 5-14 and in the chronic phase on Day 15 downward. Levels of not more than 130 mEq/l were regarded as hyponatremia. Cases showing other evident causes such as heart failure and renal insufficiency were excluded. In the normal control group (n = 20) which was admitted to this hospital for a close check-up, serum ANP was 26.5 +/- 11.6 pg/ml (10-50); levels of more than 50 pg/ml were regarded as being abnormally high. 1) Hyponatremia was observed in 7 cases (26-9%); the day of onset was 11.9 hospital day. The duration was 5.0 days and the minimum serum Na level was 126.4 mEq/l. 2) The serum ADH level was high regardless of whether or not there was the development of hyponatremia in the acute phase but tended to decrease gradually and became normal in the hyponatremia phase. 3) The serum ANP level in the cases of hyponatremia was 40.7 +/- 9.1 pg/ml in the acute phase, 69.0 +/- 25.7 pg/ml in the hyponatremia phase and 40.2 +/- 21.5 pg/ml in the chronic phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Atrial Natriuretic Factor; Humans; Hyponatremia; Subarachnoid Hemorrhage; Vasopressins

It is commonly taught that retention of free water is the dominant factor reducing the serum sodium concentration in hyponatremia. To determine whether the concentrations of other electrolytes are similarly diluted, we identified 51 patients with hyponatremia (Na = 121 +/- 1 mmol/L [mEq/L]) and compared electrolyte and laboratory values at the time of hyponatremia with values at a time when serum sodium was in the normal range (138 +/- 1 mmol/L). The medium interval between these measurements was 12 days. At the time of hyponatremia, serum sodium and chloride were substantially and significantly reduced by 12% to 15%. Although many hyponatremic patients had overtly increased or decreased concentrations of the other measured electrolytes, there were no significant changes in the mean concentration for any of these at the time of hyponatremia. Unchanged mean values were found for the plasma concentration of bicarbonate (26.1 +/- 0.6 normal v 25.2 +/- 0.8 mmol/L at the time of hyponatremia), potassium (4.31 +/- 0.10 v 4.33 +/- 0.15 mmol/L), albumin, phosphate, and creatinine. The stability of these laboratory values was observed both in patients with clinically normal extracellular fluid (ECF) volume and in those with true or effective ECF depletion. The urinary sodium (UNa) concentration was found to be a reliable predictor of the ECF volume status, whereas the fractional sodium excretion (FENa) was not. Electrolyte derangements are common in patients with hyponatremia, but are usually confined to patients on diuretics or who have an abnormal ECF volume. In the absence of these complicating situations, the plasma electrolytes are typically normal and are not reduced by dilution to the same extent as Na and CI. Based on a review of both the classic and recent knowledge concerning electrolyte regulation in hyponatremia, we propose that two factors explain these observations. First, the degree of dilution is overestimated because of Na losses in urine and perhaps Na shift into cells. Second, both renal and extrarenal adaptive mechanisms are activated by hyponatremia that stabilizes the concentration of other ions. One of these mechanisms is cell swelling, which triggers a volume-regulatory response leading to the release of ions and water into the ECF. Other adaptive mechanisms are mediated by antidiuretic hormone (ADH) per se, and by atrial natriuretic peptide (ANP).

Topics: Adaptation, Physiological; Animals; Atrial Natriuretic Factor; Bicarbonates; Extracellular Space; Humans; Hyponatremia; Incidence; Potassium; Retrospective Studies; Urea; Uric Acid; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Topics: Atrial Natriuretic Factor; Brain Injuries; Child; Female; Humans; Hyponatremia; Natriuresis; Vasopressins

To clarify the role of the sugar polyols, sorbitol and myo-inositol, in cerebral cell volume regulation, we studied the effect of sorbinil, an inhibitor of aldose and aldehyde reductase, on the size of the cerebral water compartments in rats with hypernatremia, hyponatremia and normonatremia. Experimental animals were pretreated with sorbinil, while comparison rats received the drug vehicle. Rats were made hypernatremic for 96 h by water deprivation and injections of hypertonic saline, while hyponatremia was provoked over 48 h by daily administration of 5% dextrose in water and vasopressin. Sorbinil treatment was continued throughout the hyper- and hyponatremic periods. The severity of hypernatremia and hyponatremia was similar in sorbinil-treated and corresponding vehicle-treated rats. Brain electrolyte content and the size of the cerebral intracellular water compartment were comparable in sorbinil-treated rats vs. controls under hypernatremic and hyponatremic conditions. Sorbinil reduced the cerebral sorbitol content by approximately 50%, irrespective of the serum Na+ concentration. In contrast, sorbinil had no effect on brain myo-inositol content which rose by 114% during chronic hypernatremia (P less than 0.0001). Cerebral levels of myo-inositol did not decline in hyponatremic rats. We conclude that (1) sorbitol is not an essential cerebral osmolyte; and (2) myo-inositol is involved in the maintenance of brain cell volume during severe hypernatremia but not under hyponatremic conditions.

Topics: Aldehyde Reductase; Analysis of Variance; Animals; Brain; Electrolytes; Hypernatremia; Hyponatremia; Imidazoles; Imidazolidines; Inositol; Male; Rats; Rats, Inbred Strains; Sorbitol; Vasopressins; Water-Electrolyte Balance

Topics: Body Water; Humans; Hyponatremia; Tuberculosis, Pulmonary; Vasopressins

Renal function and plasma antidiuretic hormone (ADH) levels were studied basally and after oral water load in four groups of subjects: 15 healthy controls (group I), 15 cirrhotics without ascites (group II), 15 cirrhotics with ascites (group III), and 10 decompensated cirrhotics with hyponatremia (group IV). Renal function and ADH levels were normal in group II. In groups III and IV water diuresis and fractional proximal sodium excretion were significantly decreased, whereas fractional distal sodium resorption and fractional excretion of potassium did not differ from those of controls. Basal ADH was significantly increased only in patients of group IV. In these patients ADH remained abnormally high after water loading. ADH did not correlate with water diuresis, plasma osmolality, mean arterial pressure, and plasma renin activity. We conclude that impaired water excretion in decompensated cirrhotics without hyponatremia cannot be ascribed to high serum levels of ADH. On the contrary, it seems to be related mainly to a reduced delivery of filtrate to the diluting segment of the nephron. In cirrhotic patients with hyponatremia high levels of ADH may play an additional role.

Topics: Adult; Female; Humans; Hyponatremia; Kidney; Liver Cirrhosis; Male; Middle Aged; Sodium; Vasopressins; Water

Vasopressin is synthesized in the perikarya of magnocellular neurons and is transported down long axons to the storage terminals of the posterior pituitary. To maintain stable pituitary stores following vasopressin secretion, the hypothalamus must synthesize and transport an amount of new vasopressin, equivalent to the amount released. Vasopressin release and synthesis rate can be chronically upregulated or suppressed relative to basal levels, depending on the demand for vasopressin. We studied whether vasopressin transport was similarly regulated during situations of varying demand. During chronic hyponatremia, when synthesis of vasopressin was reduced to undetectable levels, transport of vasopressin was also markedly decreased, as evidenced by continued presence of vasopressin in the transport system. Upregulation of transport was demonstrated by measuring pituitary accumulation of vasopressin in rats whose pituitary stores were initially depleted by hypernatremia and in whom subsequent release was suppressed by hyponatremia. In hypernatremic rats, transport of vasopressin was increased fivefold over baseline as determined by pituitary accumulation, and this elevated rate persisted for 7 days in the absence of release. This study demonstrates that axonal transport of vasopressin is a regulated process and is linked to synthesis rate rather than release.

Topics: Animals; Biological Transport; Colchicine; Deamino Arginine Vasopressin; Hypernatremia; Hyponatremia; Hypothalamus; Male; Pituitary Gland; Rats; Rats, Inbred Strains; Sodium Chloride; Vasopressins

One hundred patients affected by S.A.H. have been studied, evaluating the possible correlations between clinical findings and hyponatremia. For a better understanding of hyponatremia during S.A.H., the hematic concentration of A.D.H. and A.N.P. have been determined and correlated with hyponatremia.

Topics: Atrial Natriuretic Factor; Cerebral Arterial Diseases; Female; Humans; Hyponatremia; Male; Prognosis; Spasm; Subarachnoid Hemorrhage; Vasopressins

Topics: Blood Proteins; Cardenolides; Digoxin; Humans; Hyponatremia; Intracranial Aneurysm; Plasma Volume; Renin; Saponins; Sodium-Potassium-Exchanging ATPase; Subarachnoid Hemorrhage; Vasopressins

We report a case of 47-year-old woman with an isolated deficiency of adrenocorticotropic hormone. She was admitted complaining of fatigue and frequent loss of consciousness. The patient developed severe hyponatremia (100 mEq/l) after five days of the admission. Her plasma renin activity and plasma aldosterone concentration were low though she was dehydrated. After the treatment of dehydration, plasma osmolality was low but high plasma antidiuretic hormone (ADH) level sustained. Both high urinary sodium excretion and low urinary aldosterone excretion still remained after one month of replacement therapy with prednisolone. But, glomerular filtration rate and a response of urinary volume to acute water loading were normalized. These results suggested that severe hyponatremia of the patient was caused by an inappropriate secretion of ADH and suppression of renin-aldosterone system. We consider the suppression of renin-aldosterone system was partially independent of an inappropriate secretion of ADH.

Topics: Adrenocorticotropic Hormone; Aldosterone; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Middle Aged; Renin-Angiotensin System; Vasopressins

Hyponatremia due to inappropriate secretion of vasopressin is a common disorder in human pathophysiology, but vasopressin synthesis during hypoosmolality has not been investigated. We used a new method to quantitate synthesis of vasopressin in rats after 3, 7, and 14 d of hyponatremia induced by administering dDAVP (a vasopressin agonist) and a liquid diet. Vasopressin synthesis was completely turned off by 7 d. Vasopressin mRNA levels in the hypothalamus paralleled the reduction in synthesis and were reduced to levels of only 10-15% of the content in control rats. When hyponatremia was corrected by withdrawal of dDAVP, vasopressin mRNA slowly returned to normal over 7 d. The observation that vasopressin synthesis can be so completely turned off leads to several conclusions: under normal physiological conditions the neurohypophysis is chronically upregulated; there must be an osmotic threshold for initiation of vasopressin synthesis (and release); the large store of hormone in the posterior pituitary is essential for vasopressin to be available during times of decreased synthesis; and, finally, some nonosmolar stimulus for synthesis must be present during clinical disorders when vasopressin is secreted (and synthesized) despite hypoosmolality.

Topics: Animals; Deamino Arginine Vasopressin; Down-Regulation; Hyponatremia; Male; Neurophysins; Osmolar Concentration; Oxytocin; Pressoreceptors; Rats; Rats, Inbred Strains; RNA, Messenger; Vasopressins

Myelinolysis occurs following rapid correction of hyponatremia in both humans and experimental animals. Although the mechanism of this effect at present is unknown, we have examined the possibility that a rapid rise in serum sodium following hyponatremia potentiates an oxidative stress and results in the oxidation of cellular proteins. In these studies, rats treated with 1 M NaCl following 3 days of vasopressin-induced hyponatremia exhibited myelinolysis in the corpus striatum and thalamus as well as significant increases in soluble oxidized proteins in the brain. These changes did not occur in rats treated with 0.155 M (0.9%) NaCl following 3 days of hyponatremia.

Topics: Animals; Arginine Vasopressin; Brain; Hyponatremia; Male; Myelin Sheath; Nerve Tissue Proteins; Organ Specificity; Oxidation-Reduction; Potassium; Rats; Rats, Inbred Strains; Reference Values; Sodium; Sodium Chloride; Vasopressins

Topics: Adult; Female; Humans; Hypernatremia; Hyponatremia; Thirst; Vasopressins; Water-Electrolyte Balance

Patients with hyponatremia due to tuberculosis have shown variable responses to water loading in previous small studies, ranging from persistent antidiuresis to a normal diuresis. Although tuberculosis is considered a cause of the syndrome of inappropriate antidiuretic hormone secretion (SIADH), circulating vasopressin has been documented in only a few cases. We studied a larger group of patients to determine whether it can be suppressed by a short-term reduction in osmolality.. Twenty-eight hyponatremic patients (mean age +/- SD: 40 +/- 10 years) with pulmonary or miliary tuberculosis underwent a clinical evaluation, measurement of blood and urine chemistry values, and (in 22) a water load of 20 mL/kg. Volume status was evaluated by urine sodium concentration, blood and urine urea nitrogen, and plasma renin activity. Endocrine, renal, and other recognized causes of SIADH were excluded.. All 22 patients exhibited a decline in urine osmolality and an increase in free water clearance after water loading. Water excretion was fully normal in seven of 22, with the remainder showing variable impairment of diluting ability and/or volume excreted. Plasma vasopressin, measured in 11 of 22 patients as well as in six others not subjected to water loading, was detectable despite hypo-osmolality in 16 of 17. Vasopressin levels declined after water loading, from 1.85 +/- 1.32 to 0.77 +/- 0.25 pg/mL (p less than 0.05). The majority of patients had the euthyroid sick syndrome but normal adrenal responses to cosyntropin. Although several patients had mild volume depletion when studied, this factor did not appear to explain the defect in water excretion. Hyponatremia resolved predictably within days to weeks of antituberculous therapy.. Circulating vasopressin remains detectable in hyponatremic patients with tuberculosis and is responsive to changes in osmolality. A downsetting of osmoregulation induced by active tuberculosis ("reset osmostat") could explain this abnormality, but we cannot exclude an unidentified non-osmotic stimulus that can be counteracted by water loading.

Topics: Adult; Hemodynamics; Humans; Hyponatremia; Osmolar Concentration; Thyroid Function Tests; Tuberculosis, Miliary; Tuberculosis, Pulmonary; Vasopressins; Water

We studied 13 children subjected to elective tonsillectomy, 6 of whom (study patients) received supplemental intravenous isotonic saline during and after operation, and 7 of whom (controls) did not. Clinical and biochemical evidence of hypovolaemia was present in the control but not in the study patients. Plasma antidiuretic hormone (ADH) and urine osmolality were higher in controls (p less than 0.005 and p less than 0.05 respectively). Plasma sodium concentration and osmolality were similar in the two groups. We conclude that hypovolaemia is the principal stimulus to ADH release following surgery and that, in addition to replacement of observed losses of blood and other fluids by fluids of appropriate composition, hypovolaemia should be prevented by the administration of maintenance quantities of isotonic fluid, rather than exacerbated by fluid restriction, in patients in whom oral fluid intake is interrupted for more than a brief period. Hypotonic and sodium free fluids should be avoided because of the risk of hyponatraemia.

Topics: Catecholamines; Child; Child, Preschool; Dehydration; Fluid Therapy; Humans; Hyponatremia; Isotonic Solutions; Plasma Volume; Postoperative Complications; Sodium Chloride; Surgical Procedures, Operative; Tonsillectomy; Vasopressins

Hypouricemia in coexistence with hyponatremia often differentiates the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from most other causes of hyponatremia. We report clearance studies in 5 cases of hyponatremia and hypouricemia that were not due to SIADH. One had metastatic pancreatic carcinoma with ascites, edema, hypoalbuminemia and hypophosphatemia. Two had adenocarcinoma of the lung with metastasis to the brain in 1, 1 had disseminated cryptococcus and 1 had Hodgkin's disease. None received radiation or known nephrotoxins at least 4 months prior to study. None had serum creatinine greater than 106.1 mumol/l (1.2 mg/dl). Two had postural hypotension and hyponatremia that responded to saline therapy. Fluid restriction corrected the hyponatremia in all patients, but the hypouricemia, high fractional excretion (FE) of urate, and high urine sodium concentration persisted. In 2 patients studied, ADH was appropriately suppressed after volume repletion but there was a defect in free water clearance due to high renal solute excretion. In contrast to patients with SIADH who correct their defect in renal urate transport with correction of hyponatremia by water restriction, our patients appear to have a persistent renal urate transport defect and abnormality in sodium conservation. Elevated FE urate of greater than 10% after correction of hyponatremia can thus differentiate these patients from SIADH. The diametrically opposing goals of fluid therapy emphasize the importance of differentiating one group from the other.

Topics: Adult; Diagnosis, Differential; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Male; Middle Aged; Sodium; Uric Acid; Vasopressins; Xanthine Oxidase

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

The authors describe a case of subarachnoid hemorrhage with hyponatremia accompanied by elevation of plasma atrial natriuretic peptide (ANP). The early phase of hyponatremia was classified as the syndrome of inappropriate secretion of antidiuretic hormone (ADH) due to subarachnoid hemorrhage. However, in the later phase, hyponatremia and natriuresis were accompanied by suppression of ADH while plasma ANP remained elevated. The patient was effectively treated with demeclocycline and hypertonic saline. The significance of ANP in the pathophysiology of increased natriuresis is discussed.

Topics: Aged; Atrial Natriuretic Factor; Demeclocycline; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Intracranial Aneurysm; Natriuresis; Saline Solution, Hypertonic; Subarachnoid Hemorrhage; Vasopressins

Measurement of plasma alpha-humanANP (ANP) and antidiuretic hormone (ADH) in 28 cases with aneurysmal subarachnoid haemorrhage (SAH) was carried out, and then compared with control subjects who were infused with hypertonic saline. In cases with hyponatremia (HN), statistical correlation between control subjects and cases without HN was not evident with regards to ANP and plasma osmolality (Posm), excreted fraction of filtrated sodium (FENa) and urinary Na/K. Furthermore, they secreted supernumerarilly in spite of HN. Cases with HN were further subdivided into two groups, they were those cases with negative total sodium balance at the time of appearance of HN, and those cases without total negative sodium balance. In the former, central venous pressure had a tendency to decrease, however, secretion of ANP and ADH was statistically not different in either groups. It appears that ANP regulated urinary sodium excretion against an osmotic or sodium load acts as a maintenance of homeostasis as an osmotic regulator. Cases with HN in which secretion of ADH was physiological, ANP secreted supernumerarilly in spite of hypoosmonaemia and hypovolaemia. Our findings may contribute to a better understanding of the pathophysiological processes leading to hyponatremia in cases with cerebral disorders, and may help to improve the treatment possibilities.

Topics: Adult; Aged; Atrial Natriuretic Factor; Female; Humans; Hyponatremia; Intracranial Aneurysm; Male; Middle Aged; Peptide Fragments; Rupture, Spontaneous; Subarachnoid Hemorrhage; Vasopressins

Patients with intracranial disease are at risk of developing clinical deterioration due to a hyponatremic syndrome associated with an inappropriate degree of natriuresis, the "syndrome of inappropriate secretion of anti-diuretic hormone (ADH)" or SIADH. To investigate the hypothesis that atrial natriuretic peptide (ANP) is related to the natriuresis in SIADH, serum samples were obtained from 8 neurosurgical patients with intracranial disease seen consecutively who fulfilled the traditional clinical and laboratory criteria for SIADH. In one patient with a hemorrhagic cerebral infarction an elevation of serum ADH (5.7 pg/ml; normal = 1 to 5 pg/ml) in association with a normal level of serum ANP (49.8 pg/ml; normal = 10 to 60 pg/ml) was seen. Six patients (2 with intracerebral hemorrhage and 1 with hemorrhagic cerebral infarction, 1 with aneurysmal subarachnoid hemorrhage, 1 with glioblastoma multiforme, and 1 with Creutz-feldt-Jakob disease) had elevated serum ANP levels (197.0, 112.0, 92.0, 432.0, 97.5, and 138.0 pg/ml, respectively) associated with either normal or low ADH levels (1.3, 2.5, 1.2, 0.7, 2.3, and 0.5 pg/ml, respectively). Another patient with an intracerebral hemorrhage had a normal serum ANP level (37.0 pg/ml) and undetectable ADH level (less than 0.5 pg/ml). In the 7 patients in whom either ADH or ANP alone was elevated, a reciprocal relationship was observed between serum ADH and ANP levels, which could be expressed in logarithmic form (correlation coefficient, r = 0.727). In the 6 patients in whom serum ANP level alone was elevated, a near linear relationship was observed between serum ANP levels and urine sodium excretion (r = 0.851).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Atrial Natriuretic Factor; Brain Diseases; Humans; Hyponatremia; Sodium; Vasopressins

Severe hyponatremia occurs in some patients with untreated hypopituitarism, but it is not known whether such hyponatremia is caused by the hypersecretion of vasopressin (antidiuretic hormone). This report describes severe, symptomatic hyponatremia in five women 59 to 83 years old (serum sodium, 111 to 118 mmol per liter) who presented with hypopituitarism (which had been previously undiagnosed in four). Plasma vasopressin was inappropriately high (1.3 to 25.8 pmol per liter [1.4 to 28 ng per liter]) in relation to plasma osmolality (236 to 260 mOsm per kilogram of body weight). All five patients had normal renal function and no signs of dehydration or volume depletion. The hyponatremia was resolved within a few days after the institution of hydrocortisone therapy, after infusion of normotonic or hypertonic saline had been found to be less effective. When four of the patients were later restudied while receiving maintenance hydrocortisone treatment, the relation between plasma vasopressin and osmolality was normal. We conclude that ACTH deficiency may cause the syndrome of inappropriate secretion of antidiuretic hormone. The beneficial effect of hydrocortisone is probably exerted through the suppression of vasopressin secretion.

Topics: Adrenocorticotropic Hormone; Aged; Aged, 80 and over; Female; Humans; Hydrocortisone; Hyponatremia; Hypopituitarism; Inappropriate ADH Syndrome; Middle Aged; Osmolar Concentration; Retrospective Studies; Vasopressins

Changes in blood plasma content of hormones which are observed in the different periods of hemorrhagic fever and the attendant renal syndrome are directed to the maintenance of significantly deranged water-electrolyte homeostasis. Adequate secretion of vasopressin and aldosterone in response to the changes in sodium concentration and plasma osmolality point to the absence of significant functional disorders of the corresponding glands. Pronounced hypernatremia in fatal cases is evidence of the deranged processes of osmoregulation associated primarily with kidney areactivity to vasopressin and prognostically is an unfavourable sign. The presence of pituitary necrosis in deceased subjects does not rule out the role of vasopressin deficiency in the pathogenesis of pronounced hypernatremia.

Topics: Acute Kidney Injury; Adolescent; Adult; Aldosterone; Female; Hemorrhagic Fever with Renal Syndrome; Humans; Hypernatremia; Hyponatremia; Male; Middle Aged; Nephrotic Syndrome; Osmotic Pressure; Renin; Vasopressins

Topics: Adult; Animals; Cell Membrane; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Male; Syndrome; Vasopressins; Water

Topics: Chronic Disease; Clinical Laboratory Techniques; Female; Humans; Hyponatremia; Kidney; Middle Aged; Osmolar Concentration; Referral and Consultation; Urodynamics; Vasopressins

Vasopressin levels, together with plasma and urinary electrolytes, were measured in the acute and convalescent stages of 17 patients with malaria and 11 patients with other febrile illnesses. There was a significantly lower serum sodium in the acute stages of both groups (p less than 0.01 and p less than 0.02). There was no significant difference between the malaria and control groups. There were no significant changes in the vasopressin levels, although one patient with malaria showed evidence of inappropriate vasopressin secretion which returned to normal after treatment. This study suggests the mild hyponatraemia sometimes seen in the acute stages of malaria is not related to inappropriate secretion of vasopressin, although this condition may be of importance in more severe cases of hyponatraemia.

Topics: Adolescent; Adult; Animals; Electrolytes; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Malaria; Male; Middle Aged; Plasmodium falciparum; Vasopressins

The effect of therapy for hyponatremia with central origin (cerebrovascular disease and head injury) was investigated in order to examine contributing factors. Out of a total of 58 subjects admitted to the hospital during the previous three years with cerebrovascular disease (49 cases), and head injuries (9 cases), hyponatremia with central origin occurred within 2 weeks. Special treatment for hyponatremia was not given in 30 of the 58 cases (control group). The group (28 cases) which underwent therapy was optionally selected in terms of the following-SIADH, natriuretic polypeptide involvement and sick cells resulting from Na-K pump disorder. These 28 cases were classified into subgroups: water restricted (7 cases), hypertonic NaCl load (9 cases), glucose/insulin/potassium (GIK) therapy (4 cases), phenytoin administration (8 cases). In all of the 58 patients, the serum sodium, potassium and osmolarity and urinary sodium and potassium were measured daily. The balance of water, sodium and potassium were calculated on hyponatremic phase. Plasma levels of such hormones as antidiuretic hormone, aldosterone and cortisol were measured on hyponatremic phase. For each group, onset day and duration of hyponatremia and lowest sodium value were investigated for the sake of comparison. No significant difference for onset day and lowest sodium value was found between each group. Duration was as follows: control group 9.4 +/- 3.3 days, water restricted 7.4 +/- 2.1 days, hypertonic NaCl load 3.3 +/- 1.4 days, GIK therapy 7.3 +/- 2.9 days and phenytoin administration 8.9 +/- 3.7 days. Hypertonic NaCl load indicated a significantly shorter duration compared with the other groups. Hypertonic NaCl load was found to be most effective for hyponatremia with central origin.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aldosterone; Cerebrovascular Disorders; Craniocerebral Trauma; Glucose; Humans; Hydrocortisone; Hyponatremia; Inappropriate ADH Syndrome; Insulin; Phenytoin; Potassium; Saline Solution, Hypertonic; Sodium; Vasopressins; Water-Electrolyte Balance

The syndrome of inappropriate secretion of antidiuretic hormone is associated with head trauma; however, there are no reports concerning vasopressin levels in pediatric patients with head trauma. Urine vasopressin in eight children (mean +/- SEM, age 7.5 +/- 1.6 years, range 1 to 15 years) was measured by radioimmunoassay during their hospitalization for head trauma. Urine vasopressin values for ten healthy children (mean age 5.4 +/- 1.3 years) and for eight children hospitalized for systemic antibiotic treatment of infections (age 5.9 +/- 1.8 years) also were obtained. Urine vasopressin, urine and serum sodium concentration and osmolality, urea nitrogen, creatinine, and fluid intake were measured within 24 hours of admission and daily for the following two days. For the first three days following head trauma, mean urine vasopressin levels in pediatric patients with head trauma were increased (P less than .05) compared with those of healthy children. Despite fluid restriction to 85% of maintenance level, 25% of patients with head trauma exhibited the clinical syndrome of inappropriate secretion of antidiuretic hormone (hyponatremia, increased urinary sodium, diminished serum osmolality, and urine osmolality greater than serum osmolality). Urine osmolality greater than 800 mosm/kg was associated with markedly increased urine vasopressin levels (200 to 1,650 pg/mL); children with this finding may be at particular risk for the syndrome of inappropriate secretion of anti-diuretic hormone without restrictive water intake.

Topics: Adolescent; Child; Child, Preschool; Craniocerebral Trauma; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Osmolar Concentration; Sodium; Vasopressins

Hyponatremia, in patients with central nervous system disease, can be attributable to impaired free water excretion (syndrome of inappropriate secretion of antidiuretic hormone) or to excessive sodium excretion (cerebral salt wasting). We present a patient with a parietal glioma and hyponatremia characterized by salt wasting and dehydration. Rehydration and sodium repletion corrected the sodium and volume deficits; withdrawal of supplemental sodium resulted in recurrence of dehydration and hyponatremia. We determined sodium and water balance and measured plasma atriopeptin, antidiuretic hormone, and aldosterone. Plasma atriopeptin ranged from 8 to 44 pg/mL (normal, less than 45 pg/mL); antidiuretic hormone was not elevated at 4 to 5 pg/mL, and aldosterone was slightly elevated at 1040.25 pmol/L. The concentrations of these hormones could not directly explain the natriuresis; interactions with neural or other humoral factors may be involved. In evaluating such patients, careful attention to sodium and water balance is important to guide appropriate therapy.

Topics: Adult; Aldosterone; Brain Neoplasms; Dehydration; Glioma; Humans; Hyponatremia; Male; Sodium; Vasopressins; Water-Electrolyte Balance

In neurosurgical patients with hyponatraemia (plasma sodium less than 130 mmol/l) and natriuresis, increased antidiuretic hormone (ADH) secretion may be appropriate rather than inappropriate. Ten such patients were studied prospectively to assess circulating ADH concentration and body fluid volumes. Compared with a control group, the mean plasma ADH level was significantly elevated (0.9 pmol/l (s.e.m. = 0.2) versus 0.2 pmol/l (s.e.m. = 0.1], the total body water was normal (101% (s.e.m. = 3) versus 100% (s.e.m. = 6], while the blood volume was significantly reduced (89% (s.e.m. = 3) versus 104% (s.e.m. = 5]. The elevated ADH level was therefore appropriate to a reduced blood volume. This suggests that, in neurosurgical patients with hyponatraemia, fluid restriction could be dangerous. Serial observations in this small group of patients showed that salt replacement and normal fluid intake resulted in a fall in the elevated ADH levels.

Topics: Acute Disease; Adult; Blood Volume; Body Water; Brain Diseases; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Natriuresis; Plasma Volume; Prospective Studies; Vasopressins

Some days after the administration of a third bolus of ABVD (adriamycin, bleomycin, vinblastine, dacarbazine) a patient affected by immunoblastic lymphoma underwent a neurotoxic crisis. The episode lasted 1 week and was followed by a dramatic fall in plasma sodium (104 mEq I-1), associated with a proportionally lesser decrease in plasma chloride and phosphate. Despite the lowest plasma osmolality, detectable levels of circulating ADH were present. After 36 h the hyponatremic episode improved after the infusion of hypertonic sodium chloride. Nevertheless the patient lapsed into a hypotonic coma. The urinary concentrations of the main tubular enzymes (gamma-glutamyltranspeptidase, N-acetyl-glucosaminidase, alpha-glucosidase) proved very high and successively decreased slowly. The most likely cause of such hyponatremic episode is vinblastine. The drug acted through: (a) an already known inappropriate release of ADH, and (b) a hitherto unreported tubular lesion, which impaired the reabsorption of sodium and other coupled solutes.

Topics: Adult; Antineoplastic Combined Chemotherapy Protocols; Bleomycin; Dacarbazine; Doxorubicin; Female; Humans; Hyponatremia; Kidney Tubules; Lymphoma, Non-Hodgkin; Vasopressins; Vinblastine; Vincristine

Topics: Atrial Natriuretic Factor; Diuresis; Humans; Hyponatremia; Psychotic Disorders; Vasopressins

Topics: Angiotensin-Converting Enzyme Inhibitors; Blood Pressure; Glomerular Filtration Rate; Heart Failure; Humans; Hyponatremia; Hypotension; Renin-Angiotensin System; Risk Factors; Vasopressins

Topics: Adenoma; Female; Humans; Hyponatremia; Middle Aged; Osmolar Concentration; Pituitary Neoplasms; Polyuria; Thirst; Vasopressins

Water intoxication is a serious problem in many patients with chronic psychiatric illness. In an effort to determine the mechanism of this disorder, we investigated the osmoregulation of water intake and antidiuretic function in psychiatric patients with polydipsia and hyponatremia and in matched controls with psychiatric illness but neither polydipsia nor hyponatremia. We found that a water load suppressed plasma osmolality and vasopressin and urine osmolality in both groups, but that urinary dilution and free water clearance were impaired in the patients with hyponatremia, even though plasma levels of vasopressin and solute clearance were similar in the two groups. Moreover, during water loading and infusion of hypertonic saline, the plasma level of vasopressin was higher at any given plasma osmolality in the test patients than in the controls, indicating a downward resetting of the osmostat. Patients' estimates of the amount of water they desired were shown to correlate significantly with the amount of water consumed and, at any given level of plasma osmolality, appeared to be higher in the test patients than in the controls. We conclude that psychiatric patients with polydipsia and hyponatremia have unexplained defects in urinary dilution, the osmoregulation of water intake, and the secretion of vasopressin.

Topics: Adult; Body Water; Drinking; Female; Humans; Hyponatremia; Kidney Concentrating Ability; Male; Osmolar Concentration; Psychotic Disorders; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Aged; Humans; Hyponatremia; Hypothyroidism; Male; Vasopressins

This prospective study is based on 256 patients with severe brain injury. Six patients (2.3%) developed the clinical picture of inappropriate secretion of antidiuretic hormone (SIADH): 3 in the first 3 days following the injury, 3 after more than a week. Their ADH plasmatic level were measured by radio-immunoassay. In the former, many factors, largely iatrogenic, can explain the increased secretion of ADH we found and which is then definitely "appropriate". It should be prevented by fluid restriction. In the latter, we found adequately low ADH levels, when the hypo-osmolarity is taken into account. Here, the aetiology seems to be a renal salt loss, eventually in relation to a natriuric factor (e.g. atrial natriuretic factor), justifying the term: "Cerebral salt wasting syndrome". With the resistance to fluid restriction, the treatment still remains a problem.

Topics: Adult; Brain Injuries; Child; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Osmolar Concentration; Prospective Studies; Vasopressins

Topics: Adult; Aged; Aldosterone; Blood Urea Nitrogen; Cerebrovascular Disorders; Humans; Hyponatremia; Middle Aged; Potassium; Vasopressins

Two cases of hyponatremia with intracranial lesions are reported with emphasis on diagnostic value of measurement of antidiuretic hormone (ADH) and atrial natriuretic polypeptide (ANP). Case 1. A 77-year-old female was transferred to our hospital for further care of vegetative state after subarachnoid bleeding on May 23, 1986. She was operated by neck clipping of rt-IC bifurcation aneurysm and lt-internal carotid-posterior communicating aneurysm at another hospital. On admission, computed tomography showed diffuse low density at bilateral thalamus and centrum semiovale. Biochemical analysis revealed hyponatremia (120 mEq/t) with increased natriuresis. Endocrinological date revealed normal plasma ADH and high plasma ANP levels. Patient was treated with infusion of 1% NaCl. Case 2. A 65-year-old male was admitted to our department because of gradual impairment of consciousness and generalized convulsion. Computed tomography showed small low density area at rt-thalamus and lt-cerebellar hemisphere. Biochemical date revealed severe hyponatremia (91 mEq/t) with normal plasma level of ADH and high plasma ANP. He was treated with infusion of 3% NaCl and hyponatremia was improved. The hyponatremia is frequently associated with intracranial disorders such as brain tumor, subarachnoid hemorrhage and head injury. Originally, hyponatremia with natriuresis was thought to be caused by salt wasting. This syndrome was defined as the inability to prevent salt loss in the urine due to undefined natriuretic factor in the brain. However, since 1957, because of introduction of concept of SIADH, it has generally become accepted that patients with natriuresis had SIADH. (ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aged; Atrial Natriuretic Factor; Brain; Brain Diseases; Female; Humans; Hyponatremia; Male; Natriuresis; Vasopressins

The pathogenesis of hyponatremia remains debated; therefore, we determined the roles of plasma vasopressin, fluid intake and renal free water excretion in hyponatremic medical patients. We evaluated 100 consecutive hypo-osmolar hyponatremic patients (PNa = 127 +/- 0.7 mM l-1) in a prospective manner. We observed: hyponatremia was often found in association with advanced congestive cardiac failure (twenty-five of 100 patients), liver cirrhosis (16%) and primary volume contraction (29%). There was a 17% in-hospital mortality of hyponatremic patients. This was primarily related to the severity of underlying illnesses rather than to hyponatremia per se. The most consistently observed laboratory finding of hyponatremia was non-osmotic vasopressin stimulation; mean observed PADH was 4.7 +/- 0.7 pg ml-1 and vasopressin was detectable by radioimmunoassay (RIA) in 91% of all patients. In addition to vasopressin stimulation we also found evidence of advanced 'circulatory underfilling' in most hyponatremic patients. Mean urinary osmolality was hypertonic to plasma (441 +/- 17.4 m0sm kg H2O-1). This applied to patients with hyponatremic cardiac failure, liver cirrhosis and volume contraction. Almost all of these patients received high ceiling diuretics. (v) Spontaneous mean daily fluid intake was 2.4 +/- 0.2 l. In summary, our findings suggest that disturbances of vasopressin, fluid intake and renal free water excretion co-operate in the pathogenesis of hyponatremia. In clinical states of advanced circulatory underfilling the occurrence of hyponatremia indicates a poor prognosis of the patient.

Topics: Aged; Drinking; Female; Heart Failure; Humans; Hyponatremia; Kidney Diseases; Liver Cirrhosis; Male; Middle Aged; Vasopressins

Hyponatremia is usual during myxedema coma. Hereafter we report two cases with increased plasma arginine vasopressin (AVP). Patients were admitted because of hypothyroid coma. In each case, there was an hyponatremia with normal urine sodium and low serum osmolality. Renal function was normal. On hormonal results, primary hypothyroidism was evident. Plasma AVP was increased. The plasma cortisol of one patient was high. Immediate therapy associated: water restriction, hypertonic saline infusion, furosemide, oral thyroid hormones with low doses. On the fourth day, conscience improved obviously. Natremia and plasma AVP went back to normal state before returning to euthyroid state. Patients went on improving along with normalizing thyroid status. Hyponatremia can be a serious sign of hypothyroidism. In case of myxedema coma with hyponatremia, clinical improvement seems to be related to fast correction of water and electrolyte disturbances and we prefer to give low doses of thyroid hormones at first. The hyponatremia and increased plasma AVP mechanisms are complex. However, in each of these cases, plasma AVP come back to normal before returning to euthyroid state. In one case, high plasma cortisol level rules out adrenal insufficiency as causal mechanism of electrolyte disorders.

Topics: Aged; Coma; Female; Humans; Hyponatremia; Hypothyroidism; Male; Myxedema; Vasopressins

Topics: Child; Child, Preschool; Hospitalization; Humans; Hyponatremia; Infant; Infant, Newborn; Natriuresis; Osmotic Pressure; Vasopressins

Topics: Burns; Fluid Therapy; Humans; Hyponatremia; Infant; Male; Vasopressins; Water Intoxication

It is increasingly evident that many disorders common in the aging individual may be accompanied by disturbances of fluid and sodium balance, especially hyponatremia. Physiological alterations in water and sodium regulation have been identified as part of the normal aging process which may contribute to the relative frequency of fluid and electrolyte disorders in the elderly. Hyponatremia may present with a wide variety of symptoms and may be a clue to the existence of an underlying major disease process. Treatment involves both acute and long-term management based on identification of the causative disorder and understanding of the pathophysiologic mechanism which has led to development of hyponatremia.

Topics: Aged; Aging; Humans; Hyponatremia; Male; Sodium; Vasopressins; Water-Electrolyte Balance

Severe hyponatremia developed within 2 weeks of head injuries in three elderly patients. Before the head injuries occurred, normal serum levels of sodium had been found in two of the three patients. Hyponatremia (105 to 117 meq/L) was associated with persistently increased urinary excretion of sodium. The patients appeared dehydrated and had lost weight. The mean plasma level of antidiuretic hormone was 5.0 +/- 1.6 (SD) pg/mL, which was relatively high despite decreased osmolality. Plasma renin activity was suppressed to 0.25 +/- 0.13 ng/mL X h, and plasma aldosterone levels measured low-normal or normal. Plasma renin activity and plasma aldosterone levels remained unchanged after the patients were given furosemide and placed in an upright position. The hyponatremia promptly resolved after the administration of fludrocortisone acetate, 0.1 to 0.4 mg/d. These observations indicate that severe hyponatremia occurs in elderly persons rapidly after head injuries, that it responds well to mineralocorticoid hormone therapy, and that both central nervous system and renal components may be involved in the mechanisms of action of the disorder.

Topics: Aged; Aged, 80 and over; Craniocerebral Trauma; Female; Fludrocortisone; Humans; Hyponatremia; Male; Natriuresis; Renin-Angiotensin System; Vasopressins

In hypoosmolar hyponatremia, vasopressin is commonly observed to be less than maximally suppressed. This is attributed to the presence of nonosmolar vasopressin stimuli. However, the exact relationship of nonsuppressed antidiuretic hormone to specific circulatory parameters is controversial. Therefore, in the present study, we examined this question in 100 hypoosmolar hyponatremic patients in the Department of Medicine. Despite plasma hypoosmolality, vasopressin was found to be measurable in 92% of patients. Seventy patients suffered from edematous disorders (congestive heart failure, cirrhosis) or volume contraction per se; in these patients we observed unequivocal, though indirect, evidence of advanced circulatory alterations. These were associated with hyponatremia and nonsuppressed vasopressin. However, the latter could not be related directly to a specific circulatory parameter such as mean arterial blood pressure, creatinine clearance, plasma renin activity (PRA), norepinephrine, or aldosterone. However, patients with nondetectable vasopressin (n = 8) differed significantly from those with high vasopressin concentrations (n = 8: PADH greater than 9 pg/ml); in the latter, pulse rate (104 +/- 3 vs. 82 +/- 5 beats/min), plasma urea concentration (90 +/- 5 vs. 32 +/- 5 mg/dl), plasma urate concentration (7.2 +/- 0.8 vs. 3.6 +/- 0.8 mg/dl), and PRA (36 +/- 7 vs. 9.5 +/- 4.6 ng AI/ml/h) were all significantly higher than in the former. It is concluded that, in hyponatremia, the relationship between circulatory impairment and vasopressin is complex.

Topics: Creatinine; Hemodynamics; Humans; Hyponatremia; Vasopressins

The present study was designed to investigate in rats the influence of converting enzyme inhibition with captopril on blood pressure, plasma urea, plasma renin concentration (PRC), plasma aldosterone and plasma vasopressin, and to define the interrelationships between PRC and these variables during equal degrees of either hyponatraemic (furosemide, 40 mg/kg for 2 days) or hypernatraemic (48-h water deprivation) dehydration. Chronic treatment with captopril (40 mg/kg daily) decreased blood pressure by 19% in normally hydrated treated rats, by 27% in water-deprived treated rats and by 40% in furosemide-treated rats. Plasma renin concentration, plasma aldosterone and plasma vasopressin were increased during both hypo- and hypernatraemic dehydration. Captopril decreased plasma aldosterone in water-deprived and furosemide-treated rats, whereas plasma vasopressin was unchanged. The significant correlation observed between plasma aldosterone and PRC in non-treated rats persisted in treated rats, the same level of plasma aldosterone being observed at values of PRC 10 times higher. On the other hand, the correlation between plasma vasopressin and PRC did not persist in captopril-treated rats. An increase in plasma urea was observed in both water-deprived treated rats and furosemide-treated rats. These data indicate that during hypo- and hypernatraemic dehydration, the renin-angiotensin system plays a role in regulating blood pressure, urea elimination and plasma aldosterone, but vasopressin regulation is not modified by its inhibition.

Topics: Aldosterone; Angiotensin-Converting Enzyme Inhibitors; Animals; Blood Pressure; Captopril; Dehydration; Hypernatremia; Hyponatremia; Kidney; Male; Rats; Renin; Renin-Angiotensin System; Urea; Vasopressins

Topics: Absorption; Body Water; Fluid Therapy; Humans; Hyponatremia; Kidney; Osmolar Concentration; Sodium; Thirst; Vasopressins

Topics: Acetazolamide; Acid-Base Imbalance; Biological Transport; Diuretics; Drug Resistance; Ethacrynic Acid; Furosemide; Humans; Hydrochlorothiazide; Hyperkalemia; Hypernatremia; Hypokalemia; Hyponatremia; Indapamide; Kidney Tubules, Distal; Kidney Tubules, Proximal; Loop of Henle; Metolazone; Osmolar Concentration; Spironolactone; Triamterene; Vasopressins

We investigated the antidiuretic hormone (ADH) response in 12 infants with bronchopulmonary dysplasia during acute respiratory distress. All of the infants had hypoxemia with air-trapping in the chest at the time of admission to the hospital. None had documented infection. There was a dramatic increase in the plasma levels of ADH during acute respiratory distress, with a subsequent reduction of levels toward normal when the respiratory distress decreased to the preadmission well state. Three of 12 infants manifested hyponatremia at 24 hours after admission, with two of them exhibiting persistent hypertension for up to three days. The mechanism for elevated ADH levels is air-trapping in the chest, causing pulmonary hypovolemia and decreased left atrial filling and/or decreased transmural pressure of the left atrium.

Topics: Bronchopulmonary Dysplasia; Female; Furosemide; Humans; Hyponatremia; Hypoxia; Infant; Infant, Newborn; Male; Respiratory Distress Syndrome, Newborn; Vasopressins

Topics: Adult; Aged; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Vasopressins; Water-Electrolyte Imbalance

Topics: Humans; Hyponatremia; Kidney Concentrating Ability; Kidney Failure, Chronic; Osmolar Concentration; Renal Dialysis; Vasopressins; Water-Electrolyte Balance

Topics: Humans; Hyponatremia; Hypothalamus; Infant; Male; Osmolar Concentration; Vasopressins; Water-Electrolyte Balance

Topics: Aged; Humans; Hyponatremia; Inappropriate ADH Syndrome; Middle Aged; Vasopressins; Water-Electrolyte Balance

Topics: Addison Disease; Adrenal Glands; Humans; Hyponatremia; Male; Middle Aged; Tuberculosis; Vasopressins

Topics: Blood Volume; Humans; Hyponatremia; Serum Albumin; Vasopressins

Hyponatremia developing some days after transsphenoidal pituitary adenectomy is a treacherous complication of uncertain cause. Of 19 patients monitored in a pilot study at the Wessex Neurological Centre, plasma sodium fell below 125 mmol/liter in three patients at times ranging from 6 to 9 days postoperatively. One patient had evidence of inappropriate secretion of arginine vasopressin (AVP), and the other two probably had steroid insufficiency despite apparently adequate steroid cover. In a more detailed study, the fluid and sodium balance of a further 16 patients was monitored for 7 to 11 days following transsphenoidal surgery together with plasma cortisol, renin, and AVP concentrations. No patient became severely hyponatremic. Three developed partial diabetes insipidus. Two patients with Cushing's disease had evidence of postoperative corticosteroid insufficiency despite normal steroid protection. An inappropriately low plasma cortisol concentration was recorded in both. Plasma AVP concentrations did not show a delayed surge postoperatively. Delayed hyponatremia appears to occur most often in patients with hypoadrenalism, as glucocorticoid cover is decreased. It results from water retention combined with natriuresis, and is reversed by glucocorticoid treatment.

Topics: Adenoma; Adult; Arginine Vasopressin; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Pituitary Neoplasms; Vasopressins; Water-Electrolyte Imbalance

Topics: Diagnosis, Differential; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

Topics: Aged; Aging; Humans; Hyponatremia; Vasopressins

Topics: Captopril; Diuretics; Heart Failure; Humans; Hyponatremia; Osmolar Concentration; Plasma; Renin-Angiotensin System; Thirst; Vasopressins

The effects of lorcainide, a new antiarrhythmic drug, on serum electrolytes and osmolality are described in a series of 33 patients with organic heart disease and complex ventricular arrhythmias treated with lorcainide. In eight patients, a mean decrease in serum Na+ of 8.25 +/- 3.2 mEq/L was observed after a single 200 mg intravenous dose of lorcainide. Sixteen of 33 patients developed significant hyponatremia and hypoosmolality during oral treatment with lorcainide. In all except two patients, serum Na+ returned to normal values within 3 to 12 months of continued lorcainide therapy. Low serum Na+ and hypoosmolality in the absence of volume depletion, clinically manifest edema, and unaltered renal, adrenal, cardiac, or thyroid function suggest that this antiarrhythmic drug produced the syndrome of inappropriate antidiuretic hormone secretion (SIADH). SIADH appeared to be transient and asymptomatic in our patients. One patient developed severe hyponatremia with serum Na+ of 108 mEq/L when hydrochlorothiazide was given to control hypertension. It is concluded that SIADH is an important side effect of lorcainide therapy. We recommend that serum Na+ be carefully monitored in patients started on lorcainide therapy, and extreme caution should be exercised in prescribing diuretics to patients with persistent hyponatremia.

Topics: Adult; Aged; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Benzeneacetamides; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Piperidines; Potassium; Sodium; Vasopressins

Topics: Diagnosis, Differential; Humans; Hyponatremia; Vasopressins

Hyponatremia and hypo-osmolality developed in a 70-year-old patient. It was probably mediated by hypersecretion of antidiuretic hormone, which, in turn, was due to prolonged nausea and vomiting. Severe esophagitis was the cause of the nausea. The patient was not given large amounts of fluids intravenously, and it is likely that she continued to drink for nondipsetic reasons. In view of her medical history of neurosyphilis, the possibility of a disturbance in the mechanism of thirst regulation is discussed, but remains unproved.

Topics: Aged; Esophagitis, Peptic; Female; Humans; Hyponatremia; Nausea; Osmolar Concentration; Syndrome; Time Factors; Vasopressins; Vomiting; Water-Electrolyte Imbalance

A monkey model of subarachnoid hemorrhage (SAH) was used to study both the incidence of hyponatremia and natriuresis and the associated changes in antidiuretic hormone (ADH) secretion and salt and water balance. Following SAH, seven of nine monkeys became natriuretic and hyponatremic. The natriuretic period lasted an average of 4.4 +/- 0.4 days. The mean nadir of serum sodium content was 125.7 +/- 1.6 mEq/liter, and occurred on the average on the 5th day following SAH. The sodium balance after SAH was negative as compared to the preoperative positive sodium balance (p less than 0.001). The plasma vasopressin level was usually elevated for a day following surgery, but there was no significant difference in the levels during the preoperative period and during the period of natriuresis following SAH. The daily urine output and aldosterone levels were not significantly different, and the plasma volume was slightly, but not significantly, decreased after SAH. Four of the animals that had a hyponatremic and natriuretic response following SAH showed a normal regulation of vasopressin in response to both a water challenge and hypertonic saline challenge. The three monkeys that underwent sham procedures did not become hyponatremic and natriuretic postoperatively. The sham-operated monkeys did not show significant differences in their plasma vasopressin levels, urine volume, plasma volume, and aldosterone levels following surgery. These observations are more consistent with primary natriuresis as the cause of hyponatremia rather than the syndrome of inappropriate secretion of ADH. The cause of the renal loss of sodium is not known, but the possibility of a brain natriuretic factor or an alteration in the neural control of the kidney should be considered.

Topics: Animals; Hyponatremia; Inappropriate ADH Syndrome; Macaca fascicularis; Male; Models, Biological; Natriuresis; Subarachnoid Hemorrhage; Vasopressins

A rat model of the Schwartz-Bartter syndrome was created by the administration of a high dose of a long-acting vasopressin preparation (pitressin tannate ) together with a forced water intake. The treatment led to water retention, hypernatriuria , marked hyponatraemia (in 4-5 days) and severe cerebral oedema. These changes could be prevented by the simultaneous administration of [1-(beta-mercapto-beta, beta- cyclopentamethylene -propionic acid),2-0- ethyltyrosine ,4-valine]arginine vasopressin. The observations indicate that this vasopressin antagonist analogue might be of use in the future as an effective drug against the Schwartz-Bartter syndrome.

Topics: Animals; Arginine Vasopressin; Body Water; Brain; Brain Edema; Diuresis; Hyponatremia; Inappropriate ADH Syndrome; Male; Osmolar Concentration; Rats; Rats, Inbred Strains; Urination; Vasopressins

Topics: Adenoma, Chromophobe; Adrenocorticotropic Hormone; Aged; Humans; Hyponatremia; Male; Osmolar Concentration; Pituitary Neoplasms; Vasopressins

Topics: Aged; Humans; Hyponatremia; Hypopituitarism; Hypothalamic Neoplasms; Kidney Concentrating Ability; Lung Neoplasms; Male; Pituitary Neoplasms; Polyuria; Vasopressins

A 54-year-old woman had seizures and a focal neurologic deficit associated with hyponatremia induced by a thiazide diuretic. Prompt correction of hyponatremia by administration of hypertonic saline solution was followed by resolution of all neurologic defects. Metabolic balance studies and rechallenge with hydrochlorothiazide were undertaken to investigate the mechanism of the thiazide-induced hyponatremia. Abnormal vasopressin secretion was shown by a plasma vasopressin concentration of 0.5 microU/ml with a plasma osmolality of 268 mOsm/kg water after administration of a fluid challenge consisting of 45 ml/kg body weight. Rechallenge with chlorothiazide while on a sodium- and potassium-controlled balanced diet resulted in a decrease in serum sodium concentration (136 to 124 mEq/L) and plasma osmolality (283 to 261 mOsm/kg) within 18 hours. During this period, urine losses of monovalent cation were only 55 mEq and body weight was constant at 48.2 kg. A second challenge while the patient received all fluids and electrolytes intravenously again resulted in decreased serum sodium concentration (134 to 126 mEq/L) after urinary loss of only 69 mEq of cation. Thus this patient's hyponatremia cannot be accounted for solely by changes in external water and electrolyte balance; the rapidity with which changes were produced suggests that osmolar inactivation, probably intracellularly, may contribute to the severe hypotonicity seen in some patients.

Topics: Drug Combinations; Female; Humans; Hydrochlorothiazide; Hypertension; Hyponatremia; Middle Aged; Neurologic Manifestations; Osmolar Concentration; Recurrence; Seizures; Sodium; Triamterene; Vasopressins

Topics: Adrenal Cortex; Aged; Humans; Hyponatremia; Hypothyroidism; Male; Vasopressins

Topics: Ascites; Body Water; Humans; Hyponatremia; Kidney; Liver Cirrhosis; Peritoneovenous Shunt; Vasopressins

Topics: Humans; Hyponatremia; Hypotension, Orthostatic; Inappropriate ADH Syndrome; Infusions, Parenteral; Osmolar Concentration; Rocky Mountain Spotted Fever; Sodium Chloride; Vasopressins

To explore a possible downward setting of the hypothalamic osmoreceptors in the hyponatremia of hypothyroidism, 4 adolescent patients with hypothyroidism were studied. Plasma and urine osmolality were measured on random paired simultaneous samples, and following a water load. The osmotic threshold was determined by the isovolemic infusion of hypertonic NaCl, and compared to the osmotic threshold of 6 healthy subjects. Random paired urine and plasma osmolality revealed inappropriately high urine osmolality for the given plasma osmolality. A water load produced a normal dilution of urine. Osmotic threshold was found at plasma osmolality of 286-287 mosm/kg, compared to 286.7 +/- 1.0 in 6 normal individuals. It is concluded that none of the known types of the syndrome of inappropriate ADH secretion could account for the hyponatremia in the hypothyroid patients, and that patients with hypothyroidism have normal osmoreceptors as measured by the osmotic threshold test.

Topics: Adolescent; Blood; Child; Female; Humans; Hyponatremia; Hypothyroidism; Male; Osmolar Concentration; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Child, Preschool; Female; Humans; Hyponatremia; Infant; Male; Prospective Studies; Retrospective Studies; Seizures, Febrile; Sodium; Vasopressins

A patient with a four-year history of unexplained hyponatremia was seen with recurrent nasal discharge and was found to have a typical olfactory neuroblastoma. The clinical laboratory diagnostic studies suggested that the patient's sodium deficiency was secondary to the syndrome of inappropriate antidiuretic hormone. Subsequent resection of the neoplasm led to resolution of the hyponatremia, suggesting that a (tumor-associated) humoral factor, such as vasopressin or a vasopressinlike substance, was responsible for the electrolyte disturbance. A search of the literature disclosed one previous case of vasopressin-secreting nasal neuroblastoma.

Topics: Adult; Female; Hormones, Ectopic; Humans; Hyponatremia; Inappropriate ADH Syndrome; Neuroectodermal Tumors, Primitive, Peripheral; Nose Neoplasms; Vasopressins

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) as a cause of hypotonic hyponatremia is well recognized. The syndrome is commonly associated with cranial and thoracic infectious disease or malignancy. An idiopathic form of the syndrome has been reported, but poorly documented. Our patient, an 88-year-old man without any associated disease, had SIADH confirmed by a standard water load test. The pattern of antidiuretic hormone release corresponded to the "vasopressin leak" pattern. A review of ten cases of "idiopathic" SIADH showed that each of these cases has been associated with neuropsychiatric or other medical disturbances. We conclude that idiopathic inappropriate antidiuresis does exist and is a discrete category of SIADH. Data suggest that advanced age may be a risk factor for this disease. This syndrome may account for the increased susceptibility to hyponatremia among older patients.

Topics: Adolescent; Aged; Child, Preschool; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Mental Disorders; Middle Aged; Osmolar Concentration; Vasopressins

Two cases of Schwartz-Bartter syndrome are reported. Both were due to malignant anaplasic tumours of the APUD type with multiple abnormal endocrine secretion, and both were accompanied with hypouricaemia of uncertain significance. The authors believe that the association of hypernatraemia with hypouricaemia should alert clinicians to the possibility of a syndrome of inappropriate antidiuretic hormone secretion (SIADH) of malignant origin.

Topics: Apudoma; Carcinoma, Small Cell; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Uric Acid; Vasopressins

In advanced heart failure, severe edema develops associated with hyponatremia. In 20 patients with severe congestive heart failure, we studied plasma antidiuretic hormone (ADH) concentrations related to hemodynamics and plasma osmolality. Prazosin was used to test the acute response to changes in atrial receptors and hemofiltration to test the response to changes in volume receptors. One group of the patients had inappropriately high ADH values (14.5 +/- 8.8 pg/ml) in relation to their plasma osmolality, which was well below normal values (276 +/- 23 mosmol/kg water) with no apparent osmoregulatory control. The other group showed a normal relationship of ADH and plasma osmolality (3.9 +/- 1.0 pg/ml; 289 +/- 8 mosmol/kg water), Only in the normal regulating group did lowering of left atrium pressure by prazosin result in a rise in ADH related to the decrease in pressure. Inappropriately high ADH secretion could be reversed by hemofiltration. This suggests that the syndrome of "dilutional hypo-osmolality" in severe congestive heart failure may be caused by an inappropriately high ADH secretion in which the osmoreceptor system is dominated by nonosmolar stimuli; however, it cannot be ruled out that associated hemodynamic effects in the kidney or other intrarenal or hormonal factors contribute to this mechanism.

Topics: Adult; Edema; Heart Failure; Hemodynamics; Humans; Hyponatremia; Middle Aged; Osmolar Concentration; Prazosin; Vasopressins

Topics: Adult; Beer; Female; Humans; Hyponatremia; Vasopressins

The pathophysiology of hyponatremia in adrenal insufficiency has been a subject of intense controversy. The controversy centers on whether the inability of the kidney to maximally dilute the urine is secondary to increased levels of antidiuretic hormone (ADH) or is independent of ADH. Review of the pertinent studies allows us to conclude that (1) in prolonged glucocorticoid deficiency, plasma ADH levels are elevated because of decreased effective circulating blood volume; (2) in mineralocorticoid deficiency, plasma ADH levels may also be elevated, but in this case because of decreased absolute circulating blood volume; (3) in both instances the elevated ADH levels impair the ability to dilute the urine; and (4) in both glucocorticoid and mineralocorticoid deficiency hemodynamic changes may also contribute, independently of ADH, by limiting delivery of tubular fluid to the diluting site.

Topics: Adrenal Insufficiency; Glucocorticoids; Hemodynamics; Humans; Hyponatremia; Kidney; Mineralocorticoids; Vasopressins

Topics: Adult; Aged; Extracellular Space; Humans; Hypernatremia; Hyponatremia; Infant; Osmolar Concentration; Sodium; Vasopressins

Topics: Humans; Hyponatremia; Vasopressins

Topics: Aged; Body Water; Diuretics; Humans; Hydrochlorothiazide; Hypertension; Hyponatremia; Male; Sodium Chloride Symporter Inhibitors; Vasopressins

Topics: Diagnosis, Differential; Edema; Humans; Hyponatremia; Vasopressins; Water; Water-Electrolyte Balance

A 45-year-old woman with myxedema coma due to primary hypothyroidism manifested hyponatremia, impaired water excretion, and elevated urine osmolarity as well as natriuresis suggestive of a syndrome of inappropriate antidiuretic hormone secretion. However, plasma vasopressin was undetectable or very low and plasma aldosterone levels were suppressed in the presence of hyponatremia. Subsequent replacement therapy with levothyroxine caused a rapid decline in sodium clearance which was independent of the change in glomerular filtration rate, and corrected the impaired water excretion and hyponatremia. Plasma vasopressin levels returned to the normal range after the correction of hyponatremia. Thus, the results indicate that neither vasopressin nor aldosterone plays a dominant role in the pathogenesis of the hyponatremia in this patient. It appears that thyroid hormone deficiency itself caused the derangement of tubular cell function, which resulted in the development of the impaired water excretion and hyponatremia.

Topics: Coma; Female; Glomerular Filtration Rate; Humans; Hyponatremia; Hypothyroidism; Inappropriate ADH Syndrome; Middle Aged; Myxedema; Osmolar Concentration; Sodium; Thyroxine; Vasopressins

Topics: Adrenal Insufficiency; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Vasopressins

Topics: Arginine Vasopressin; Heart Failure; Humans; Hyponatremia; Radioimmunoassay; Vasopressins

Topics: Arginine Vasopressin; Body Water; Deamino Arginine Vasopressin; Diabetes Insipidus; Humans; Hypernatremia; Hypoglycemia; Hyponatremia; Inappropriate ADH Syndrome; Pharmacology; Radioimmunoassay; Vasopressins; Water-Electrolyte Imbalance

The release of vasopressin (AVP) was assessed by measuring urinary excretion of the hormone in ten neonates who had an acute and symptomatic pneumothorax in the first three days after birth. AVP excretion rose significantly (paired t analysis) after the pneumothorax occurred. When apparent re-expansion of the lungs occurred after treatment, excretion of AVP returned to prepneumothorax levels within eight to 16 hours. If the pneumothorax persisted or worsened. AVP excretion remained elevated. Urine osmolality rose significantly (paired t analysis) after pneumothorax, presumably in response to the increased AVP levels. Two of the ten infants had hyponatremia in the period studied, while in a state of sodium balance. It was concluded that AVP release is increased after a pneumothorax occurs. This increase is apparently not due to osmoregulatory requirements. Fluid intake in these infants may need adjustment to prevent an inappropriate positive water balance.

Topics: Drinking; Humans; Hyponatremia; Infant, Newborn; Infant, Newborn, Diseases; Osmolar Concentration; Pneumothorax; Respiration, Artificial; Urine; Vasopressins

Degenerative lesions in the superior vermis of the cerebellum were produced in 8 of 14 rats that were first made hyponatremic for three days with vasopressin and water and then given hypertonic saline. Within the superior vermis, lesions were predominantly localized to the crests of the folia. These lesions were characterized by demyelination of folial white matter and necrosis of granule cells at the junction with the white matter. In severe degeneration, the entire width of the granule cell layer was involved and Purkinje cell necrosis was found as well. Hyponatremia alone or administration of hypertonic saline to normonatremic rats did not result in lesions. Because of the topographical and histopathological similarity of these lesions to those of alcoholic cerebellar degeneration, our findings raise the possibility of a contribution of electrolyte-induced injury to the pathogenesis of alcoholic cerebellar degeneration.

Topics: Animals; Arginine Vasopressin; Cerebellum; Hyponatremia; Male; Myelin Sheath; Necrosis; Nerve Degeneration; Rats; Rats, Inbred Strains; Saline Solution, Hypertonic; Sodium; Sodium Chloride; Vasopressins

Water intoxication with seizures secondary to excessive fluid ingestion occurred in four apparently healthy infants in two families; we also review five previously reported cases.

Topics: Diseases in Twins; Drinking; Female; Humans; Hyponatremia; Infant; Infant Care; Male; Seizures; Vasopressins; Water Intoxication

A 36-yr-old woman with a chronic wasting illness associated with hyponatremia and hypotension proved to have secondary adrenal insufficiency and low levels of GH and PRL. TSH, LH, and FSH responses remained normal. Aldosterone excretion was markedly reduced (0.74 microgram/day) before replacement therapy was started, but normal renin and aldosterone responses to sodium restriction were observed after 6 months of corticosteroid treatment. These responses were maintained after acute steroid withdrawal despite the continued absence of ACTH. Chronically adequate glucocorticoid levels were necessary to maintain a normal aldosterone response in this patient. If there is also a pituitary factor required for this response, it does not appear to be ACTH.

Topics: Adrenocorticotropic Hormone; Adult; Aldosterone; Blood Glucose; Dexamethasone; Female; Fludrocortisone; Follicle Stimulating Hormone; Growth Hormone; Humans; Hypoglycemia; Hyponatremia; Insulin; Luteinizing Hormone; Prolactin; Sodium; Thyrotropin; Vasopressins

Antidiuretic hormone (ADH) immunoactivity (28--164 pg/mg wet weight) was detected in the tumour tissue of only three out of thirty-two patients with carcinoma of the bronchus. All three patients had small oat-cell tumours and two had persistent hyponatraemia prior to death. Serum sodium was not obtained in the third patient. Serum sodium was normal in the remaining twenty-nine patients with undetectable ADH immunoactivity.

Topics: Adenocarcinoma; Aged; Carcinoma, Small Cell; Carcinoma, Squamous Cell; Female; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Radioimmunoassay; Vasopressins

Topics: Adrenocorticotropic Hormone; Cushing Syndrome; Erythropoietin; Gonadotropins; Hormones, Ectopic; Humans; Hypercalcemia; Hypoglycemia; Hyponatremia; Insulin; Melanocyte-Stimulating Hormones; Paraneoplastic Endocrine Syndromes; Parathyroid Hormone; Pigmentation Disorders; Vasopressins

In five hyponatremic, cirrhotic patients, demeclocycline hydrochloride was used to inhibit the hydroosmotic effect of vasopressin. In four, renal impairment developed during the 7 to 20 days of demeclocycline hydrochloride (900 to 1,200 mg/day) administration. In these four patients, creatinine clearance fell (72 to 20 mL/min, P less than .01) as BUN (12 to 47 mg/dl, P less than .02) and serum creatinine (0.9 to 4.2 mg/dl, P less than .01) levels rose. The azotemic effect of the drug could not be accounted for consistently by volume depletion secondary to its natriuretic effect. However, a close correlation between plasma demeclocycline levels and its azotemic effect was observed. We conclude that a nephrotoxic effect of demeclocycline severly limits its usefulness in treating hyponatremia in the cirrhotic patient.

Topics: Adult; Creatinine; Demeclocycline; Glomerular Filtration Rate; Humans; Hyponatremia; Kidney; Kidney Diseases; Liver Cirrhosis, Alcoholic; Male; Natriuresis; Vasopressins

Topics: Demeclocycline; Female; Humans; Hyponatremia; Hypothyroidism; Inappropriate ADH Syndrome; Middle Aged; Vasopressins; Water-Electrolyte Imbalance

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Urea; Vasopressins

Topics: Adult; Aged; Diuretics; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Sodium; Sodium Chloride; Vasopressins; Water-Electrolyte Balance

Topics: Extracellular Space; Humans; Hyponatremia; Natriuresis; Vasopressins

Known physiologic mechanisms explain the elevated blood ADH levels observed in most patients with the syndrome of inappropriate ADH. Therefore the word "inappropriate" is a misnomer. It implies that the mechanisms that regulate ADH release are not functioning normally--which is not true. The term misleads the physician who, ideally, should determine why a patient has an excessive blood ADH level and initiate appropriate treatment. Patients with ectopic production of ADH and hyponatremia should be so labeled: "Hyponatremia due to ectopic ADH production." The term SIADH, if used at all, should be reserved for the rare patient with CNS injury or disease that causes increased ADH release and in which the hypothalamic center does not respond normally to afferent peripheral stimuli.

Topics: Blood; Demeclocycline; Furosemide; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lithium; Osmolar Concentration; Pressoreceptors; Saline Solution, Hypertonic; Vasopressins

Topics: Adrenal Cortex Function Tests; Adrenocorticotropic Hormone; Cosyntropin; Drug Contamination; Humans; Hyponatremia; Pituitary-Adrenal Function Tests; Vasopressins

Topics: Adrenal Cortex Diseases; Adrenocorticotropic Hormone; Humans; Hyponatremia; Vasopressins

Topics: Child, Preschool; Face; Female; Humans; Hyponatremia; Hypothalamus; Inappropriate ADH Syndrome; Osmolar Concentration; Vasopressins

Following some remarks on the hyposomolar-hyponatraemic syndrome and on the formation of free water, the possible aetiopathogenetic mechanisms of hyponatraemia in ascitogenous cirrhosis of the liver and in particular the role of ADH are considered. 3 cases out of 18 suffering from ascitic phase cirrhosis in whom inability to produce free water was accompanied by conserved urinary excretion of sodium are reported. One explanation might be the intervention of ADH or of an antidiuretic substance.

Topics: Adult; Aged; Ascites; Female; Humans; Hyponatremia; Liver Cirrhosis; Male; Middle Aged; Osmolar Concentration; Vasopressins; Water-Electrolyte Imbalance

Topics: Extracellular Space; Homeostasis; Humans; Hyponatremia; Kidney Diseases; Kidney Glomerulus; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Blood Volume; Diuretics; Heart Failure; Hospitalization; Humans; Hyperglycemia; Hyponatremia; Kidney Failure, Chronic; Liver Cirrhosis; Stress, Physiological; Surgical Procedures, Operative; Vasopressins

Three patients with head injury are described to illustrate certain features of the development, treatment and recovery of hyponatraemia. The hyponatraemia is initially due to water retention but true sodium depletion may develop because of an associated urine sodium loss. The mechanism of the latter is discussed.

Topics: Adult; Craniocerebral Trauma; Extracellular Space; Female; Humans; Hyponatremia; Male; Sodium; Urea; Vasopressins

Topics: Adult; Body Water; Diabetes Insipidus; Diuresis; Extracellular Space; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Intracellular Fluid; Kidney Concentrating Ability; Kidney Failure, Chronic; Osmolar Concentration; Sodium; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Pontine myelinolysis can be suspected clinically on the basis of the following criteria: (1) Electrolyte disturbance manifested mainly by hyponatremia; (2) progressive neurologic deficits resulting in a "locked-in" syndrome; (3) usually, but not necessarily, alcohol abuse; and (4) frequent iatrogenic precipitation of the syndrome by inappropriate rehydration of patients at risk. A major pathophysiologic mechanism for this disorder seems to be the anatomic grid structure of the base of the pons, which is more vulnerable to edema than the cerebral hemispheres. Treatment should be focused on rapid reversal of electrolyte imbalance and judicious use of dehydrating agents. Early diagnosis and treatment might reverse an otherwise malignant syndrome.

Topics: Adolescent; Adult; Aged; Alcoholism; Brain Edema; Brain Stem; Child; Child, Preschool; Demyelinating Diseases; Female; Humans; Hyponatremia; Male; Middle Aged; Pons; Vasopressins; Water-Electrolyte Imbalance

17 patients with severe hyponatraemia (none had cardiac failure or had lately had an operation) all had excessively high plasma-antidiuretic hormone (A.D.H.). Only 13 had features typical of the syndrome of inappropriate secretion of A.D.H. (S.I.A.D.H.). Plasma-A.D.H. was not related to either plasma-sodium or diagnosis. There were as many patients with chest infection as with carcinoma of the lung. Plasma-sodium and plasma-A.D.H. returned rapidly towards normal in the patients with chest infection or volume depletion but these concentrations corrected much more slowly in patients with carcinoma of the lung. The increase in plasma-sodium in patients with chest infection was too rapid to be produced by water-deprivation treatment and was due to return of plasma-A.D.H. to normal. The term S.I.A.D.H. implies an understanding of pathophysiology that does not exist. As a diagnosis it does not help in management or prognosis. A simpler, more descriptive terminology such as "hyponatraemia with carcinoma of the lung" would be more useful and less confusing in the clinical situation.

Topics: Aged; Female; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Respiratory Tract Infections; Sodium; Syndrome; Terminology as Topic; Vasopressins

Topics: Humans; Hyponatremia; Vasopressins; Water-Electrolyte Balance

Topics: Ascites; Demeclocycline; Edema; Humans; Hyponatremia; Osmolar Concentration; Vasopressins; Water Intoxication

Topics: Adrenocorticotropic Hormone; Humans; Hyponatremia; Male; Middle Aged; Vasopressins

We evaluated demeclocycline and lithium therapy in 10 patients with the syndrome of inappropriate secretion of antidiuretic hormone. Despite severe water restriction, all patients had hyponatremia (mean +/- S.E.M. serum sodium of 122 +/- 1.1 meq per liter) and elevated urine osmolality (744 +/- 59 mOsm per kilogram) before treatment. Demeclocycline (600 to 1200 mg daily) restored serum sodium concentration to 139 +/- 1.1 meq per liter within five to 14 days, permitting unrestricted water intake in all patients. In three patients given lithium carbonate (900 mg daily) the serum sodium concentration, urine osmolality and urine volume were unchanged; since two patients had adverse central-nervous-system symptoms during lithium therapy, further study of this agent was abandoned. A patient with an unusual 22-year history of the syndrome was unresponsive to lithium, whereas long-term treatment with demeclocyline was markedly effective. Demeclocycline is superior to lithium in the treatment of the syndrome and may obviate the need for severe water restriction.

Topics: Adult; Aged; Child; Chronic Disease; Demeclocycline; Drug Evaluation; Female; Humans; Hyponatremia; Lithium; Male; Middle Aged; Osmolar Concentration; Sodium; Syndrome; Vasopressins

Topics: Demeclocycline; Humans; Hyponatremia; Lithium; Osmolar Concentration; Syndrome; Vasopressins

A hypothyroid, 72-year-old woman with idiopathic hypopituitarism manifested severe hyponatremia, plasma hypoosmolality, and inappropriately elevated urine osmolality suggestive of a syndrome of inappropriate antidiuretic hormone secretions. The hyponatremia did not respond to demeclocycline hydrochloride, and antidiuretic hormone (ADH) levels measured by a specific radioimmunoassay were appropriately suppressed. Subsequent replacement therapy with levothyroxine sodium resulted in correction of the hyponatremia. Thus, both direct assay as well as hormone blockade failed to show an action of ADH in mediating the water retention.

Topics: Aged; Demeclocycline; Female; Humans; Hyponatremia; Hypopituitarism; Hypothyroidism; Sodium; Thyroxine; Vasopressins

Twenty-four h urinary vasopressin excretion was measured by bioassay in 15 patients with untreated hypothyroidism and compared with plasma sodium concentration. Four patients had raised excretion of an antidiuretic substance and in 3 of these patients excretion was reduced after thyroid replacement therapy. The criteria applied supported the view that the antidiuretic substance was arginine vasopressin. Plasma sodium concentration was normal in all these 4 patients. A further 4 patients had hyponatraemia without raised arginine vasopressin excretion. The results suggest that: (1) excess arginine vasopressin secretion is not the cause of the hyponatraemia of hypothyroidism and (2) an increased secretion of arginine vasopressin does occur in some cases of normonatraemic hypothyroidism, the cause requiring further elucidation.

Topics: Adult; Aged; Arginine Vasopressin; Female; Humans; Hyponatremia; Hypothyroidism; Male; Middle Aged; Osmolar Concentration; Sodium; Vasopressins

Topics: Carcinoma, Bronchogenic; Deficiency Diseases; Humans; Hyponatremia; Male; Methods; Middle Aged; Syndrome; Vasopressins

Topics: Diseases in Twins; Humans; Hyponatremia; Hypothyroidism; Infant; Kidney; Male; Sodium; Syndrome; Vasopressins; Water-Electrolyte Imbalance

In a study of 23 children admitted to hospital with a febrile convulsion, mild hyponatraemia was found on 8 occasions. In 6 of these cases there was evidence of inappropriate secretion of antidiuretic hormone. The hyponatraemia is unlikely to be the cause of the convulsion, but probably predisposes the child to a subsequent convulsion during the same febrile illness.

Topics: Child, Preschool; Humans; Hyponatremia; Infant; Osmolar Concentration; Prospective Studies; Seizures; Seizures, Febrile; Vasopressins

The syndrome of inappropriate antidiuretic hormone secretion, with marked hyponatremia, was observed in an elderly women who was taking carbamazepine for trigeminal neuralgia. Subsequent studies revealed this effect to be directly related to the administration of the drug. Substantial water retention has not been previously described in patients taking normal volumes of fluid and taking standard doses of carbamazepine. Additionally, it was determined that the antidiuretic effect of carbamazepine could be blocked by phenytoin. The actions of both drugs on renal water excretion, and the interactions of the drugs were observed to be dose-related.

Topics: Aged; Carbamazepine; Diuresis; Dose-Response Relationship, Drug; Drug Therapy, Combination; Female; Humans; Hyponatremia; Phenytoin; Syndrome; Trigeminal Neuralgia; Vasopressins

Topics: Adolescent; Asphyxia Neonatorum; Brain; Brain Edema; Female; Humans; Hyponatremia; Hypoxia, Brain; Infant, Newborn; Ischemia; Male; Vasopressins

Topics: Aged; Depression; Drinking; Humans; Hyponatremia; Male; Tranylcypromine; Vasopressins; Water

Topics: Cyclophosphamide; Humans; Hyponatremia; Leukemia; Sodium Chloride; Vasopressins; Vincristine

Topics: Adult; Bronchial Neoplasms; Carcinoma; Guanidines; Humans; Hyponatremia; Male; Muscular Diseases; Osmolar Concentration; Syndrome; Vasopressins

Topics: Adult; Humans; Hyponatremia; Male; Pituitary Diseases; Pituitary Gland, Posterior; Vasopressins

The authors report the case of a patient who presented, during two exacerbations of intermittent acute porphyria, a grave psychiatric syndrome secondary to severe hyponatraemia. The later was due to inappropriate secretion of anti-diuretic hormone confirmed by laboratory tests and the stimation of anti-diuretic activity in the urine. The course was favourable under the effects of symptomatic treatment including sodium supplements and fluid restriction. The anti-diuretic syndrome disappeared on each occasion without sequelae at the time of regression of the exacerbation of porphyria.

Topics: Acute Disease; Hyponatremia; Porphyrias; Recurrence; Vasopressins

Plasma and urinary arginine vasopressin (AVP) in normal subjects and in patients with various water metabolism disorders was measured using a sensitive, specific radioimmunoassay. The AVP plasma levels in normal subjects were 3.1 +/- 1.2 pg/ml. The parallel changes in plasma osmolality, plasma AVP concentration, and urinary osmolality were observed after water load. In patients with various kinds of hyponatremia and impaired water excretion, plasma AVP concentrations were within or over normal levels, suggesting that persistent secretion of AVP may play an important role in the pathogenesis of hyponatremia. Variable levels of plasma AVP were observed in patients with essential hypernatremia, which in turn suggested that osmoreceptors may be selectively damaged in some patients, and that ADH-secreting neurons are also involved in others. Our radioimmunoassay facility made it possible for us to measure plasma and urinary DDAVP in the treatment of diabetes insipidus.

Topics: Adrenal Insufficiency; Adult; Animals; Arginine Vasopressin; Ascites; Diabetes Insipidus; Dogs; Edema; Humans; Hypernatremia; Hyponatremia; Hypotension, Orthostatic; Infant; Neoplasms; Osmolar Concentration; Radioimmunoassay; Vasopressins; Water

Topics: Aged; Cavernous Sinus; Humans; Hyponatremia; Male; Phenytoin; Pituitary Diseases; Secretory Rate; Syndrome; Thrombosis; Vasopressins

Topics: Adult; Aged; Female; Humans; Hyponatremia; Hypothyroidism; Male; Middle Aged; Vasopressins

Topics: Acute Disease; Arginine Vasopressin; Humans; Hyponatremia; Kidney Concentrating Ability; Vasopressins

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is described in a 67-year-old man with cerebellar and cerebral atrophy. This is the first reported case of this association.

Topics: Aged; Brain Diseases; Cerebellar Diseases; Electroencephalography; Humans; Hyponatremia; Male; Vasopressins

Topics: Child; Craniopharyngioma; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Male; Pituitary Neoplasms; Postoperative Care; Postoperative Complications; Sodium; Time Factors; Vasopressins; Water-Electrolyte Imbalance

A case report is presented in which myxedema coma and inappropriate antidiuretic hormone secretion developed as a result of radiation therapy and surgery to the neck area in a patient with recurrent metastatic squamous cell carcinoma of the floor of the mouth. Laboratory findings of low thyroxine level and the findings of persistent hyponatremia and hypoosmolality of serum in spite of persistent sodium loss in the urine were helpful in diagnosing the problem. Treatment included thyroid hormone replacement and fluid restriction resulting in complete reversal of her condition. We believe that patients with head and neck cancer who have undergone a course of radiation to the neck, and particularly when thyroid function might have been altered by previous subtotal thyroidectomy as part of a curative resection, should be carefully followed with periodic thyroid function assays and serum electrolytes with particular attention to serum sodium values.

Topics: Carcinoma, Squamous Cell; Coma; Female; Head and Neck Neoplasms; Humans; Hyponatremia; Hypothyroidism; Middle Aged; Myxedema; Neoplasm Metastasis; Radiation Injuries; Vasopressins

The syndrome of inappropriate secretion of antidiuretic hormone has been associated with many pulmonary diseases, including tuberculosis and bacterial and viral pneumonia: however, it has not been reported with anaerobic infections or empyema in the absence of pneumonia. We report a patient with empyema due to Bacteroides melaninogenicus, Bacteroides oralis, and Peptostreptococcus who developed the syndrome. Eight hours before the start of therapy, his serum sodium concentration was 127 mEq per liter; serum osmolality, 255 mOsm per kg; urine osmolality, 522 mOsm per kg; urinary sodium concentration, 39 mEq per liter. The creatinine clearance and the adrenocorticotropic hormone stimulation test were normal, and there was no evidence of dehydration. No other causes of the syndrome of inappropriate secretion of antidiuretic hormone were apparent. With drainage and antimicrobial drug therapy, the empyema cleared, and the syndrome resolved in 8 days. The patient has been well, without evidence of inappropriate secretion of antidiuretic hormone, for 9 months. Anaerobic infections and/or empyema without pneumonia can be associated with the syndrome of inappropriate secretion of antidiuretic hormone.

Topics: Adult; Anaerobiosis; Bacterial Infections; Bacteroides Infections; Empyema; Humans; Hyponatremia; Male; Osmolar Concentration; Peptostreptococcus; Prevotella melaninogenica; Syndrome; Vasopressins

Topics: Adult; Deamino Arginine Vasopressin; Hemophilia A; Hemostasis, Surgical; Humans; Hyponatremia; Male; Tooth Extraction; Vasopressins; Water Intoxication

The efficacy of demeclocycline hydrochloride in suppressing the tubular action of tumoral antidiuretic products was tested in seven patients with the syndrome of inappropriate antidiuretic hormone secretion. In all patients, demeclocycline hydrochloride (1,200 mg/day) induced production of hypotonic urine and corrected hyponatremia despite large fluid intakes. Comparison of the response to a standard water load before and during treatment showed a notable improvement in the response to water ingestion. Even though demeclocycline moderately impairs renal function, it appears to be the treatment of choice in the chronic form of the syndrome.

Topics: Administration, Oral; Aged; Carcinoma, Small Cell; Chronic Disease; Demeclocycline; Depression, Chemical; Dose-Response Relationship, Drug; Humans; Hyponatremia; Kidney Concentrating Ability; Lung Neoplasms; Male; Middle Aged; Syndrome; Vasopressins

Topics: Adrenal Gland Diseases; Adrenal Glands; Age Factors; Aged; Brain Edema; Female; Humans; Hyponatremia; Iatrogenic Disease; Kidney; Liver Cirrhosis; Male; Sodium; Vasopressins; Water-Electrolyte Imbalance

The authors report a case of coma due to peripheral myxoedema with severe hyponatremia (111 mq) and low urinary sodium. The clinical and metabolic disorders regressed within ten days under treatment with thyroid. The frequency of hyponatremia during myxoedema coma is recalled and the pathogenic mechanism discussed. Although the adrenal origin seems excluded, there is possibly some hypervasopresinism, but it seems finally that the thyroxin-dependent hyponatremia is of renal origin.

Topics: Coma; Female; Humans; Hydrocortisone; Hyponatremia; Hypothyroidism; Kidney; Male; Mineralocorticoids; Myxedema; Vasopressins

Four children aged between 7 and 19 months with severe bronchopneumonia due to adenovirus type 7, proved by virology and/or serology developed severe hyponatraemia. One of them is reported in detail: it was possible to estimate plasma ADH levels and thereby prove the existence of reversible hypersecretion of the hormone. Whilst the syndrome of hyponatraemia with inappropriate secretion of ADH has not yet been reported in association with severe pneumonia in the child, it is known in adults. The limits of the syndrome and its physiopathology are discussed. It may be due either to vagal stimulation as a result of a fall in left aressure, or to central involvement. Therapeutic implications of the problem are emphasized.

Topics: Adenoviridae Infections; Adenovirus Infections, Human; Diuresis; Hormones, Ectopic; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Infant; Lung; Male; Pituitary Gland, Posterior; Vagus Nerve; Vasopressins

Topics: Carcinoma, Small Cell; Demeclocycline; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Paraneoplastic Endocrine Syndromes; Phosphorus; Uric Acid; Vasopressins

Topics: Demeclocycline; Humans; Hyponatremia; Male; Middle Aged; Osmolar Concentration; Syndrome; Vasopressins

Autopsy in a patient with severe hyponatremia showed central pontine myelinolysis. Review of our patients with central pontine myelinolysis and those described in the English literature to data disclosed that 61 percent had documented hyponatremia. While the exact mechanism involving hyponatremia and central pontine myelinolysis cannot be defined, a circumstantial relationship is apparent. The purpose of this paper is to emphasize this relationship and to suggest that the possibility of central pontine myelinolysis be considered in any patient with hyponatremia and neurologic dysfunction.

Topics: Alcoholism; Demyelinating Diseases; Diuretics; Fatty Liver; Female; Humans; Hypertension; Hyponatremia; Liver Function Tests; Middle Aged; Pons; Sodium; Vasopressins

Topics: Blood; Diagnosis, Differential; Extracellular Space; Humans; Hyponatremia; Osmolar Concentration; Syndrome; Urine; Vasopressins

Topics: Humans; Hyponatremia; Syndrome; Vasopressins

The syndrome of inappropriate secretion of antidiuretic hormone was observed in two patients with cystic fibrosis during acute exacerbation of chronic pulmonary disease. It was diagnosed by the accepted clinical and laboratory criteria and confirmed in one case by values for immunoreactive vasopressin that were inappropriately high for plasma osmolality. The severe hyponatremia was corrected by fluid restriction, alone or combined with intravenous treatment with diuretic and hypertonic saline solution. In addition, there was simultaneous therapy of the pulmonary disease. SIADH thus must be added to salt loss as a cause of hyponatremia in CF, and may be more common than realized in patients with CF and severe pulmonary disease.

Topics: Adult; Cystic Fibrosis; Female; Humans; Hyponatremia; Male; Vasopressins

A 51-year-old man with serologically confirmed Rocky Mountain spotted fever was believed to have inappropriate antidiuretic hormone (ADH) secretion. He was observed for four days in the hospital until the correct diagnosis was made. During this period, he progressively became more hyponatremic, despite a low BUN level and the administration of large amounts of sodium and water. At the time, his serum sodium concentration was 117 mEq/liter, and his urine was hypertonic to that of serum. Thereafter, his serum sodium level rose with fluid restriction. Rickettsia-induced CNS damage may have lead to the inappropriate ADH release that was observed in this patient.

Topics: Humans; Hyponatremia; Male; Middle Aged; Rocky Mountain Spotted Fever; Sodium; Vasopressins

The syndrome of inappropriate ADH secretion ("SIADH") was first recognized 1935 by Roth et al. and described in detail 1957 by Schwartz et al. The clinical symptoms (hyponatremia, hypertonicity of urine and inability to excrete a water load) are caused by inadequately elevated ADH secretion under a variety of situations and diseases. Some recent work was focused on the pathogenesis of this syndrome and new clinical findings (low plasma levels of uric acid and potassium) as well as special forms ("SIADH" without elevated vasopressin levels in plasma) are thought to be of relevance. New therapeutical recommendations will be discussed.

Topics: Diuresis; Hormones; Hormones, Ectopic; Humans; Hyponatremia; Osmolar Concentration; Potassium; Syndrome; Uric Acid; Vasopressins

The authors have developed a radioimmunoassay for human plasma vasopressin (AVP) which permits the estimation of antidiuretic hormon (ADH) levels as low as 0,8 pg/ml. The average plasma level of AVP after overnight water restriction was found to be 14,3 pg/ml (sd = 4,4 pg/ml) in normal subjects. They provoked a hypersecretion of ADH by the intravenous injection of 1-2 mg of nicotine. In 11 volunteer normal subjects this stimulation by nicotine provoked ADH hypersecretion which reached a maximum between 2nd and 15th minutes after injection. In 3 cases of diabetes insipidus, nicotine injection did not induce ADH hypersecretion; in 1 case of potomania this response was weak; in 2 cases of syndrome of inappropriate ADH secretion, AVP plasma levels were elevated and the response after nicotine stimulation was exaggerated.

Topics: Arginine Vasopressin; Blood; Diabetes Insipidus; Hormones, Ectopic; Humans; Hyponatremia; Nicotine; Osmolar Concentration; Psychoses, Alcoholic; Radioimmunoassay; Vasopressins

The concentration of serum sodium is determined by the external balance of water. Hyponatremia occurs when total body water is in excess of sodium, and hypernatremia develops when body water is relatively decreased in relation to sodium. Both disorders may be present in patients with various disease states in which total body sodium is either decreased, normal or increased. The symptomatology in both disorders is related to the disturbance in central nervous system due to brain edema in patients with hyponatremia and brain dehydration, and cerebrovascular hemorrhages in patients with hypernatremia. The treatment of hypo and hypernatremia is achieved by correcting the abnormalities in body water content.

Topics: Adult; Blood Volume; Edema; Endocrine System Diseases; Humans; Hypernatremia; Hyponatremia; Infant; Kidney Concentrating Ability; Kidney Diseases; Syndrome; Thirst; Vasopressins; Water; Water Loss, Insensible

A case of carcinoma of the bladder complicated by the syndrome of inappropriate anti-diuretic hormone secretion is reported. Management of the syndrome is discussed.

Topics: Aged; Carcinoma, Squamous Cell; Female; Fludrocortisone; Hormones, Ectopic; Humans; Hyponatremia; Urinary Bladder Neoplasms; Vasopressins

Topics: Humans; Hyponatremia; Vasopressins

Topics: Blood Volume; Body Weight; Cystic Fibrosis; Humans; Hyponatremia; Vasopressins

The syndrome of inappropriate secretion of antidiuretic hormone is characterized by production of less than maximally dilute urine in the presence of hypotonic plasma. It may be secondary to malignant disease, central nervous system disorders, or pulmonary disease, among other conditions, or it may be idiopathic. Manifestations are those of water intoxication, eg, confusion, fatigue, nausea, headache, and neurologic signs. The pathogenesis is not completely understood. Restriction of fluid intake to obtain a negative water balance is effective treatment.

Topics: Drug-Related Side Effects and Adverse Reactions; Humans; Hyponatremia; Sodium; Syndrome; Urine; Vasopressins

Topics: Acid-Base Imbalance; Adult; Alcoholism; Beer; Heart Diseases; Humans; Hyponatremia; Liver Diseases; Male; Nutrition Disorders; Vasopressins

Topics: Dehydration; Diagnosis, Differential; Humans; Hyponatremia; Infant, Newborn; Infant, Premature, Diseases; Syndrome; Vasopressins

Lithium carbonate, useful in the treatment of manic-depressive disorders, can produce nephrogenic diabetes insipidus. The drug, therefore, has been used to facilitate renal waster excretion when severe hyponatremia occurs in the syndrome of inappropriate antidiuretic hormone secretion. Symptomatic dilutional hyponatremia developed in a patient with pulmonary carcinoma whom we treated. Lithium carbonate was administered and renal sodium wasting, hypovolemia, and hypotension occurred. Hyperkalemia was also observed, and since adrenal steroid levels were not decreased, impairment of distal tubular function was suggested. Lithium carbonate blocks antidiuretic hormone effect by decreasing collecting duct cyclic adenosine monophosphate generation. These observations suggest that more generalized inhibitory effects on renal tubular function may also result from its use. An alternative drug, demeclocycline, may be preferable.

Topics: Carcinoma, Squamous Cell; Humans; Hyponatremia; Lithium; Lung Neoplasms; Male; Middle Aged; Neoplasm Metastasis; Potassium; Sodium; Vasopressins

Topics: Anemia, Sickle Cell; Chronic Disease; Diabetes Insipidus; Diet; Humans; Hydrogen-Ion Concentration; Hypernatremia; Hyponatremia; Kidney; Kidney Concentrating Ability; Kidney Diseases; Osmolar Concentration; Vasopressins; Water-Electrolyte Imbalance

Topics: Demeclocycline; Hormones, Ectopic; Humans; Hyponatremia; Male; Middle Aged; Paraneoplastic Endocrine Syndromes; Tracheal Neoplasms; Vasopressins

Four cases of cerebral edema associated with therapy for diabetic ketoacidosis are reported. One patient had an inappropriate ADH-like syndrome at the time of onset of clinical symptoms of cerebral edema; he survived. The remaining patients had hyponatremia at or near the time of onset of clinical symptoms of cerebral edema, and they subsequently died. The literature is reviewed and some aspects of therapy, which might be casually related to cerebral edema observed in association with therapy of diabetic ketoacidosis, are discussed.

Topics: Blood; Brain Edema; Child; Child, Preschool; Diabetic Ketoacidosis; Female; Hormones, Ectopic; Humans; Hyponatremia; Infusions, Parenteral; Insulin; Male; Osmolar Concentration; Vasopressins; Water-Electrolyte Imbalance

A 6-week-old infant born prematurely had severe hyponatremia and other features of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). This disturbance was believed to be secondary to extensive bilateral pneumonia with collapse of the right upper lobe. Although this association has been recognized in adults, this is the first report of its occurrence in an infant. SIADH must be considered in the differential diagnosis of hyponatremia in association with pneumonia in an infant.

Topics: Humans; Hyponatremia; Infant; Infant, Newborn; Infant, Premature, Diseases; Male; Pneumonia, Viral; Radiography; Secretory Rate; Vasopressins

Topics: Animals; Blood Pressure; Body Fluids; Cardiovascular Physiological Phenomena; Dogs; Heart; Heart Diseases; Humans; Hyponatremia; Immersion; Plasma Volume; Pressoreceptors; Reflex; Sodium; Thirst; Vasopressins; Water-Electrolyte Balance

Clinical aspects with disturbances in fluid and electrolytes metabolism in brain diseases were discussed reviewing 41 cases experienced in our department. These 41 cases were found in 377 patients with diseases of the central nervous system in our hospital during recent 14 months. Hyponatremia was found in 19 cases and aneurysms of A-C, A1 and A2 had the majority of the cases. The cerebral angiography suggested an unstable blood supply to the anterior portion of the hypothalamus, for instance, showing remarkable shift, spasm or obstruction A-C, A1 or A2. The duration of hyponatremia was transient and mostly less than 2 weeks after the last attack of subarachnoid hemorrhage. On the contrary, hypernatremia was seen in 9 cases and 6 of them were found in cases of tumors in the pineal region and A-C, A1 and A2 were intact angiographically. The hypernatremia was continuous and did not response to V-P shunt or any kinds of infusion therapy. The hypernatremia due to cerebral disease is thought to be a result of destruction of the supraoptic and paraventricular nuclei or adjacent area in the anterior potion of the hypothalamus in most of presumed these cases. It might be that the decreased blood supply to the anterior position of the hypothalamus offers an information not of hypoosmolarity but of hypovolemic state, and this information increases the secretion of ADH. This mechanism of hyponatremia could play an important role in S.I.A.D.H.

Topics: Adolescent; Adult; Aged; Brain Diseases; Brain Neoplasms; Child; Female; Humans; Hypernatremia; Hyponatremia; Infant; Intracranial Aneurysm; Male; Middle Aged; Pinealoma; Postoperative Complications; Vasopressins

A 29-year-old woman with severe idiopathic diabetes insipidus, while being treated by a combination of chlorpropamide and chlorothiazide, developed the syndrome of inappropriate secretion of ADH (SIADH) following an overdose of chlorpropamide. The syndrome resolved as the serum chlorpropamide level fell. This report demonstrates that a chlorpropamide-induced SIADH can occur in a patient with idiopathic diabetes insipidus, and it appears that the antidiuretic effect of the drug is dose-related.

Topics: Adult; Chlorpropamide; Diabetes Insipidus; Female; Humans; Hyponatremia; Vasopressins

Recent studies have shown that chronic hypotonic volume expansion (HVE) induced by administration of vasopressin and water stimulates distal hydrogen ion secretion and thereby (a) permits dogs with HCl-acidosis to restore acid-base equilibrium to normal despite continued acid feeding and (b) permits normal dogs to conserve filtered bicarbonate quantitatively despite the natriuresis induced by water retention. To examine whether these effects of chronic HVE are mediated by augmented mineralocorticoid secretion, urinary and plasma aldosterone levels were monitored during prolonged administration of vasopressin. In HCl-fed animals, the HVE-induced rise in plasma [HCO3] (from 13.8 to 21.3 meq/liter) was associated with a rise in aldosterone excretion from 0.45 to 0.88 mug/day (P less than 0.02). In normal animals, in which plasma [HCO3] remained stable during HVE (21.9 vs. 20.0 meq/liter), aldosterone excretion rose from 0.51 to 2.28 mug/day (P less than 0.02) and plasma aldosterone concentration rose from 8.1 to 39.8 ng/100 ml (P less than 0.01). Vasopressin and water were also administered to adrenalectomized animals maintained on glucocorticoids and a slightly subphysiologic replacement schedule of mineralocorticoids. In the HCl-fed adrenalectomized group, plasma [HCO3], instead of rising to normal, showed no significant change (16.9 vs. 15.0 meq/liter). In the non-HCl-fed adrenalectomized group, plasma [HCO3], rather than remaining stable, fell significantly (20.3 vs 16.5 meq/liter, P less than 0.1). Two conclusions can be drawn from this study: (a) the well-known inhibitory effect of volume expansion on aldosterone secretion can be overridden by a potent stimulatory effect on the adrenal produced by severe chronic hypotonicity, and (b) the response of plasma [HCO3] observed during severe chronic HVE is mediated by augmented mineralocorticoid secretion. These findings, furthermore, offer a possible explanation for the puzzling observation that plasma [HCO3] in patients with the syndrome of inappropriate antidiuretic hormone secretion is maintained at normal levels even in the face of severe hyponatremia.

Topics: Acid-Base Equilibrium; Acidosis; Adrenal Glands; Adrenalectomy; Aldosterone; Animals; Bicarbonates; Blood Volume; Dogs; Extracellular Space; Female; Hyponatremia; Kidney; Vasopressins; Water

Topics: Anemia, Sickle Cell; Child; Female; Humans; Hyponatremia; Syndrome; Vasopressins; Water-Electrolyte Imbalance

Twenty-six patients with the syndrome of inappropriate secretion of antidiuretic hormone were reviewed. The underlying diseases were bronchogenic carcinoma (12 cases); myxoedema (five cases); diseases of the nervous system (five cases); bronchopneumonia, carcinoma of the oesophagus, acute intermittent porphria and chlorpropamide therapy (each one case). Serum sodium levels ranged between 104 and 125 mEq per litre. Eighteen patients presented neurological manifestations, which in 14 were considered to be due to hyponatraemia. Neurological signs included disorders of consciousness (stage I and II coma), extrapyramidal signs, asterixis and epileptic seizures. An hyponatraemic coma was the first manifestation of the syndrome in five cases. In all cases where the EEG was recorded it showed non-specific signs of metabolic coma. The fundi never showed signs of intracranial hypertension. Blood urea and creatinine levels were invariably low in the euthyroid patients; these values were normal or elevated in patients with myxoedema and hyponatraemia. Hypokalaemia was frequent, and hypocalcaemia constant. In eleven cases an excess of water intake revealed the clinical syndrome: six patients were excessive beer drinkers and five had received extensive intravenous infusions. In one case the deleterious effect of diuretics was evident, and in another, the syndrome became evident during radiotherapy of an oesophageal tumour. Treatment of the syndrome was successful in all cases. A review of the literature concerning the various pathogenic mechanisms corresponding to the different underlying diseases is presented. The concept of aberrant hormonal production by a tumour is illustrated by an electron microscopic study.

Topics: Adult; Aged; Carcinoma, Bronchogenic; Cerebrovascular Disorders; Esophageal Neoplasms; Female; Hormones, Ectopic; Humans; Hyponatremia; Hypothyroidism; Lung Neoplasms; Male; Middle Aged; Myxedema; Neurologic Manifestations; Vasopressins; Water Intoxication

A study of plasma arginine vasopressin in 17 patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) associated with bronchogenic carcinoma, revealed that the arginine vasopressin levels were distinctly elevated in most. In 14 patients with bronchogenic carcinoma, but without overt SIADH, plasma levels of arginine vasopressin were significantly higher than in normal subjects (p less than 0.001). This, together with the finding of a lower than normal plasma osmolality in this group, suggests that inappropriate ADH excess might be much more common in patients with bronchogenic carcinoma than previously thought. The normal positive correlation between plasma osmolality and plasma arginine vasopressin was found to be reversed in SIADH. Seven of nine patients with overt SIADH, studied after fluid deprivation, showed an increase in plasma arginine vasopressin coincident with an increase in plasma osmolality (r = +0.8, p less than 0.01); in one patient, plasma arginine vasopressin returned to the original level following rehydration. The possibility that this might imply a degree of physiologic control to what is generally considered an autonomous secretion is discussed. It is, however, considered more likely that other factors, including changes in plasma volume and glomerular filtration, might explain the increase in plasma levels of arginine vasopressin.

Topics: Adult; Aged; Arginine Vasopressin; Carcinoma, Bronchogenic; Female; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Osmolar Concentration; Syndrome; Vasopressins; Water Deprivation

Topics: Aged; Bronchopneumonia; Female; Humans; Hyponatremia; Hypothyroidism; Secretory Rate; Vasopressins

Topics: Female; Humans; Hyponatremia; Middle Aged; Osmolar Concentration; Sodium; Vasopressins; Water-Electrolyte Imbalance

A case has been presented in which a patient sustained a closed head injury with concomitant maxillofacial injuries; early signs of water intoxication and ISADH developed six days after injury. This disorder was corrected by restricting free water intake for six days until equilibration occurred. Successful reduction of the facial fractures was accomplished after stabilization of the patient's neurological condition and correction of her metabolic disorder. The ISADH and resulting hyponatremia have been documented in a variety of disease states including trauma to the central nervous system. Disruption or irritation to the hypothalamic-neurohypophyseal system has been proposed as the mechanism of dysfunction after cerebral injury. The results of the secretion of inappropriate amounts of ADH relative to renal function and homeostatis have been discussed. Clinical and laboratory diagnosis as well as the elective and emergency management of ISADH have been reviewed. The fact that the sequelae of this abnormal metabolic state may mimic or mask the neurological deterioration which may follow cerebral injury is significant. This may contribute to the difficulty in making a correct diagnosis and designing proper therapy. The problem is basically one of differentiating a correctable metabolic disorder from a lesion that can be fatal unless surgically removed.

Topics: Adult; Blood; Blood Volume; Brain Injuries; Extracellular Space; Female; Humans; Hyponatremia; Hypothalamus; Kidney; Osmolar Concentration; Sodium; Vasopressins; Water-Electrolyte Balance

Schwartz-Bartter-syndrome as a consequence of severe cerebral alterations like bacterial and tuberculous meningitis, encephalitis, hydrocephalus and brain haemorrhage has been observed in 7 cases. Massive natriuresis is followed by marked hyponatremia and hypochloremia which may lead to an intracellular brain edema. Sodium administered even in high dosage is lost rapidly through the kidney, and does not normalize the serum level of sodium. The Schwartz-Bartter-syndrome is caused by inadequatly elevated ADH-secretion with consecutive water retention and an increase in plasma volume. Consecutively an increased excretion of sodium takes place causing a substantial loss of bound water. An analogous situation was seen in a child with neurohormonal diabetes insipidus after an overdosage of ADH, which resulted in a hypervolemia, marked hyponatremia and massive natriuresis. The increased excretion of sodium may be the result of reduced reabsorption of sodium in the proximal tubuli of the kidney, caused by a humeral natriuretic factor (the socalled "third factor"). In the serum of one of our patients an increased natriuretic activity could be shown; this is the first time in a child with Schwartz-Bartter-syndrome.

Topics: Blood Volume; Brain Diseases; Brain Edema; Cerebral Hemorrhage; Child; Chlorides; Encephalitis; Female; Humans; Hydrocephalus; Hyponatremia; Infant; Infant, Newborn; Male; Meningitis; Natriuresis; Osmolar Concentration; Syndrome; Tuberculosis, Meningeal; Vasopressins

Four patients with chronic illnesses and stable hyponatremia and plasma hypotonicity had normal urinary diluting capacity, with excretion of greater than 80% of a standard water load (20 ml/kg) within 4 hours and maintenance of a urine osmolality less than 100 mosmol/kg, during sustained water diuresis. Administration of a chronic salt load did not correct the hyponatremia. However, it was stabilized after treatment of the underlying medical condition. These subjects may represent a true resetting of the osmostat or a variant of the syndrome of inappropriate antidiuretic hormone secretion.

Topics: Aged; Alcoholism; Diagnosis, Differential; Female; Humans; Hyponatremia; Kidney; Kidney Concentrating Ability; Male; Middle Aged; Osmolar Concentration; Tuberculosis, Pulmonary; Vasopressins; Water-Electrolyte Balance

Topics: Aged; Body Weight; Diuretics; Humans; Hypertension; Hyponatremia; Polythiazide; Potassium; Potassium Chloride; Potassium Deficiency; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adenylyl Cyclases; Animals; Carbonates; Cyclic AMP; Diabetes Insipidus; Humans; Hyperthyroidism; Hyponatremia; Lithium; Osmolar Concentration; Rats; Sodium; Syndrome; Thyrotropin; Vasopressins

Among the malignant tumors of nonendocrine origin that are capable of producing polypeptide hormones and of manifesting as different endocrine syndromes discussed here are ectopic ACTH syndrome, SIADH, and ectopic gonadotropin-producing tumors.

Topics: Adrenocorticotropic Hormone; Carcinoma, Hepatocellular; Carcinoma, Small Cell; Chorionic Gonadotropin; Cushing Syndrome; Diagnosis, Differential; Erythropoietin; Follicle Stimulating Hormone; Gynecomastia; Hormones, Ectopic; Humans; Hyperthyroidism; Hypoglycemia; Hyponatremia; Liver Neoplasms; Lung Neoplasms; Luteinizing Hormone; Male; Paraneoplastic Endocrine Syndromes; Polycythemia; Puberty, Precocious; Thyrotropin; Vasopressins; Water Intoxication

A patient with acute lymphocytic leukemia is described who developed meningeal leukemia 14 months after the initial diagnosis was made. As part of his antileukemic therapy, at that time, he received prednisone and vincristine, given prophylactically to maintain a bone marrow remission. He inadvertently received 15 mg of vincristine instead of 1.5 mg. Following this overdosage he developed pancytopaenia, mild neurotoxicity and subsequently a grand mal seizure associated with the delayed onset of hyponatremia. This was presumed to be due to the inappropriate secretion of antidiuretic hormone (ADH) secondary to vincristine toxicity. This responded to fluid restriction and anti-epileptiform therapy.

Topics: Adolescent; Anemia, Aplastic; Epilepsy, Tonic-Clonic; Humans; Hyponatremia; Male; Medication Errors; Peripheral Nervous System Diseases; Vasopressins; Vincristine

Metabolic abnormalities compatible with inappropriate secretion of ADH developed during the course of severe viral pneumonia in a 17-year-old Navy recruit. With a regimen of strict fluid restriction, normalization of these abnormalities occurred. Marked leukopenia and hypoxia were also present, but gradually improved with resolution of the pneumonia. Inappropriate ADH secretion has been associated most often with bacterial pneumonia and this patient represents one of the few with viral pneumonia complicated by this syndrome. While the previous cases were assoicated with influenza virus, this patient was infected with adenovirus-7 which is endemic in the military recruit population.

Topics: Adenoviridae; Adenoviridae Infections; Adolescent; Hormones, Ectopic; Humans; Hyponatremia; Male; Pneumonia, Viral; Vasopressins; Water-Electrolyte Imbalance

Topics: Carcinoma, Small Cell; Demeclocycline; Diuresis; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Syndrome; Vasopressins

We have studied the effects of demeclocycline on the water metabolism of a patient with the syndrome of inappropriate antidiuretic hormone (ADH) secretion who presented with a serum sodium concentration of 110 meq/litre. Free water clearance was studied before, during, and after treatment with demeclocycline. This study shows that demeclocycline (900 mg/day) can at least partially inhibit the action of ADH in the setting of tumor-induced ADH secretion, with the production of a reversible, partial nephrogenic diabetes insipidus, and with few or no side effects. Demeclocycline may be useful in the treatment of chronic inappropriate ADH secretion.

Topics: Carcinoma, Small Cell; Demeclocycline; Diabetes Insipidus; Humans; Hyponatremia; Kidney Diseases; Lung Neoplasms; Male; Middle Aged; Osmolar Concentration; Syndrome; Urine; Vasopressins

Each of the five true hyponatremias is discussed as a defect in the free water-excreting mechanisms of the body, in order to formulate a rational approach to diagnosis and treatment. One artificial and three real causes of elevations in plasma sodium are also discussed.

Topics: Adult; Extracellular Space; Humans; Hypernatremia; Hyponatremia; Sodium; Vasopressins; Water

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) has been recognized to occur following treatment with vincristine. None of the reports have provided information regarding its potential for recurrence on further challenge with vincristine (VCR), an agent generally required for repeated use in patients with malignancies. Symptomatic hyponatremia and SIADH that occurred 8 days following administration of VCR in a child with acute lymphatic leukemia was documented with specific radioimmunoassay of urinary ADH levels. The further occurrence of recurrent elevations in ADH excretion 8-10 days following repeated treatment with VCR was also observed. However, SIADH was prevented by prophylactic rigorous fluid restriction. The occurrence of SIADH following VCR therefore does not preclude the further safe usage of this drug.

Topics: Child, Preschool; Dexamethasone; Female; Humans; Hyponatremia; Leukemia, Lymphoid; Radiation Effects; Radioimmunoassay; Skull; Vasopressins; Vincristine; Water-Electrolyte Balance

Lithium, an established inhibitor of antidiuretic hormone action, was used (as the carbonate salt) to treat a patient with the syndrome of inappropriate secreation of antidiuretic hormone. The patient was studied by balance technics, and after a stablized hyponatremic state developed, 0.9 g of lithium carbonate was administered daily. A prompt water diuresis ensued, with correctionof hyponatremia in two days. Discontinuation of the drug resulted in a gradual return of the hyponatremic state. No change in urinary cyclic AMP occurred during the period of lithium effect. Lithium carbonate may be an effective treatment for both the acute and the chronic forms of the syndrome.

Topics: Administration, Oral; Blood; Carbonates; Humans; Hyponatremia; Lithium; Male; Middle Aged; Osmolar Concentration; Sodium; Syndrome; Urine; Vasopressins; Water-Electrolyte Balance

A case of excessive water retention after hypophysectomy is recorded. Its probable cause, inappropriate secretion of ADH, is explained and the diagnosis and management discussed. Three other recorded cases occurring after hypophyseal surgery are mentioned. The importance of postoperative electrolyte measurements in early diagnosis and management is emphasized.

Topics: Diuretics; Female; Humans; Hyponatremia; Hypophysectomy; Mannitol; Middle Aged; Vasopressins; Water Intoxication

Topics: Animals; Dogs; Humans; Hyponatremia; Isoproterenol; Osmolar Concentration; Oxytocin; Rats; Syndrome; Vasopressins

Topics: Aged; Amitriptyline; Cognition Disorders; Depression; Female; Humans; Hyponatremia; Syndrome; Vasopressins

Topics: Biopsy; Humans; Hyponatremia; Male; Middle Aged; Osmolar Concentration; Syndrome; Thymoma; Thymus Neoplasms; Vasopressins

A 6-week-old boy with severe pneumonia developed hyponatremia as a result of the syndrome of inapropriate antidiuretic hormone secretion (SIADH). Cerebral edema and seizures occurred after administration of fluids and diuretics. Fluid restriction and resolution of the pneumonia corrected the severe electrolyte imbalance. The possibility of SIADH should be considered in cases of severe and resistant pneumonia in infancy.

Topics: Humans; Hyponatremia; Infant; Male; Pituitary Gland, Posterior; Pneumonia; Vasopressins

Topics: Diagnosis, Differential; Drinking; Humans; Hyponatremia; Vasopressins; Water-Electrolyte Balance

Topics: Blood Volume; Body Water; Cell Membrane Permeability; Humans; Hyponatremia; Kidney Tubules, Proximal; Osmolar Concentration; Pituitary Gland, Posterior; Vasopressins; Water Intoxication; Water-Electrolyte Balance

The effect of different doses of clofibrate and carbamazepine on water metabolism was compared in a patient with psychogenic polydipsia. A definite relationship was found between the doses of both drugs and the antidiuretic effect. Daily 2--4 g clofibrate was ineffective, but 6--8 g induced the syndrome of inappropriate secretion of ADH. 600 mg carbamazepine a day induced a marked antidiuretic response which could be further augmented by administering daily 1200--1800 mg. The discrepancy between the effective "hypolipidemic" and "antidiuretic" dose of clofibrate may perhaps explain the lack of reports on water intoxication induced by this agent, despite of its entensive use in clinical practice.

Topics: Adult; Carbamazepine; Clofibrate; Diuresis; Dose-Response Relationship, Drug; Female; Glomerular Filtration Rate; Humans; Hyponatremia; Osmolar Concentration; Vasopressins; Water Intoxication

Topics: Female; Humans; Hyponatremia; Infant; Male; Pneumonia; Saline Solution, Hypertonic; Seizures; Vasopressins

Topics: Confusion; Humans; Hyponatremia; Male; Middle Aged; Pneumonia, Pneumococcal; Vasopressins

A radioimmunoassay method for the measurement of arginine-vasopressin (AVP) in human plasma has been developed which requires 5 ml of plasma and has a lower limit of detection of 1-8 pg/ml plasma. Arginine-vasopressin was found to be stable in whole blood for up to 1 h at room temperature and for at least 4 h at 4 degrees C, while in plasma stored at -20 degrees C no loss was seen over 10 days. Dehydration and rehydration in normal subjects produced appropriate changes in AVP concentration but there was considerable variability in the levels attained by individual subjects and no obvious correlation with plasma osmolality. No consistent increase in plasma AVP concentration was seen on change of posture from the recumbent to the upright position. Vigorous exercise produced a marked rise in plasma AVP concentrations in most subjects which could not be attributed simply to an increase in plasma osmolality. In fusion studies with Pitressin in normal subjects showed a mean half-life of 6-4 min with an overall plasma clearance rate of 8-5 ml/min/kg body weight and a mean volume of distribution of 5-33 l. In patients with a biochemical picture suggestive of inappropriate antidiuretic hormone secretion, markedly raised plasma AVP concentrations were found only in patients with bronchial carcinoma.

Topics: Arginine Vasopressin; Blood Preservation; Bronchial Neoplasms; Dehydration; Furosemide; Growth Hormone; Humans; Hydrocortisone; Hyponatremia; Leukemia; Osmolar Concentration; Physical Exertion; Posture; Radioimmunoassay; Thyrotropin; Urine; Vasopressins

Topics: Diagnosis, Differential; Humans; Hyponatremia; Kidney Function Tests; Osmolar Concentration; Syndrome; Vasopressins

Topics: Adrenal Insufficiency; Humans; Hyperglycemia; Hyperlipidemias; Hyponatremia; Pituitary Gland, Posterior; Syndrome; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Transient episodes of the syndrome of inappropriate anti-diuresis developped in two severe colchicine poisonings. These are the first cases reported. On patient also developped a reversible periphal neuropathy. The similarity of such accidents with vicristine neuro-toxicity is emphasized.

Topics: Adolescent; Alopecia; Bone Marrow Diseases; Diarrhea; Disseminated Intravascular Coagulation; Female; Humans; Hyponatremia; Psychomotor Disorders; Vasopressins; Water Intoxication; Water-Electrolyte Imbalance

A radioimmunoassay for [8-arginine]-vasopressin (AVP), previously described (Czernichow et al. 1975) has been used for the determination of antidiuretic hormone in a 4 ml urine sample. AVP is extracted from acidified urine with a cation exchanger (Amberlite CG 50) with an overall recovery of 72%. The blank value measured in extracted samples of urine was 0.29 pg/ml +/- 0.21 (SEM) and calculated by extrapolation of the regression line of the recovery experiment was 0.49 pg/ml. The coefficient of variation within-assay was 13% and between-assay 18%. Addition of the amounts of AVP found in each specimen of urine voided gave results nearly identical to those of the amounts found in 24 h pool of urine, indicating that the assay was not affected by changes in concentration of the other urinary components during the day. The daily urinary excretion of AVP measured in 34 subjects was found to be 34 ng in 17 women and 70 ng in 17 men, a significant difference. Urinary concentration and excretion rate of AVP rose during thirst test and during Carter-Robbins test performed in 13 healthy subjects. In the latter test it was observed that the women displayed a strikingly more pronounced AVP elevation after the osmolar stimulus than the men. In both sexes a significant correlation was found between AVP excretion rate and plasma osmolality as well as free water clearance. Three cases of complete or incomplete diabetes insipidus and potomania could be clearly differentiated according to the total output of AVP during the thirst test. Extremely high values of AVP were found in the urine of 5 subjects with Schwartz-Bartter syndrome associated with bronchogenic tumours.

Topics: Arginine Vasopressin; Diabetes Insipidus; Female; Humans; Hyponatremia; Lung Neoplasms; Male; Osmolar Concentration; Radioimmunoassay; Sex Factors; Syndrome; Thirst; Vasopressins

Topics: Biological Transport, Active; Cell Membrane Permeability; Cells; Diffusion; Extracellular Space; Humans; Hyponatremia; Ion Exchange; Osmolar Concentration; Sodium; Syndrome; Vasopressins; Water-Electrolyte Balance

Topics: Calcitonin; Carcinoma, Small Cell; Hormones, Ectopic; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Osmolar Concentration; Paraneoplastic Endocrine Syndromes; Sodium; Syndrome; Vasopressins

Topics: Blood Glucose; Cell Membrane Permeability; Humans; Hydrogen-Ion Concentration; Hyponatremia; Osmolar Concentration; Potassium; Sodium; Urea; Vasopressins; Water-Electrolyte Balance

Topics: Female; Humans; Hyponatremia; Infant; Tuberculosis, Meningeal; Vasopressins

Topics: Adrenocorticotropic Hormone; Alkalosis; Bicarbonates; Breast Neoplasms; Calcium; Carcinoma, Bronchogenic; Carcinoma, Small Cell; Female; Gentamicins; Hodgkin Disease; Hormones, Ectopic; Humans; Hydrocortisone; Hyponatremia; Hypothalamus; Lung Neoplasms; Paraneoplastic Endocrine Syndromes; Phosphates; Potassium; Vasopressins

Topics: Aged; Alcohol Drinking; Beer; Carcinoma, Small Cell; Coma; Hormones, Ectopic; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Osmolar Concentration; Paraneoplastic Endocrine Syndromes; Sodium; Vasopressins

Topics: Adrenocorticotropic Hormone; Adult; Cushing Syndrome; Diagnosis, Differential; Female; Follicle Stimulating Hormone; Growth Hormone; Hormones, Ectopic; Humans; Hyperthyroidism; Hypocalcemia; Hypoglycemia; Hyponatremia; Insulin; Luteinizing Hormone; Mediastinal Neoplasms; Middle Aged; Osmolar Concentration; Parathyroid Hormone; Pigmentation Disorders; Syndrome; Thymus Neoplasms; Thyrotropin-Releasing Hormone; Vasopressins

Topics: Adrenal Gland Neoplasms; Autopsy; Bone Neoplasms; Bronchial Neoplasms; Calcitonin; Carcinoma; Carcinoma, Small Cell; Humans; Hyponatremia; Liver Neoplasms; Lymphatic Metastasis; Male; Middle Aged; Neoplasm Metastasis; Osmolar Concentration; Paraneoplastic Endocrine Syndromes; Syndrome; Vasopressins

Topics: Benzothiadiazines; Body Water; Carcinoma, Bronchogenic; Chlorpropamide; Dehydration; Diuretics; Edema; Humans; Hyponatremia; Sodium; Sodium Chloride Symporter Inhibitors; Vasopressins; Water Intoxication

Topics: 11-Hydroxycorticosteroids; 17-Hydroxycorticosteroids; 17-Ketosteroids; Adenoma, Chromophobe; Cortisone; Drinking; Ethanol; Growth Hormone; Humans; Hyponatremia; Hypopituitarism; Male; Middle Aged; Osmolar Concentration; Pituitary Neoplasms; Urination; Vasopressins

Topics: Arginine; Diabetes Insipidus; Humans; Hypertension; Hyponatremia; Radioimmunoassay; Vasopressins

Topics: Adult; Hormones, Ectopic; Humans; Hyponatremia; Male; Syndrome; Tuberculosis, Pulmonary; Vasopressins

Topics: Body Weight; Chemical Phenomena; Chemistry; Humans; Hyponatremia; Male; Middle Aged; Natriuresis; Osmolar Concentration; Schizophrenia; Syndrome; Thiothixene; Vasopressins; Water

Topics: Adult; Bronchial Neoplasms; Carcinoma; Diagnosis, Differential; Humans; Hyponatremia; Lung Neoplasms; Male; Muscular Diseases; Muscular Dystrophies; Osmolar Concentration; Syndrome; Vasopressins

Topics: Animals; Body Water; Brain; Erythrocytes; Hyponatremia; Kidney; Liver; Lysine; Magnetic Resonance Spectroscopy; Mathematics; Muscles; Osmolar Concentration; Rats; Sodium; Vasopressins

Topics: Acute Disease; Adult; Ataxia; Barbiturates; Consciousness Disorders; Craniocerebral Trauma; Electroencephalography; Epilepsy; Female; Humans; Hyponatremia; Nystagmus, Pathologic; Porphobilinogen; Porphyrias; Urinary Incontinence; Vasopressins; Water-Electrolyte Balance

Topics: Humans; Hyponatremia; Leukemia, Myeloid; Natriuresis; Vasopressins

Topics: Humans; Hyponatremia; Leukemia, Myeloid, Acute; Sodium; Vasopressins; Water Intoxication

Topics: Child, Preschool; Humans; Hyponatremia; Infant; Leukemia, Myeloid, Acute; Male; Syndrome; Vasopressins; Vincristine

Topics: Adolescent; Adult; Amino Acids; Body Weight; Calcium; Cyclophosphamide; Cystitis; Diuresis; Female; Glomerular Filtration Rate; Humans; Hyponatremia; Kidney; Kidney Concentrating Ability; Male; Middle Aged; Natriuresis; Neoplasms; Osmolar Concentration; Phosphorus; Potassium; Proteinuria; Uric Acid; Vasopressins

Topics: Amitriptyline; Cognition Disorders; Fatigue; Female; Humans; Hyponatremia; Middle Aged; Osmolar Concentration; Sodium; Syndrome; Vasopressins

Topics: Blood; Drinking; Female; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Infusions, Parenteral; Isotonic Solutions; Mineralocorticoids; Osmolar Concentration; Sodium; Sodium Chloride; Urine; Vasopressins; Water; Water-Electrolyte Balance

Topics: Humans; Hyponatremia; Infant, Newborn; Natriuresis; Respiratory Distress Syndrome, Newborn; Vasopressins

Topics: Animals; Dogs; Humans; Hyponatremia; Kidney Tubules, Proximal; Microsurgery; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Body Water; Body Weight; Diuresis; Epilepsy, Tonic-Clonic; Female; Furosemide; Humans; Hypertonic Solutions; Hyponatremia; Injections, Intravenous; Male; Osmolar Concentration; Potassium; Potassium Chloride; Sodium; Sodium Chloride; Syndrome; Urine; Vasopressins

Topics: Adrenocorticotropic Hormone; Aldosterone; Catecholamines; Craniocerebral Trauma; Dehydration; Electrolytes; Glucagon; Glucose; Growth Hormone; Humans; Hydrocortisone; Hypernatremia; Hyponatremia; Metabolic Diseases; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Bronchial Neoplasms; Carcinoma, Small Cell; Diabetes Insipidus; Humans; Hyponatremia; Iodine Isotopes; Radioimmunoassay; Vasopressins; Water; Water Deprivation

Topics: Adrenocorticotropic Hormone; Cell Transformation, Neoplastic; Cushing Syndrome; Humans; Hypercalcemia; Hyponatremia; Neoplasms; Parathyroid Hormone; Precancerous Conditions; Vasopressins

Topics: Adult; Aldosterone; Autopsy; Bronchoscopy; Carcinoma, Bronchogenic; Hormones, Ectopic; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Renin; Vasopressins

Topics: Aldosterone; Catecholamines; Heart Failure; Hemodynamics; Humans; Hyperaldosteronism; Hypokalemia; Hyponatremia; Kidney; Potassium; Renin; Sodium; Vasopressins; Water; Water-Electrolyte Balance

Topics: Adult; Body Water; Brain Injuries; Diabetes Insipidus; Facial Injuries; Female; Fractures, Bone; Humans; Hyponatremia; Hypothalamus; Male; Natriuresis; Osmolar Concentration; Pituitary Gland, Posterior; Prospective Studies; Skull Fractures; Sodium; Vasopressins

Topics: Edema; Furosemide; Hemodynamics; Humans; Hyponatremia; Kidney; Osmolar Concentration; Sodium; Vasopressins; Water

Topics: Heart Failure; Humans; Hyponatremia; Liver Cirrhosis; Myxedema; Pituitary Diseases; Radioimmunoassay; Vasopressins

Topics: Body Fluids; Body Weight; Central Venous Pressure; Extracellular Space; Humans; Hypernatremia; Hyponatremia; Kidney; Osmolar Concentration; Osmotic Pressure; Sodium; Surgical Procedures, Operative; Tongue, Fissured; Vasopressins; Water Deprivation; Water-Electrolyte Balance

Topics: Acid-Base Equilibrium; Acidosis, Respiratory; Chlorides; Diuretics; Electrolytes; Glucose; Humans; Hyperkalemia; Hypokalemia; Hyponatremia; Respiratory Insufficiency; Respiratory Tract Diseases; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Female; Humans; Hyponatremia; Porphyrias; Pregnancy; Pregnancy Complications; Sodium; Syndrome; Vasopressins

Three cases of coma after vincristine therapy are described. One patient had hyponatraemia and other features of inappropriate secretion of antidiuretic hormone. The effects were temporary, and full recovery occurred in all three patients.

Topics: Adolescent; Aged; Coma; Electroencephalography; Female; Hodgkin Disease; Humans; Hyponatremia; Leukemia; Lymphadenitis; Male; Vasopressins; Vincristine

Topics: Adrenal Gland Neoplasms; Carcinoma; Female; Humans; Hyponatremia; Middle Aged; Neoplasm Metastasis; Osmolar Concentration; Sodium; Syndrome; Vasopressins

Topics: Age Factors; Aldosterone; Desoxycorticosterone; Diuresis; Female; Fludrocortisone; Humans; Hyponatremia; Infant; Osmolar Concentration; Pituitary Diseases; Pituitary-Adrenal System; Renin; Seizures; Sodium Chloride; Vasopressins; Water Intoxication

Topics: Adrenocorticotropic Hormone; Animals; Biological Assay; Body Weight; Chromatography, Ion Exchange; Diabetes Insipidus; Drug Contamination; Drug Synergism; Female; Growth Hormone; Humans; Hyponatremia; Middle Aged; Rats; Swine; Vasopressins; Water Intoxication

Topics: Age Factors; Aged; Chlorpropamide; Cyclic AMP; Humans; Hyponatremia; Syndrome; Tolbutamide; Vasopressins

Topics: Biological Assay; Child, Preschool; Extracellular Space; Female; Humans; Hyponatremia; Kidney Neoplasms; Medication Errors; Osmolar Concentration; Sodium Chloride; Specific Gravity; Urine; Vasopressins; Vincristine; Water-Electrolyte Balance; Wilms Tumor

Topics: Carcinoma, Small Cell; Diabetes Insipidus; Hormones, Ectopic; Humans; Hyponatremia; Lung Neoplasms; Osmolar Concentration; Plasma Volume; Polyuria; Radioimmunoassay; Syndrome; Vasopressins

Topics: Adult; Autopsy; Bicarbonates; Bronchial Neoplasms; Carcinoma, Bronchogenic; Carcinoma, Small Cell; Chlorides; Cyclophosphamide; Hormones, Ectopic; Humans; Hyponatremia; Injections, Intravenous; Male; Osmolar Concentration; Sodium; Urea; Vasopressins

Topics: Coma; Diet Therapy; Electroencephalography; Endocrine System Diseases; Female; Humans; Hypokalemia; Hyponatremia; Injections, Intravenous; Kidney Function Tests; Middle Aged; Natriuresis; Potassium; Psychophysiologic Disorders; Sodium; Vasopressins; Water

Topics: Acute Disease; Age Factors; Diuresis; Female; Glomerular Filtration Rate; Humans; Hyponatremia; Middle Aged; Natriuresis; Neurologic Manifestations; Porphyrias; Vasopressins; Water-Electrolyte Balance

Topics: Bronchial Neoplasms; Carcinoma, Bronchogenic; Carcinoma, Squamous Cell; Diet; Hormones, Ectopic; Humans; Hyponatremia; Male; Natriuresis; Paraneoplastic Endocrine Syndromes; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Blood; Child, Preschool; Humans; Hyponatremia; Leukemia, Lymphoid; Male; Osmolar Concentration; Vasopressins; Vincristine; Water Deprivation

Topics: Female; Humans; Hyponatremia; Lymphoma, Large B-Cell, Diffuse; Middle Aged; Tonsillar Neoplasms; Vasopressins; Vincristine

Topics: Blood Vessels; Cell Movement; Coronary Vessels; Diabetes Insipidus; Female; Humans; Hyponatremia; Lactation; Male; Muscle Contraction; Oxytocin; Pituitary Hormones, Posterior; Pregnancy; Spermatozoa; Uterus; Vasopressins; Water-Electrolyte Balance

Tumors from patients with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) have been found to contain large amounts of the antidiuretic hormone vasopressin. A lung tumor from a patient with hyponatremia most likely due to SIADH was removed at surgery and found to contain 23.5 mU vasopressin/g wet weight by radioimmunoassay Slices of this tumor were incubated with phenylalanine-(3)H. Arginine vasopressin-(3)H was purified from the incubate by Sephadex G-25 column chromatography in two different systems, performic acid oxidation, and gradient elution column chromatography with diethylaminoethyl Sephadex. As oxidation of vasopressin results in drastic conformational change with breaking of the ring of the cyclic polypeptide and addition of two cysteic acid residues per molecule, the radioactive material which eluted coincident with vasopressin both before and after this procedure was considered to be arginine vasopressin-(3)H. To our knowledge this is the first demonstration of in vitro biosynthesis of vasopressin by a tumor from a patient with SIADH.Ultrastructurally, the bronchogenic carcinoma was composed of small undifferentiated and granulated cells. The granulated neoplastic cells had well developed organelles (endoplasmic reticulum, free ribosomes) concerned with protein synthesis. Secretion granules present in the tumor cells were small, surrounded by a limiting membrane, and resembled those reported in polypeptide hormone-secreting cells.

Topics: Aged; Carcinoma, Bronchogenic; Chromatography, DEAE-Cellulose; Culture Techniques; Cytoplasmic Granules; Endoplasmic Reticulum; Hormones, Ectopic; Humans; Hyponatremia; Lung; Lung Neoplasms; Male; Microscopy, Electron; Radioimmunoassay; Ribosomes; Vasopressins

Topics: Animals; Brain; Disease Models, Animal; Hyponatremia; Male; Muscles; Organ Size; Osmolar Concentration; Potassium; Rats; Sodium; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Adult; Female; Humans; Hyponatremia; Influenza, Human; Osmolar Concentration; Pituitary Gland, Posterior; Pneumonia; Pneumonia, Staphylococcal; Pregnancy; Pregnancy Complications, Infectious; Vasopressins

Topics: Hormones, Ectopic; Humans; Hyponatremia; Infant, Newborn; Infant, Newborn, Diseases; Male; Meningitis; Natriuresis; Osmolar Concentration; Pituitary Gland, Posterior; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Diabetes Insipidus; Facial Injuries; Female; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Kidney Diseases; Male; Natriuresis; Vasopressins; Water Deprivation; Water-Electrolyte Balance

Topics: Aged; Central Nervous System Diseases; Chlorpropamide; Diabetes Mellitus; Female; Humans; Hyponatremia; Natriuresis; Osmolar Concentration; Syndrome; Time Factors; Urination Disorders; Vasopressins

Topics: Acromegaly; Edema; Endocrine System Diseases; Humans; Hyperaldosteronism; Hyperthyroidism; Hyponatremia; Hypothyroidism; Syndrome; Vasopressins

Topics: Diuretics; Extracellular Space; Humans; Hyperlipidemias; Hypoglycemia; Hyponatremia; Osmolar Concentration; Plasma Volume; Sodium; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Hormones, Ectopic; Humans; Hyponatremia; Liver Cirrhosis; Male; Middle Aged; Tuberculosis, Meningeal; Tuberculosis, Pulmonary; Vasopressins

Topics: Aged; Female; Fludrocortisone; Humans; Hyponatremia; Male; Mannitol; Natriuresis; Urologic Diseases; Vasopressins; Water-Electrolyte Balance

Topics: Carcinoma, Bronchogenic; Craniocerebral Trauma; Diuresis; Drinking; Extracellular Space; Humans; Hypertonic Solutions; Hyponatremia; Lung Neoplasms; Methods; Nicotine; Osmolar Concentration; Pituitary Function Tests; Porphyrias; Sodium Chloride; Vasopressins

Topics: Aged; Aspergillosis; Female; Humans; Hyponatremia; Lung Diseases; Lung Diseases, Fungal; Male; Middle Aged; Tuberculosis, Pulmonary; Vasopressins

Topics: Humans; Hyponatremia; Metabolic Diseases; Osmolar Concentration; Vasopressins; Water; Water-Electrolyte Balance

Topics: Brain Diseases; Carcinoma, Bronchogenic; Humans; Hypernatremia; Hyponatremia; Vasopressins

Topics: Adult; Aged; Autopsy; Beer; Blood Urea Nitrogen; Coma; Diarrhea; Electroencephalography; Feeding and Eating Disorders; Female; Hemiplegia; Humans; Hypokalemia; Hyponatremia; Male; Middle Aged; Nutrition Disorders; Sodium; Tremor; Vasopressins; Vomiting; Water Intoxication

Topics: Adenocarcinoma, Bronchiolo-Alveolar; Adrenocortical Hyperfunction; Bronchial Neoplasms; Carcinoma, Bronchogenic; Female; Hormones, Ectopic; Humans; Hypercalcemia; Hyponatremia; Neoplasm Metastasis; Vasopressins

Topics: Angiotensin II; Animals; Blood Volume; Body Weight; Deficiency Diseases; Dogs; Female; Hematocrit; Hyponatremia; Male; Renin; Sodium Chloride; Vasopressins

Topics: Adult; Aged; Alkalosis; Bendroflumethiazide; Biological Assay; Blood Urea Nitrogen; Bromine; Carbon Dioxide; Chlorides; Chlorpropamide; Chlorthalidone; Creatinine; Diagnosis, Differential; Diuretics; Female; Furosemide; Humans; Hydrochlorothiazide; Hypokalemia; Hyponatremia; Hypopituitarism; Hypothyroidism; Male; Methyclothiazide; Middle Aged; Natriuresis; Osmolar Concentration; Polythiazide; Potassium Isotopes; Radioisotope Dilution Technique; Radioisotopes; Sodium Isotopes; Tritium; Vasopressins; Vomiting; Water-Electrolyte Balance

Topics: Adult; Craniocerebral Trauma; Epilepsy, Tonic-Clonic; Hematoma, Subdural; Humans; Hyponatremia; Male; Middle Aged; Osmolar Concentration; Vasopressins

Topics: Aged; Chlorpropamide; Diabetes Mellitus; Female; Humans; Hyponatremia; Kidney Tubules; Male; Tolazamide; Vasopressins; Water Intoxication

Topics: Humans; Hyponatremia; Leukemia; Male; Middle Aged; Pituitary Gland, Posterior; Vasopressins; Vincristine

Topics: Adrenal Cortex Hormones; Body Weight; Coma; Electrocardiography; Electroencephalography; Female; Humans; Hyponatremia; Hypopituitarism; Middle Aged; Sodium; Vasopressins; Water; Water-Electrolyte Balance

Topics: Bronchial Neoplasms; Carcinoma, Bronchogenic; Female; Hormones, Ectopic; Humans; Hyponatremia; Middle Aged; Vasopressins

Topics: Animals; Dogs; Hyponatremia; Kidney Tubules; Sodium; Vasopressins

Topics: Aged; Carcinoma, Bronchogenic; Hormones, Ectopic; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Pituitary Diseases; Tuberculosis; Vasopressins

Topics: Biopsy; Carcinoma, Bronchogenic; Electromyography; Hormones, Ectopic; Humans; Hyponatremia; Hypoventilation; Lung Neoplasms; Male; Middle Aged; Muscular Diseases; Vasopressins

Topics: Acute Disease; Adult; Amino Acids; Chlorides; Extracellular Space; Female; Humans; Hypokalemia; Hyponatremia; Levulinic Acids; Male; Nitrogen; Porphobilinogen; Porphyrias; Porphyrins; Uremia; Vasopressins; Water-Electrolyte Balance

Topics: Bronchial Neoplasms; Carcinoma; Carcinoma, Bronchogenic; Hormones, Ectopic; Humans; Hyponatremia; Hypoventilation; Lung Neoplasms; Male; Middle Aged; Muscular Diseases; Myositis; Vasopressins

Topics: Adolescent; Adult; Aged; Animals; Carcinoma, Bronchogenic; Central Nervous System Diseases; Child; Diuretics; Dogs; Electroencephalography; Female; Glomerular Filtration Rate; Humans; Hyponatremia; Hypothyroidism; Iatrogenic Disease; Kidney; Kidney Concentrating Ability; Lung Neoplasms; Male; Middle Aged; Neurologic Manifestations; Polyradiculopathy; Rats; Vasopressins

Topics: Edema; Female; Humans; Hyponatremia; Middle Aged; Neurologic Manifestations; Polyradiculopathy; Pulmonary Edema; Vasopressins

Topics: Female; Humans; Hyponatremia; Middle Aged; Subarachnoid Hemorrhage; Vasopressins

Topics: Aged; Blood; Chlorpropamide; Diabetes Mellitus; Diuresis; Female; Humans; Hyponatremia; Kidney Function Tests; Middle Aged; Natriuresis; Osmolar Concentration; Sodium; Vasopressins

Topics: Blood Urea Nitrogen; Blood Volume; Craniocerebral Trauma; Hematocrit; Hodgkin Disease; Humans; Hypernatremia; Hyperpituitarism; Hyponatremia; Hypothyroidism; Male; Middle Aged; Renin; Sodium; Suicide; Vasopressins; Water-Electrolyte Balance

Topics: Blood; Brain Neoplasms; Child; Dehydration; Glioma; Humans; Hyponatremia; Hypothalamus; Osmolar Concentration; Sodium; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Blood; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Natriuresis; Osmolar Concentration; Urine; Vasopressins

Topics: Brain; Brain Edema; Craniocerebral Trauma; Craniotomy; Humans; Hyponatremia; Natriuresis; Nutrition Disorders; Osmolar Concentration; Pituitary Gland; Postoperative Complications; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Carcinoma, Bronchogenic; Humans; Hyponatremia; Lung Neoplasms; Vasopressins

Topics: Aged; Bronchial Neoplasms; Carcinoma, Bronchogenic; Carcinoma, Squamous Cell; Hormones, Ectopic; Humans; Hyponatremia; Male; Mental Disorders; Vasopressins; Water-Electrolyte Balance

Topics: Amino Acid Sequence; Arginine; Carcinoma, Bronchogenic; Chromatography, Gel; Hormones, Ectopic; Humans; Hyponatremia; Iodine Isotopes; Lysine; Methods; Nicotine; Osmolar Concentration; Plasma; Radioimmunoassay; Urine; Vasopressins; Water Deprivation

Topics: Adult; Chlorides; Diagnosis, Differential; Epilepsy; Female; Humans; Hypertension; Hyponatremia; Porphyrias; Porphyrins; Pregnancy; Puerperal Disorders; Vasopressins

Topics: Adult; Aged; Body Weight; Cholesterol; Diuresis; Female; Glomerular Filtration Rate; Humans; Hydrocortisone; Hyponatremia; Kidney; Male; Middle Aged; Myxedema; Osmolar Concentration; Potassium; Sodium; Thyroid Gland; Thyroid Hormones; Thyroxine; Vasopressins; Water-Electrolyte Balance

Topics: Aldosterone; Angiotensin II; Blood Volume; Hormones, Ectopic; Humans; Hyponatremia; Lung Neoplasms; Mental Disorders; Middle Aged; Renin; Vasopressins

Topics: Adrenalectomy; Adrenocorticotropic Hormone; Alkalosis; Autoimmune Diseases; Bone Diseases; Carcinoma, Bronchogenic; Cushing Syndrome; Endocrine System Diseases; Hypercalcemia; Hyperparathyroidism; Hyponatremia; Lung Neoplasms; Metabolic Diseases; Neoplasm Metastasis; Neurologic Manifestations; Neuromuscular Diseases; Skin Diseases; Skin Manifestations; Vascular Diseases; Vasopressins

Topics: Aged; Chlorpropamide; Female; Humans; Hyponatremia; Natriuresis; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Adult; Carotid Arteries; Diagnosis, Differential; Electroencephalography; Hematoma, Subdural; Humans; Hyponatremia; Male; Osmolar Concentration; Radiography; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Aged; Female; Humans; Hyponatremia; Injections, Intravenous; Myxedema; Osmolar Concentration; Thyroid Hormones; Thyroxine; Vasopressins

Topics: Biological Assay; Hormones, Ectopic; Humans; Hyponatremia; Lung; Male; Middle Aged; Pituitary Gland, Posterior; Tuberculosis, Pulmonary; Vasopressins

Topics: Adenine Nucleotides; Aldosterone; Brain Neoplasms; Child; Ethanol; Glioma; Humans; Hypertonic Solutions; Hyponatremia; Hypothalamus; Male; Osmolar Concentration; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Adult; Aged; Aldosterone; Blood Glucose; Fasting; Fever; Glomerular Filtration Rate; Glucose; Humans; Hyponatremia; Insulin; Middle Aged; Natriuresis; Neoplasms; Osmolar Concentration; Sodium; Tuberculosis; Vasopressins

Topics: Aged; Endocrine System Diseases; Female; Humans; Hyponatremia; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Asphyxia Neonatorum; Humans; Hypertonic Solutions; Hyponatremia; Infant, Newborn; Male; Meningitis; Osmolar Concentration; Osmosis; Punctures; Sodium; Sodium Chloride; Urine; Vasopressins

Topics: Humans; Hyponatremia; Natriuresis; Vasopressins; Water-Electrolyte Balance

Topics: Alkalosis; Bicarbonates; Blood Pressure; Blood Urea Nitrogen; Diet, Sodium-Restricted; Diuresis; Edema; Ethacrynic Acid; Female; Furosemide; Humans; Hyponatremia; Hypotension, Orthostatic; Kidney Concentrating Ability; Middle Aged; Potassium Deficiency; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Dogs; Electrolytes; Hormones, Ectopic; Humans; Hyponatremia; Lung Neoplasms; Lymphoma; Neoplasms; Pancreatic Neoplasms; Stomach Neoplasms; Vasopressins

Topics: Adenoma; Cerebral Angiography; Female; Humans; Hyponatremia; Middle Aged; Pituitary Function Tests; Pituitary Neoplasms; Pituitary-Adrenal Function Tests; Vasopressins

Topics: Carcinoma; Diagnosis, Differential; Exudates and Transudates; Female; Humans; Hyponatremia; Intestinal Obstruction; Middle Aged; Myxedema; Osmolar Concentration; Pelvic Inflammatory Disease; Pelvic Neoplasms; Sodium; Thyroid Hormones; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Aged; Atrophy; Blood; Brain Diseases; Chlorpropamide; Diabetes Complications; Diabetes Mellitus; Female; Fludrocortisone; Humans; Hyperpituitarism; Hyponatremia; Natriuresis; Osmolar Concentration; Tolbutamide; Urine; Vasopressins

Topics: Aldosterone; Body Weight; Desoxycorticosterone; Humans; Hyponatremia; Male; Middle Aged; Osmolar Concentration; Potassium; Sodium; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Bronchial Neoplasms; Carcinoma, Squamous Cell; Central Nervous System Diseases; Hormones, Ectopic; Humans; Hyponatremia; Male; Middle Aged; Vasopressins

Topics: Aged; Carcinoma, Bronchogenic; Central Nervous System Diseases; Hormones, Ectopic; Humans; Hyponatremia; Lung Diseases; Male; Middle Aged; Vasopressins

Topics: Adult; Hormones, Ectopic; Humans; Hyponatremia; Male; Middle Aged; Porphyrias; Vasopressins; Water-Electrolyte Balance

Topics: Acute Disease; Humans; Hyponatremia; Infusions, Parenteral; Male; Middle Aged; Tuberculosis, Miliary; Tuberculosis, Pulmonary; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Aged; Humans; Hyponatremia; Male; Pituitary Gland, Posterior; Tuberculosis, Pulmonary; Vasopressins

Topics: Central Nervous System Diseases; Endocrine System Diseases; Humans; Hyponatremia; Kidney Tubules; Lung Diseases; Neoplasms; Osmolar Concentration; Vasopressins

Topics: Acute Disease; Adult; Humans; Hyponatremia; Male; Middle Aged; Porphyrias; Syndrome; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Bronchial Neoplasms; Carcinoma; Electroencephalography; Humans; Hyponatremia; Middle Aged; Natriuresis; Neoplasm Metastasis; Vasopressins; Water Intoxication

Topics: Adrenocorticotropic Hormone; Aldosterone; Autopsy; Chlorides; Humans; Hyponatremia; Hypopituitarism; Kidney Concentrating Ability; Male; Middle Aged; Nitrogen; Pituitary-Adrenal Function Tests; Potassium; Sodium; Syphilis; Vasopressins

Topics: 17-Hydroxycorticosteroids; 17-Ketosteroids; Adrenal Insufficiency; Adrenocorticotropic Hormone; Dexamethasone; Diuresis; Ethanol; Extracellular Space; Female; Glucocorticoids; Growth Hormone; Humans; Hyponatremia; Hypopituitarism; Infusions, Parenteral; Metyrapone; Middle Aged; Natriuresis; Sodium Chloride; Vasopressins; Water-Electrolyte Balance

Topics: 17-Hydroxycorticosteroids; Acidosis, Respiratory; Adolescent; Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Adult; Aged; Brain; Carbon Dioxide; Cerebrovascular Circulation; Circadian Rhythm; Coma; Dexamethasone; Encephalitis, St. Louis; Female; Growth Hormone; Humans; Hyponatremia; Insulin; Male; Metyrapone; Middle Aged; Oxygen; Pituitary-Adrenal System; Vasopressins

Topics: Child; Coma; Epilepsy, Tonic-Clonic; Humans; Hyponatremia; Hypotension; Leukemia, Lymphoid; Male; Reflex, Abnormal; Vasopressins; Vincristine

Topics: Hyponatremia; Nursing Care; Patient Care Team; Research; Vasopressins; Water-Electrolyte Balance

Topics: Autopsy; Chlorthalidone; Demyelinating Diseases; Female; Humans; Hypertonic Solutions; Hyponatremia; Methyclothiazide; Middle Aged; Pons; Potassium; Pulmonary Embolism; Reserpine; Vasopressins; Water-Electrolyte Balance

Topics: Aged; Blood Urea Nitrogen; Brain Neoplasms; Female; Humans; Hypertonic Solutions; Hyponatremia; Hypothalamus; Lung Neoplasms; Neoplasm Metastasis; Osmolar Concentration; Plasma Volume; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adenocarcinoma; Blood Volume; Humans; Hyponatremia; Liver; Male; Middle Aged; Neoplasm Metastasis; Osmolar Concentration; Prostatic Neoplasms; Sodium; Vasopressins

Topics: Adolescent; Anti-Bacterial Agents; Brain Edema; Child; Child, Preschool; Coma; Electroencephalography; Encephalitis; Female; Humans; Hyponatremia; Male; Vasopressins

Topics: Astrocytoma; Brain Neoplasms; Child; Diet, Sodium-Restricted; Electromyography; Humans; Hyponatremia; Male; Metyrapone; Neural Conduction; Pituitary Function Tests; Sodium; Vasopressins

Topics: Electroencephalography; Hormones, Ectopic; Humans; Hypernatremia; Hypokalemia; Hyponatremia; Metabolic Diseases; Penicillins; Uremia; Vasopressins

Topics: Adult; Central Nervous System Diseases; Hormones, Ectopic; Humans; Hyponatremia; Lung Neoplasms; Male; Neurologic Manifestations; Vasopressins

Topics: Aged; Carcinoma, Bronchogenic; Hormones, Ectopic; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Vasopressins

Topics: Central Nervous System Diseases; Female; Hormones, Ectopic; Humans; Hyponatremia; Lung Diseases; Male; Neoplasms; Vasopressins

Topics: Adult; Alcoholism; Cortisone; Creatinine; Deficiency Diseases; Ethanol; Humans; Hyponatremia; Male; Middle Aged; Potassium; Sodium; Tuberculosis, Pulmonary; Vasopressins; Water

Topics: Brain Neoplasms; Carcinoma, Bronchogenic; Cerebral Cortex; Dementia; Glioma; Humans; Hyponatremia; Liver Neoplasms; Lymph Nodes; Male; Mental Disorders; Middle Aged; Neoplasm Metastasis; Seizures; Sodium; Thalamus; Vasopressins

Topics: Aged; Bronchopneumonia; Humans; Hyponatremia; Male; Tuberculosis, Pulmonary; Vasopressins

Topics: Adrenal Cortex Hormones; Alkalosis; Blood Urea Nitrogen; Blood Volume; Diuretics; Edema; Ethacrynic Acid; Furosemide; Glomerular Filtration Rate; Humans; Hyperaldosteronism; Hyperkalemia; Hypokalemia; Hyponatremia; Kidney Failure, Chronic; Kidney Tubules; Liver Cirrhosis; Spironolactone; Triamterene; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adenocarcinoma; Adrenal Gland Neoplasms; Adrenal Glands; Adrenal Insufficiency; Aldosterone; Body Weight; Female; Humans; Hyponatremia; Lung Neoplasms; Middle Aged; Neoplasm Metastasis; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Humans; Hyponatremia; Male; Pituitary Diseases; Tuberculosis, Meningeal; Vasopressins; Water-Electrolyte Balance

Topics: Breast Neoplasms; Cortisone; Desoxycorticosterone; Diabetes Insipidus; Female; Hematocrit; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Middle Aged; Neoplasm Metastasis; Nerve Degeneration; Nerve Regeneration; Neurons; Pituitary Gland; Pituitary Gland, Posterior; Postoperative Complications; Sodium; Sodium Chloride; Vasopressins; Water; Water-Electrolyte Balance

Topics: Adolescent; Diuresis; Female; Humans; Hyponatremia; Porphyrias; Vasopressins

Topics: Adult; Chlorides; Diet; Diuresis; Female; Humans; Hyponatremia; Kidney Tubules; Male; Middle Aged; Potassium; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Aldosterone; Angiotensin II; Humans; Hydrocortisone; Hypernatremia; Hyponatremia; Natriuresis; Vasopressins; Water-Electrolyte Balance

Topics: Adenocarcinoma, Bronchiolo-Alveolar; Adrenocorticotropic Hormone; Aged; Carcinoma, Bronchogenic; Electrolytes; Hormones; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Osmolar Concentration; Sodium Chloride; Vasopressins; Water-Electrolyte Balance

Topics: Adrenocortical Hyperfunction; Adrenocorticotropic Hormone; Aldosterone; Alkalosis; Bronchial Neoplasms; Carcinoma; Endocrine System Diseases; Fludrocortisone; Humans; Hypercalcemia; Hypokalemia; Hyponatremia; Male; Plasma Volume; Vasopressins

Topics: Blood Urea Nitrogen; Craniocerebral Trauma; Hematocrit; Humans; Hyperkalemia; Hypernatremia; Hypokalemia; Hyponatremia; Natriuresis; Osmosis; Potassium; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Aged; Animals; Biological Assay; Blood Chemical Analysis; Blood Urea Nitrogen; Bronchial Neoplasms; Creatinine; Dexamethasone; Diuresis; Female; Fludrocortisone; Humans; Hyperaldosteronism; Hyponatremia; Male; Middle Aged; Natriuresis; Phenytoin; Rats; Tissue Extracts; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Heart Failure; Humans; Hyponatremia; Vasopressins; Water Intoxication

Topics: Carcinoma, Bronchogenic; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Thirst; Vasopressins

Topics: Adult; Body Weight; Female; Glomerular Filtration Rate; Heart Valve Diseases; Heart Valve Prosthesis; Humans; Hydrocephalus; Hypertonic Solutions; Hyponatremia; Male; Osmolar Concentration; Sodium; Sodium Chloride; Vasopressins

Topics: Aged; Cerebrovascular Disorders; Coma; Female; Humans; Hyponatremia; Hypopituitarism; Potassium Deficiency; Vasopressins

Topics: Aged; Carcinoma, Squamous Cell; Humans; Hyponatremia; Lung Neoplasms; Male; Mental Disorders; Middle Aged; Natriuresis; Smoking; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Aged; Female; Humans; Hyponatremia; Male; Middle Aged; Vasopressins

Topics: Arthritis, Rheumatoid; Extracellular Space; Felty Syndrome; Female; Hormones, Ectopic; Humans; Hyponatremia; Middle Aged; Sjogren's Syndrome; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Humans; Hyponatremia; Thirst; Vasopressins

Topics: Diabetes Insipidus; Humans; Hyponatremia; Male; Middle Aged; Psychophysiologic Disorders; Stress, Psychological; Vasopressins; Water Intoxication

Topics: Aldosterone; Extracellular Space; Humans; Hyperkalemia; Hypernatremia; Hyponatremia; Potassium; Preoperative Care; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Brain Neoplasms; Electroencephalography; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Natriuresis; Neoplasm Metastasis; Vasopressins; Water Intoxication

Topics: Adenocarcinoma; Animals; Biological Assay; Carcinoma, Bronchogenic; Chickens; Humans; Hyponatremia; Lung Neoplasms; Male; Methods; Middle Aged; Neoplasm Metastasis; Neoplasms, Multiple Primary; Osmolar Concentration; Oxytocin; Pancreatic Neoplasms; Pneumonectomy; Rabbits; Radioimmunoassay; Rats; Vasopressins

Topics: Aged; Female; Humans; Hypokalemia; Hyponatremia; Intracranial Aneurysm; Vasopressins

Topics: Aged; Female; Humans; Hyponatremia; Hypothyroidism; Myxedema; Sodium; Thyroid Hormones; Vasopressins; Water-Electrolyte Balance

Topics: Carcinoma, Bronchogenic; Endocrine System Diseases; Hormones, Ectopic; Humans; Hyponatremia; Infections; Lung Neoplasms; Male; Middle Aged; Myxedema; Pituitary Diseases; Porphyrias; Vasopressins

Topics: Aged; Heart Failure; Humans; Hyponatremia; Hypopituitarism; Male; Myxedema; Propylthiouracil; Triiodothyronine; Vasopressins

Topics: Animals; Anura; Biological Assay; Carcinoma, Bronchogenic; Chromatography, Gel; Chromatography, Ion Exchange; Chymotrypsin; Diuresis; Hormones, Ectopic; Humans; Hyponatremia; Liver Neoplasms; Lymphatic Metastasis; Neoplasm Metastasis; Pancreatic Neoplasms; Thioglycolates; Trypsin; Vasopressins

Topics: Animals; Bronchial Neoplasms; Hormones, Ectopic; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Natriuresis; Potassium; Rats; Vasopressins

Topics: Aged; Animals; Anura; Bronchial Neoplasms; Carcinoma; Humans; Hyponatremia; Hypopituitarism; Male; Neoplasm Metastasis; Pancreatic Neoplasms; Permeability; Sodium; Urinary Bladder; Vasopressins; Water

Topics: Bronchial Neoplasms; Chromatography, Ion Exchange; Humans; Hyponatremia; Vasopressins

Topics: Adult; Bendroflumethiazide; Craniocerebral Trauma; Diabetes Insipidus; Diuresis; Humans; Hyponatremia; Kidney; Male; Vasopressins

Topics: Adult; Body Weight; Diabetic Retinopathy; Epilepsy, Tonic-Clonic; Female; Humans; Hyponatremia; Male; Middle Aged; Palliative Care; Pituitary Gland; Postoperative Complications; Tremor; Vasopressins

Topics: Adolescent; Adult; Aged; Female; Humans; Hyponatremia; Male; Middle Aged; Peripheral Nervous System Diseases; Polyneuropathies; Polyradiculopathy; Sodium; Vasopressins; Water Intoxication

Topics: Adult; Diagnosis, Differential; Female; Heart Diseases; Humans; Hyponatremia; Kidney Diseases; Male; Middle Aged; Obesity; Potassium; Potassium Isotopes; Radioisotope Dilution Technique; Sodium; Sodium Isotopes; Vasopressins

Topics: Aged; Blood Proteins; Blood Urea Nitrogen; Chlorine; Creatinine; Diagnosis, Differential; Ethacrynic Acid; Female; Hormones, Ectopic; Humans; Hyponatremia; Mental Disorders; Potassium; Sodium; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Aldosterone; Blood Volume; Bronchial Neoplasms; Carcinoma; Cyclophosphamide; Diuresis; Electroencephalography; Hormones, Ectopic; Humans; Hyponatremia; Male; Middle Aged; Natriuresis; Plasma Volume; Radioisotope Teletherapy; Renin; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adult; Aged; Cell Membrane Permeability; Cervical Vertebrae; Cordotomy; Female; Humans; Hyponatremia; Male; Middle Aged; Vasomotor System; Vasopressins; Water-Electrolyte Balance

Topics: Diagnosis, Differential; Female; Humans; Hyponatremia; Infusions, Parenteral; Middle Aged; Vasopressins

Topics: Coma; Congenital Hypothyroidism; Female; Humans; Hyponatremia; Infant; Myxedema; Vasopressins; Water Intoxication

Topics: Aged; Female; Humans; Hyponatremia; Sodium; Urine; Vasopressins

Topics: Humans; Hyponatremia; Natriuresis; Neoplasms; Urine; Vasopressins

Topics: Brain Diseases; Bronchial Neoplasms; Humans; Hyponatremia; Vasopressins; Water Intoxication

Topics: Aged; Diagnosis, Differential; Female; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Natriuresis; Neurologic Manifestations; Vasopressins; Water-Electrolyte Balance

Topics: Aldosterone; Carcinoma; Glomerular Filtration Rate; Humans; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Vasopressins; Water-Electrolyte Balance

Topics: Bronchial Neoplasms; Humans; Hyponatremia; Male; Middle Aged; Myasthenia Gravis; Vasopressins

Topics: Arginine; Carcinoma; Female; Humans; Hyponatremia; Immunoassay; In Vitro Techniques; Lung Neoplasms; Middle Aged; Natriuresis; Tissue Extracts; Vasopressins

Topics: Aged; Ethacrynic Acid; Female; Humans; Hyponatremia; In Vitro Techniques; Male; Middle Aged; Natriuresis; Secretory Rate; Vasopressins

Topics: Humans; Hyponatremia; Infant; Male; Rhabdomyosarcoma; Spermatic Cord; Urine; Vasopressins; Vincristine

Topics: Aged; Aldosterone; Body Weight; Carcinoma, Bronchogenic; Erythrocytes; Feces; Female; Humans; Hyponatremia; Male; Middle Aged; Muscles; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Anuria; Chlorpromazine; Diabetes Insipidus; Ethanol; Female; Humans; Hyponatremia; Male; Neurosecretion; Osmosis; Sensory Receptor Cells; Vasopressins

Topics: Adult; Aldosterone; Bronchial Neoplasms; Carcinoma; Humans; Hyponatremia; Male; Vasopressins

Topics: Adult; Digitoxin; Female; Humans; Hyponatremia; Natriuresis; Suicide; Vasopressins

Topics: Adult; Bronchopneumonia; Female; Hodgkin Disease; Humans; Hyponatremia; Lymphography; Male; Middle Aged; Vasopressins

Topics: Aged; Humans; Hyponatremia; Male; Vasopressins

Topics: Arginine Vasopressin; Bronchial Neoplasms; Carcinoma, Bronchogenic; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lymphatic Metastasis; Natriuresis; Neoplasms; Physiology; Urine; Vasopressins

Topics: Drug Therapy; Geriatrics; Humans; Hyponatremia; Myxedema; Thyroid Function Tests; Thyroxine; Vasopressins; Water-Electrolyte Balance

Topics: Blood; Glycolates; Hemoglobins; Humans; Hyponatremia; Magnesium; Metabolism; Pharmacology; Porphyria, Acute Intermittent; Porphyrias; Thioglycolates; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Craniocerebral Trauma; Diagnosis; Endocrine System Diseases; Humans; Hyponatremia; Inappropriate ADH Syndrome; Pathology; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Chlorides; Empyema; Extracellular Space; Hyponatremia; Models, Theoretical; Pneumococcal Infections; Rats; Research; Vasopressins; Water-Electrolyte Balance

Topics: Aldosterone; Blood Volume; Bodily Secretions; Body Fluids; Craniocerebral Trauma; Creatine; Creatinine; Extracellular Space; Fluids and Secretions; Humans; Hyponatremia; Natriuresis; Physiology; Skull Fractures; Urine; Vasopressins

Topics: Arginine Vasopressin; Bronchial Neoplasms; Carcinoma; Carcinoma, Bronchogenic; Drug Therapy; Fluids and Secretions; Humans; Hyponatremia; Mechlorethamine; Neoplasms; Urine; Vasopressins

Topics: 17-Hydroxycorticosteroids; 17-Ketosteroids; Adrenal Insufficiency; Adrenocorticotropic Hormone; Creatine; Creatinine; Diagnosis, Differential; Drug Therapy; Eosinophils; Follicle Stimulating Hormone; Humans; Hyponatremia; Hypothalamus; Pituitary Gland; Pituitary Gland, Posterior; Pituitary-Adrenal Function Tests; Prednisone; Sodium; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Humans; Hyponatremia; Vasopressins

Topics: 5-Hydroxytryptophan; Carcinoid Tumor; Carcinoma, Hepatocellular; Carotid Body Tumor; Catecholamines; Cushing Syndrome; Endocrine System Diseases; Female; Fibrosarcoma; Humans; Hyperthyroidism; Hypoglycemia; Hyponatremia; Liver Neoplasms; Lung Neoplasms; Male; Neoplasms; Polycythemia Vera; Puberty, Precocious; Vasopressins

Topics: Aged; Humans; Hyponatremia; In Vitro Techniques; Lymphoma, Non-Hodgkin; Male; Mediastinal Neoplasms; Vasopressins

Topics: Adult; Humans; Hyponatremia; Male; Middle Aged; Tuberculosis, Pulmonary; Vasopressins; Water-Electrolyte Balance

Topics: Duodenal Neoplasms; Female; Humans; Hyponatremia; Middle Aged; Vasopressins

Topics: Adult; Female; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Intracranial Aneurysm; Male; Middle Aged; Rupture, Spontaneous; Subarachnoid Hemorrhage; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Animals; Female; Humans; Hyponatremia; Male; Middle Aged; Subarachnoid Hemorrhage; Vasopressins

Topics: Blood Cell Count; Blood Chemical Analysis; Child; Cortisone; Craniopharyngioma; Diabetes Insipidus; Electroencephalography; Humans; Hyponatremia; Hypopituitarism; Male; Radiography; Sella Turcica; Vasopressins; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Calcium; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Humans; Hyponatremia; Magnesium; Physiology; Potassium; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Blood Chemical Analysis; Carbon Dioxide; Chlorides; Electroencephalography; Encephalitis; Encephalitis, Herpes Simplex; Herpes Simplex; Hyponatremia; Kidney Function Tests; Limbic System; Pathology; Physiology; Potassium; Sodium Chloride; Vasopressins; Water-Electrolyte Balance

Topics: Humans; Hyponatremia; Porphyria, Acute Intermittent; Porphyrias; Proteinuria; Seizures; Urine; Vasopressins

Topics: Arteriosclerosis; Diabetes Insipidus; Diuresis; Glucose; Heart Failure; Humans; Hypernatremia; Hyponatremia; Injections, Intravenous; Isotonic Solutions; Mannitol; Myocarditis; Osmosis; Potassium; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Adenine Nucleotides; Adenosine Triphosphate; Adrenocorticotropic Hormone; Arginine Vasopressin; Humans; Hyponatremia; Pharmacology; Vasopressins; Water-Electrolyte Balance

Topics: Addison Disease; Arginine Vasopressin; Avena; Bronchial Neoplasms; Carcinoma, Small Cell; Cushing Syndrome; Gynecomastia; Humans; Hypercalcemia; Hyperthyroidism; Hyponatremia; Hypotension; Liver Cirrhosis; Male; Metabolism; Pathology; Physiology; Small Cell Lung Carcinoma; Sodium; Vasopressins

Topics: Blood Chemical Analysis; Bronchial Neoplasms; Carcinoma; Humans; Hyponatremia; Metabolism; Neoplasms; Urine; Vasopressins

Topics: Arginine Vasopressin; Glomerular Filtration Rate; Guillain-Barre Syndrome; Humans; Hyponatremia; Kidney Function Tests; Natriuresis; Polyradiculopathy; Urine; Vasopressins; Water; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Carcinoma; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lung Neoplasms; Metabolism; Vasopressins; Water-Electrolyte Balance

Topics: Humans; Hyponatremia; Ions; Porphyria, Acute Intermittent; Porphyrias; Sodium; Vasopressins

Topics: Aldosterone; Brain Diseases; Humans; Hyponatremia; Natriuresis; Vasopressins; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Blood Chemical Analysis; Carcinoma; Carcinoma, Small Cell; Geriatrics; Humans; Hyponatremia; Lung Neoplasms; Vasopressins

Topics: Carcinoma; Carcinoma, Bronchogenic; Humans; Hyponatremia; Lung Neoplasms; Mediastinal Neoplasms; Renal Elimination; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Humans; Hyponatremia; Metabolism; Vasopressins

Topics: Aldosterone; Brain Neoplasms; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lung Neoplasms; Natriuresis; Neoplasm Metastasis; Physiology; Vasopressins

Topics: Arginine Vasopressin; Clinical Laboratory Techniques; Encephalitis; Encephalitis, Herpes Simplex; Herpes Simplex; Humans; Hyponatremia; Inappropriate ADH Syndrome; Physiology; Vasopressins; Water-Electrolyte Balance

Topics: Humans; Hyponatremia; Vasopressins

Topics: Carcinoma; Carcinoma, Bronchogenic; Humans; Hyponatremia; Sodium; Vasopressins

Topics: Brain; Brain Injuries; Brain Neoplasms; Humans; Hyponatremia; Vasopressins; Water-Electrolyte Balance

Topics: Carcinoma; Carcinoma, Bronchogenic; Diabetes Insipidus, Neurogenic; Humans; Hyponatremia; Kidney; Sodium; Vasopressins

Topics: Humans; Hyponatremia; Kidney; Sodium; Sodium, Dietary; Syndrome; Vasopressins

Topics: Humans; Hyponatremia; Kidney; Lung Neoplasms; Sodium; Vasopressins

Topics: Arginine Vasopressin; Chlorides; Dehydration; Humans; Hyponatremia; Sodium; Sodium Chloride; Sweat; Sweating; Urine; Vasopressins