pituitrin and Hypernatremia

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

In the pregnant patient, hypotonic polyuria in the setting of elevated serum osmolality and polydipsia should narrow the differential to causes related to diabetes insipidus (DI). Gestational DI, also called transient DI of pregnancy, is a distinct entity, unique from central DI or nephrogenic DI which may both become exacerbated during pregnancy. These three different processes relate to vasopressin, where increased metabolism, decreased production or altered renal sensitivity to this neuropeptide should be considered. Gestational DI involves progressively rising levels of placental vasopressinase throughout pregnancy, resulting in decreased endogenous vasopressin and resulting hypotonic polyuria worsening through the pregnancy. Gestational DI should be distinguished from central and nephrogenic DI that may be seen during pregnancy through use of clinical history, urine and serum osmolality measurements, response to desmopressin and potentially, the newer, emerging copeptin measurement. This review focuses on a brief overview of osmoregulatory and vasopressin physiology in pregnancy and how this relates to the clinical presentation, pathophysiology, diagnosis and management of gestational DI, with comparisons to the other forms of DI during pregnancy. Differentiating the subtypes of DI during pregnancy is critical in order to provide optimal management of DI in pregnancy and avoid dehydration and hypernatremia in this vulnerable population.

Topics: Dehydration; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Diagnosis, Differential; Female; Humans; Hypernatremia; Neurophysins; Osmoregulation; Polydipsia; Polyuria; Pregnancy; Pregnancy Complications; Protein Precursors; Vasopressins; Water-Electrolyte Balance

For an endocrinologist, nephrogenic diabetes insipidus (NDI) is an end-organ disease, that is the antidiuretic hormone, arginine-vasopressin (AVP) is normally produced but not recognized by the kidney with an inability to concentrate urine despite elevated plasma concentrations of AVP. Polyuria with hyposthenuria and polydipsia are the cardinal clinical manifestations of the disease. For a geneticist, hereditary NDI is a rare disease with a prevalence of five per million males secondary to loss of function of the vasopressin V2 receptor, an X-linked gene, or loss of function of the water channel AQP2. These are small genes, easily sequenced, with a number of both recurrent and private mutations described as disease causing. Other inherited disorders with mild, moderate or severe inability to concentrate urine include Bartter's syndrome and cystinosis. MAGED2 mutations are responsible for a transient form of Bartter's syndrome with severe polyhydramnios. The purpose of this review is to describe classical phenotype findings that will help physicians to identify early, before dehydration episodes with hypernatremia, patients with familial NDI. A number of patients are still diagnosed late with repeated dehydration episodes and large dilations of the urinary tract leading to a flow obstructive nephropathy with progressive deterioration of glomerular function. Families with ancestral X-linked AVPR2 mutations could be reconstructed and all female heterozygote patients identified with subsequent perinatal genetic testing to recognize affected males within 2 weeks of birth. Prevention of dehydration episodes is of critical importance in early life and beyond and decreasing solute intake will diminish total urine output.

Topics: Dehydration; Diabetes Insipidus, Nephrogenic; Female; Genetic Carrier Screening; Genetic Diseases, X-Linked; Genetic Testing; Humans; Hypernatremia; Infant, Newborn; Kidney Glomerulus; Male; Mutation; Neurophysins; Osmolar Concentration; Pregnancy; Prenatal Diagnosis; Protein Precursors; Receptors, Vasopressin; Vasopressins

Adipsic diabetes insipidus (ADI) is a very rare disorder, characterized by hypotonic polyuria due to arginine vasopressin (AVP) deficiency and failure to generate the sensation of thirst in response to hypernatraemia. As the sensation of thirst is the key homeostatic mechanism that prevents hypernatraemic dehydration in patients with untreated diabetes insipidus (DI), adipsia leads to failure to respond to aquaresis with appropriate fluid intake. This predisposes to the development of significant hypernatraemia, which is the typical biochemical manifestation of adipsic DI.. A literature search was performed to review the background, etiology, management and associated complications of this rare condition.. ADI has been reported to occur in association with clipping of an anterior communicating artery aneurysm following subarachnoid haemorrhage, major hypothalamic surgery, traumatic brain injury and toluene exposure among other conditions. Management is very difficult and patients are prone to marked changes in plasma sodium concentration, in particular to the development of severe hypernatraemia. Associated hypothalamic disorders, such as severe obesity, sleep apnoea and thermoregulatory disorders are often observed in patients with ADI.. The management of ADI is challenging and is associated with significant morbidity and mortality. Prognosis is variable; hypothalamic complications lead to early death in some patients, but recent reports highlight the possibility of recovery of thirst.

Topics: Animals; Arginine Vasopressin; Complement Factor D; Diabetes Insipidus; Humans; Hypernatremia; Vasopressins

Disorders of body fluids are among the most commonly encountered problems in the practice of clinical medicine. This is in large part because many different disease states can potentially disrupt the finely balanced mechanisms that control the intake and output of water and solute. It therefore behooves clinicians treating such patients to have a good understanding of the pathophysiology, the differential diagnosis and the management of these disorders. Since body water is the primary determinant of the osmolality of the extracellular fluid (ECF), disorders of body water homeostasis can be divided into hypoosmolar disorders, in which there is an excess of body water relative to body solute, and hyperosmolar disorders, in which there is a deficiency of body water relative to body solute. The classical hyperosmolar disorder is diabetes insipidus (DI), and the classical hypoosmolar disorder is the syndrome of inappropriate antidiuretic hormone secretion (SIADH). This chapter first reviews the regulatory mechanisms underlying water and sodium metabolism, the two major determinants of body fluid homeostasis. The major disorders of water metabolism causing hyperosmolality and hypoosmolality, DI and SIADH, are then discussed in detail, including the pathogenesis, differential diagnosis and treatment of these disorders.

Topics: Animals; Diabetes Insipidus; Diagnosis, Differential; Humans; Hypernatremia; Inappropriate ADH Syndrome; Vasopressins; Water; Water-Electrolyte Imbalance

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

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

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

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

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

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

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

In humans and most other mammals, the antidiuretic hormone (ADH) is a nonapeptide often referred to as arginine vasopressin (AVP). It is produced by large neurons that originate in the supraoptic and paraventricular nucleus of the hypothalamus and project through the pituitary stalk to terminate on capillary plexuses scattered throughout the posterior pituitary. These plexuses drain into the systemic circulation by way of the cavernous sinus and superior vena cava.

Topics: Arginine Vasopressin; Humans; Hypernatremia; Inappropriate ADH Syndrome; 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: Animals; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Kidney Concentrating Ability; 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

Cranial diabetes insipidus (DI) arises when release of arginine vasopressin (AVP, antidiuretic hormone) in response to osmotic stimuli is inadequate. The correct diagnosis and management of cranial DI is particularly important when it arises as an acute complication of surgery, trauma or in subjects who lack thirst sensation. Desmopressin (1-desamino-8-D-arginine-vasopressin, DDAVP) provides an effective and convenient replacement therapy when given by the intranasal route. However, nasal administration is difficult for some patients, and in the future oral or transcutaneous desmopressin formulations may prove to be satisfactory alternatives. By contrast, treatments for nephrogenic DI, where there is failure of the antidiuretic response to endogenous or exogenous vasopressin, have been disappointing and water replacement remains the mainstay of therapy. An understanding of the physiology and pathophysiology of water homeostasis and correct interpretation of water balance and electrolyte data are essential for correct diagnosis and management of all cases of DI.

Topics: Arginine Vasopressin; Diabetes Insipidus; Female; Humans; Hypernatremia; Kidney Diseases; Male; Pregnancy; Pregnancy Complications; Thirst; 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: 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: Brain Diseases; Diabetes Insipidus; Electrolytes; Humans; Hypernatremia; Hyponatremia; Postoperative Complications; Vasopressins; Water; Water Intoxication; 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

Topics: Acidosis; Acute Kidney Injury; Alkalosis; Amyloidosis; Hodgkin Disease; Humans; Hyperkalemia; Hypernatremia; Hypertension, Renal; Hypokalemia; Kidney; Kidney Concentrating Ability; Kidney Diseases; Multiple Myeloma; Neoplasms; Nephritis; Nephrotic Syndrome; Osmolar Concentration; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Child; Drinking; Extracellular Space; Female; Humans; Hypernatremia; Hypothalamo-Hypophyseal System; Hypothalamus; Kidney Concentrating Ability; Male; Pennsylvania; Remission, Spontaneous; Sensory Receptor Cells; Sodium; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Chlorides; Humans; Hydrogen-Ion Concentration; Hypernatremia; Hyponatremia; Infusions, Parenteral; Sodium; 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: Extracellular Space; Humans; Hypercalcemia; Hyperkalemia; Hypernatremia; Hyperparathyroidism; Hypokalemia; Kidney; Magnesium; Vasopressins; Water-Electrolyte Balance

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

Topics: Adult; Aged; Anesthetics; Blood Urea Nitrogen; Body Weight; Creatinine; Halothane; Humans; Hypernatremia; Kidney Concentrating Ability; Kidney Diseases; Male; Methoxyflurane; Middle Aged; Osmolar Concentration; Polyuria; Postoperative Care; Prospective Studies; Sodium; Surgical Procedures, Operative; Time Factors; Uric Acid; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Humans; Hypernatremia; Male; Mice; Sodium; Subfornical Organ; Vasopressins; Water

Modulation of the epithelial Na

Topics: Adenosine Triphosphate; Aldosterone; Animals; Epithelial Sodium Channels; Genotype; H(+)-K(+)-Exchanging ATPase; Homeostasis; Hypernatremia; Kidney Tubules, Collecting; Male; Mice, Inbred C57BL; Mice, Knockout; Phenotype; Renal Elimination; Renal Reabsorption; Signal Transduction; Sodium, Dietary; Time Factors; Vasopressins

Changes in osmolality or extracellular NaCl concentrations are detected by specialized neurons in the hypothalamus to increase vasopressin (VP) and stimulate thirst. Recent in vitro evidence suggests this process is mediated by an NH2-terminal variant of the transient receptor potential vanilloid type 1 (TRPV1) channel expressed by osmosensitive neurons of the lamina terminalis and vasopressinergic neurons of the supraoptic nucleus. The present study tested this hypothesis in vivo by analysis of plasma VP levels during acute hypernatremia in awake control and TRPV1(-/-) rats. TRPV1(-/-) rats were produced by a Zinc-finger-nuclease 2-bp deletion in exon 13. Intravenous injection of the TRPV1 agonist capsaicin produced hypotension and bradycardia in control rats, but this response was absent in TRPV1(-/-) rats. Infusion of 2 M NaCl (1 ml/h iv) increased plasma osmolality, electrolytes, and VP levels in both control and TRPV1(-/-) rats. However, plasma VP levels did not differ between strains at any time. Furthermore, a linear regression between plasma VP versus osmolality revealed a significant correlation in both control and TRPV1(-/-) rats, but the slope of the regression lines was not attenuated in TRPV1(-/-) versus control rats. Hypotension produced by intravenous injection of minoxidil decreased blood pressure and increased plasma VP levels similarly in both groups. Finally, both treatments stimulated thirst; however, cumulative water intakes in response to hypernatremia or hypotension were not different between control and TRPV1(-/-) rats. These findings suggest that TRPV1 channels are not necessary for VP secretion and thirst stimulated by hypernatremia.

Topics: Animals; Drinking; Hypernatremia; Male; Mice, Knockout; Osmolar Concentration; Rats; Rats, Sprague-Dawley; Thirst; TRPV Cation Channels; Vasopressins; Water-Electrolyte Balance

Elderly patients have a high prevalence of hypernatremia. The aim of this study was to determine demographic and clinical characteristics of the elderly hypernatremic patient hospitalized in the internal medicine ward and to enhance understanding of the role of antidiuretic hormone (ADH) secretion in the pathogenesis of hypernatremia.. Case-control study performed in an internal medicine ward in a university-affiliated hospital. Thirtythree elderly hypernatremic patients (admission sodium, >150 mEq/L; age, >70 years) were compared with 34 normonatremic patients. Demographic, functional (mental status and activities of daily living), clinical data (Acute Physiology and Chronic Health Evaluation [APACHE] II score), and serum copeptin levels as a marker of ADH secretion, were collected at admission. Mortality and change in the functional status were followed up to 30 days from discharge.. Patients with hypernatremia presented with significantly lower baseline functional and cognitive states and higher APACHE II score (21.3 ± 8.6 vs. 15.4 ± 6.7; P<.01). Mortality within 30 days after discharge was higher in the hypernatremic group (58% vs. 32%; P<.05). Higher copeptin levels were found in the hypernatremic group compared to the normonatremic group (100.2 ± 60.6 pmol/L vs. 66.5 ± 57.2 pmol/L; P<.05). High levels of copeptin were associated with higher in-hospital (P<.05) and 30-day (P<.01) mortality. Sodium levels were found correlated with copeptin levels; yet, an even stronger correlation was found between copeptin levels and APACHE II score (r = 0.52; P<.001).. Hypernatremia in the elderly at admission is associated with a high mortality rate. Copeptin level in the elderly seems to be a good single disease severity marker. ADH is strongly secreted in elderly hypernatremic patients.. ADH = antidiuretic hormone APACHE = Acute Physiology and Chronic Health Evaluation.

Topics: Aged; Aged, 80 and over; Biomarkers; Case-Control Studies; Female; Glycopeptides; Hospital Mortality; Hospitalization; Humans; Hypernatremia; Male; Severity of Illness Index; Vasopressins

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

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

Previous studies have indicated that the primary targets for vasopressin actions on the injured brain are the cerebrovascular endothelium and astrocytes, and that vasopressin amplifies the posttraumatic production of proinflammatory mediators. Here, the controlled cortical impact model of traumatic brain injury in rats was used to identify the sources of vasopressin in the injured brain. Injury increased vasopressin synthesis in the hypothalamus and cerebral cortex adjacent to the posttraumatic lesion. In the cortex, vasopressin was predominantly produced by activated microglia/macrophages, and, to a lesser extent, by the cerebrovascular endothelium. These data further support the pathophysiological role of vasopressin in brain injury.

Topics: Animals; Arginine Vasopressin; Brain Chemistry; Brain Injuries; Cerebral Cortex; Endothelium, Vascular; Hypernatremia; Hypothalamus; Immunohistochemistry; Macrophages; Male; Microglia; Microscopy, Confocal; Rats; Rats, Long-Evans; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Vasopressins

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

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

Hypernatremia is generally thought to be a condition in which water depletion raises the serum sodium concentration despite some salt loss. However, many patients with hypernatremia have been shown to have normal or increased total body water, indicating that these patients are salt- and frequently water-overloaded. Possible pathophysiological reasons for these abnormalities are discussed. Recognition of this clinical condition is important because therapy should avoid further worsening the salt and water overload.

Topics: Aged, 80 and over; Humans; Hypernatremia; Male; Sodium; Vasopressins; Water; Water-Electrolyte Balance

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

Topics: Body Water; Brain Edema; Child; Humans; Hypernatremia; Male; Osmolar Concentration; Thirst; Vasopressins; Water-Electrolyte Balance

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

Topics: Dehydration; Diabetes Insipidus, Nephrogenic; Humans; Hypernatremia; Polyuria; Vasopressins; Water Deprivation

The use of vasopressin for the treatment of septic shock is increasing. Few reports of fluid and electrolyte complications of this therapy have been reported. A neurologically impaired, 53-year-old man with a history of syndrome of inappropriate antidiuretic hormone developed apparent transient diabetes insipidus and acute hypernatremia after being treated with vasopressin. He was treated for presumed septic shock with intravenous vasopressin 0.01-0.10 U/minute. His blood pressure did not improve with this therapy, and his course was complicated by hyponatremia during the vasopressin infusion. Discontinuation of the infusion was followed by a profound (8.4 L) diuresis and rapid onset of hypernatremia (serum sodium concentration increased from 132 to 157 mEq/L over 8 hrs). Although urine osmolality was not measured during the patient's diuresis, the rapid changes in serum sodium concentration can be explained only by an inappropriate water diuresis. The diuresis ceased when the vasopressin infusion was resumed. We concluded that these findings are most consistent with transient diabetes insipidus. The safety and efficacy of intravenous vasopressin have not been established in patients with septic shock and underlying disorders of water homeostasis. The drug may have diminished vasoconstrictive effects in this patient population. Careful monitoring of water and sodium balance is warranted in all patients treated with vasopressin for septic shock.

Topics: Acute Disease; Diabetes Insipidus; Humans; Hypernatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Vasoconstrictor Agents; Vasopressins

Adipsic hypernatraemia is an uncommon disorder in childhood caused by a defect in the osmoregulation of thirst, leading to impairment of water homeostasis and chronic hyperosmolality of body fluids. Adipsia is often associated with an abnormality in osmoregulated vasopressin secretion due to the close proximity of the hypothalamic osmoreceptors that control thirst with those regulating vasopressin secretion. Hypothalamic lesions of diverse aetiology (vascular abnormalities, neoplasms, granulomatous diseases, trauma etc.) have been described in this syndrome. We report a 12-year-old boy with evident weight loss due to hypernatraemic dehydration with a selective defect in osmoregulation of thirst and normal vasopressin secretion with no demonstrable structural lesion. To date, only six paediatric patients with this condition have been described in the literature.. Hypothalamic adipsic hypernatraemia syndrome must be suspected when a dehydrated patient denies thirst. The study of antidiuretic function is necessary because the osmoregulation of vasopressin secretion could be altered.

Topics: Brain; Child; Dehydration; Drinking; Humans; Hypernatremia; Hypothalamic Diseases; Magnetic Resonance Imaging; Male; Prognosis; Syndrome; Vasopressins; Water-Electrolyte Balance

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

Rats normally excrete 20-25 mmol of sodium (Na+) + potassium (K+) per kilogram per day. To minimize the need for a large water intake, they must excrete urine with a very high electrolyte concentration (tonicity). Our objective was to evaluate two potential factors that could influence the maximum urine tonicity, hypernatraemia and the rate of urea excretion. Balance studies were carried out in vasopressin-treated rats fed a low-electrolyte diet. In the first series, the drinking solution contained an equivalent sodium chloride (NaCl) load at 150 or 600 mmol l(-1). In the second series, the maximum urine tonicity was evaluated in rats consuming 600 mmol l(-1) NaCl with an 8-fold range of urea excretion. Hypernatraemia (148 +/- 1 mmol l(-1)) developed in all rats that drank 600 mmol l(-1) saline. Although the rate of Na+ + K+ excretion was similar in both saline groups, the maximum urine total cation concentration was significantly higher in the hypernatraemic group (731 +/- 31 vs. 412 +/- 37 mmol l(-1)). Only when the rate of excretion of urea was very low, was there a further increase in the maximum urine total cation concentration (1099 +/- 118 mmol l(-1)). Thus hypernatraemia was the most important factor associated with a higher urine tonicity.

Topics: Animals; Diet; Electrolytes; Hypernatremia; Isotonic Solutions; Loop of Henle; Male; Models, Biological; Osmolar Concentration; Rats; Rats, Wistar; Renal Agents; Saline Solution, Hypertonic; Sodium Chloride, Dietary; Urea; Urodynamics; Vasopressins

We present a case to illustrate the importance of emphasizing elementary physiology to deduce the basis for the acute onset of polyuria and hypernatremia. An imaginary consultation with Professor McCance is utilized to illustrate how a clinician-physiologist would have explained why these abnormalities developed and how they should have been treated. His approach began with a consideration of the most impressive abnormality. His analysis relied heavily on deductions and the anticipation of the expected responses to a stimulus in quantitative terms. The goals of therapy became evident after he performed mass balance calculations. Professor McCance would not understand why modern clinicians abandoned this form of analysis.

Topics: Adult; Female; Humans; Hypernatremia; Intracranial Aneurysm; Polyuria; Urination; Vasopressins; Water-Electrolyte Imbalance

Topics: Edema; Fluid Therapy; Hospitalization; Humans; Hypernatremia; Saline Solution, Hypertonic; Vasopressins; Water-Electrolyte Balance

The aim of our work was to study the different blood parameters as well as the activity of the vasopressinergic axis in young and mature male rats under normal conditions and following a 3-day dehydration cycle by water deprivation. Under normal conditions, our study demonstrates higher levels of vasopressin in mature rats as compared to young rats. This could be due in part to the higher blood osmolality in the mature rats. After dehydration, hypovolemia, plasmatic hyperosmolality, hypernatremia and hyperproteinemia cause a stimulation in vasopressin synthesis and release, as seen in results obtained from the hypothalamus, hypophysis and plasma in both young and mature rats. However, the response of the vasopressinergic axis to dehydration is greater in young rats, suggesting a more pronounced sensitivity to osmotic factors.

Topics: Aging; Animals; Blood Proteins; Blood Volume; Dehydration; Hematocrit; Hypernatremia; Hypothalamo-Hypophyseal System; Male; Osmolar Concentration; Potassium; Rats; Rats, Wistar; Sodium; Vasopressins

Topics: Child; Craniopharyngioma; Craniotomy; Dehydration; Diagnosis, Differential; Female; Humans; Hypernatremia; Hypothalamic Diseases; Pituitary Neoplasms; Syndrome; Vasopressins

In patients with acquired immune deficiency syndrome (AIDS), hypoosmolality is frequently observed, whereas hypernatremia is distinctly rare. We report two patients with advanced AIDS and cytomegalovirus (CMV) encephalitis, who developed severe hypernatremia without any thirst sensation, that is, adipsic hypernatremia. Both developed severe hypernatremia of up to 164 and 162 mmol/L, with serum osmolalities of 358 and 344 mOsmol/kg while remaining alert and denying thirst. Serum antidiuretic hormone (ADH) levels were 0.9 and 1.5 pg/mL, inappropriately low for the concomitant serum osmolalities. Vital signs were stable. During hypernatremia, urine osmolalities were 327 and 340 mOsmol/kg, and urine Na+ levels were 56 and 119 mmol/L, respectively. Periventricular white matter lesions were seen on cerebral nuclear magnetic resonance imaging (NMRI) in case 1, but the pituitary appeared normal in both cases. Survival after onset of hypernatremia was 6 and 4 weeks, respectively. Autopsy in case 1 showed typical findings of CMV encephalitis but normal pituitary, confirming that infection with HIV or CMV most likely caused the dysfunction of the central osmostat.

Topics: Adult; AIDS-Related Opportunistic Infections; Autopsy; Cytomegalovirus Infections; Encephalitis, Viral; Fatal Outcome; Humans; Hypernatremia; Male; Osmolar Concentration; Thirst; Vasopressins

To test the hypothesis that subnormal thirst sensation could contribute to the development of the hypernatraemia characteristic of hyperosmolar coma, we studied osmoregulation in survivors of hyperosmolar coma.. Eight survivors of hyperosmolar coma, eight control subjects with Type II (non-insulin-dependent) diabetes mellitus and eight healthy control subjects underwent water deprivation during which measurements of thirst, plasma osmolality and vasopressin were taken.. Water deprivation caused greater peak plasma osmolality in the hyperosmolar coma group (301.7 +/- 2.7 mmol/kg) than in Type II diabetic (294.3 +/- 3.2 mmol/kg, p < 0.01) or control group (296.9 +/- 3.0 mmol/kg, p < 0.01) and a greater increase in plasma vasopressin concentration (hyperosmolar coma, 5.8 +/- 1.3 pmol/l, Type II diabetes, 1.8 +/- 1.3 pmol/l, p < 0.001, control subjects, 2.2 +/- 1.8 pmol/l, p < 0.001). Thirst ratings were lower following water deprivation in the hyperosmolar coma group (3.5 +/- 0.8 cm) than in Type II diabetes (7.7 +/- 1.6 cm, p < 0.001) or control subjects (7.4 +/- 1.3 cm, p <0.001), and the hyperosmolar group patients drank less in 30 min following water deprivation (401 +/- 105 ml) than Type II diabetic (856 +/- 218 ml, p < 0.001) or control subjects (789 +/- 213 ml, p < 0.001).. Survivors of hyperosmolar coma have subnormal osmoregulated thirst and fluid intake, which might contribute to the hypernatraemic dehydration typical of the condition.

Topics: Aged; Aged, 80 and over; Arginine Vasopressin; Blood; Dehydration; Diabetes Mellitus, Type 2; Female; Humans; Hyperglycemic Hyperosmolar Nonketotic Coma; Hypernatremia; Linear Models; Male; Middle Aged; Osmolar Concentration; Thirst; Vasopressins; Water Deprivation; Water-Electrolyte Balance

Topics: Adult; Colchicine; Female; Humans; Hypernatremia; Polyuria; Suicide; Vasopressins

It is well known that altitude natives differ from sea level natives in aspects of fluid and electrolyte homeostasis.. To evaluate exercise and environmental influences on the electrolyte and water status in hypoxia adapted subjects, we investigated 11 well-trained marathon runners (33.7 +/- 0.7 yr, 60.5 +/- 1.9 kg), native to an altitude above 2600 m, before and after two marathon races. One competition was held at moderate altitude (AM, 2650 m, 14 degrees C, 55% RH, running time 3 h 6 min +/- 22 min) and another under tropical conditions (HM, 470 m, 28 degrees C, 70% RH, running time 2 h 54 min +/- 30 min). Blood samples were taken 3 d before, immediately after, 1 h after, and 24 h after the races.. The loss in body fluid was calculated to be 2.15 L during AM and 5.05 L during HM, respectively. It was compensated mostly by ingested fluids without electrolyte content and by metabolically produced water, which led to hyponatremia during AM (plasma [Na+] from 144.3 +/- 0.7 to 131.7 +/- 2.1 mmol x L(-1)). Severe dehydration without significant changes in plasma [Na+] could be detected after HM. Serum antidiuretic hormone concentrations and serum aldosterone concentrations significantly increased during both races and remained at a high level for at least 1h after both competitions. Serum atrial natriuretic peptide (ANP) concentrations were at a high level at rest, increasing during HM, and decreasing during AM.. Under tropical conditions, we found a severe state of dehydration characterized by an extended ANP-response, which was not prevented by water intake during the race. Under hypoxic conditions, however, we found that hyponatremia had developed. This can be partly explained by pure water intake and metabolically produced water, and also, possibly, by a special hypoxia-induced effect.

Topics: Adult; Aldosterone; Altitude; Dehydration; Electrolytes; Humans; Hypernatremia; Hypoxia; Male; Running; Vasopressins

We report a 45 y old male patient with severe hypodipsia, but intact vasopressin secretion and maximal renal response to vasopressin. The patient presented during hot summer days, 18 months after a frontal lobe hemorrhage due to a ruptured aneurysm, with severe hypernatremia (171 mmol/L) and a plasma osmolality of 348 mosm/kg. He was awake and had no interest in fluid intake. After initial correction, a thirst test for 36 hours was performed. Plasma osmolality rose from 295 to 320, urine osmolality rose from 220 to 700 mosm/kg, while plasma vasopressin levels increased more than 3-fold. Throughout the test the patient did not exhibit appreciable thirst. The intact osmoregulation of vasopressin as evidenced by the plasma levels and the elicited renal response, indicates that a selective acquired disturbance of thirst is present. Whether the thirst center is destroyed or/and thirst recognition (frontal lobe affection) is disturbed primarily, can not be decided.

Topics: Aneurysm, Ruptured; Brain Mapping; Cerebral Hemorrhage; Frontal Lobe; Humans; Hypernatremia; Intracranial Aneurysm; Magnetic Resonance Imaging; Male; Middle Aged; Perceptual Disorders; Postoperative Complications; Thirst; Vasopressins; Water-Electrolyte Balance

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

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

Hypernatremia was detected in a dog that was evaluated because of seizures. During hospitalization, the dog was fully conscious and remained hypernatremic when drinking voluntarily and when water was added to the food. Urine volume increased and urine osmolality decreased during an infusion of hypertonic saline (2.5% NaCl) solution, despite development of progressive hyperosmolality. There was no correlation between plasma antidiuretic hormone concentration and osmolality during the infusion study. The dog released antidiuretic hormone normally after nonosmotic stimulation (ie, apomorphine administration). These findings allowed a diagnosis of hypodipsic hypernatremia caused by destruction of hypothalamic osmoreceptors. At necropsy, there was hydrocephalus, atrophy of the septum pellucidum, and neuraxonal dystrophy of the cuneate nuclei. The underlying neurologic disease responsible for the CNS lesions could not be determined, but hydrocephalus may have led to pressure atrophy in the region of the hypothalamus that contains osmoreceptors.

Topics: Animals; Brain Diseases; Dog Diseases; Dogs; Drinking; Fluid Therapy; Hypernatremia; Hypothalamus; Male; Osmolar Concentration; Seizures; Vasopressins; Water-Electrolyte Imbalance

Studies to assess the relationship between plasma arginine vasopressin concentration (Pavp) and plasma osmolality (Posm) were performed on an elderly patient with dementia who developed severe hypernatremia due to inadequate water intake following a debilitating hip fracture. Serum sodium concentrations were 174 and 196 mEq/L on two consecutive hospital admissions. During the second of these admissions, sequential measurements of Pavp and Posm were obtained as hypernatremia was gradually corrected. Pavp during this period was correlated with Posm (r = 0.887, P < 0.01), but was low despite the presence of hyperosmolality and volume depletion. Pavp decreased from 0.56 microU/mL to 0.18 microU/mL as Posm decreased from 396 to 338 mOsm/kg H2O. The regression line of this relationship intercepted the abscissa at 320 mOsm/kg H2O. Hypertonic sodium chloride infusion to reassess this relationship 2 days following the correction of hypernatremia increased Pavp only to 0.67 microU/mL while increasing Posm from 297 to 316 mOsm/kg H2O. Nevertheless, Pavp and Posm were significantly correlated (r = 0.937, P < 0.001). The slope of the regression line was 0.031, and Posm at the abscissal intercept was 292 mOsm/kg H2O. A similar increase in Posm from 290 to 310 mOsm/kg H2O during hypertonic sodium chloride infusion 11 days following the correction of hypernatremia increased Pavp to 1.95 microU/mL (r = 0.786, P < 0.05). The magnitude of the increase in Pavp at this time was equivalent to that previously observed in studies of normal subjects. The slope (0.048) and abscissal intercept (280 mOsm/kg H2O) of linear regression were also consistent with observations in studies of normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aged; Aged, 80 and over; Dehydration; Humans; Hypernatremia; Male; Regression Analysis; Vasopressins; Water-Electrolyte Balance

To test the hypothesis that enhanced expression of the vasopressin gene accompanies the development of deoxycorticosterone acetate (DOCA)-salt hypertension in the rat and to compare the response with those observed during chronic hypernatremia.. Transcript levels were determined by measurement of vasopressin messenger RNA (mRNA) in the supraoptic nucleus and paraventricular nucleus by in situ hybridization, autoradiography and image analysis. Plasma, urinary and pituitary vasopressin were determined by radioimmunoassay.. High-resolution localization and measurement of specific mRNA in the supraoptic and paraventricular nuclei before and during development of DOCA-salt hypertension were compared with corresponding results in both age-matched controls and normal rats that drank hypertonic saline.. Vasopressin mRNA levels were increased in the paraventricular nucleus during the established and chronic stages of DOCA-salt hypertension, but were unchanged in the supraoptic nucleus. Urinary excretion of vasopressin was increased in the prehypertensive, established and chronic phases of DOCA-salt hypertension, whereas plasma vasopressin levels were increased only in the chronic phase. Pituitary vasopressin levels were unchanged. In comparative studies, vasopressin mRNA levels in both the supraoptic and paraventricular nuclei and plasma vasopressin were significantly increased in normal rats drinking 2% saline.. Whereas hypernatremic rats showed markedly elevated vasopressin transcripts in the supraoptic and paraventricular nuclei, DOCA-salt hypertension is associated with increased vasopressin mRNA in the paraventricular but not the supraoptic nucleus. The response in the paraventricular nucleus may explain part of the increased peripheral vasopressin levels and suggests that this nucleus makes a critical contribution to the pathogenesis of DOCA-salt hypertension.

Topics: Animals; Desoxycorticosterone; Gene Expression; Hypernatremia; Hypertension; Male; Models, Cardiovascular; Paraventricular Hypothalamic Nucleus; Pituitary Gland; Rats; Rats, Sprague-Dawley; RNA, Messenger; Supraoptic Nucleus; Transcription, Genetic; Vasopressins

One purpose of this report is to illustrate that calculating the rate of excretion of osmoles in the urine can be of value in the differential diagnosis of hypernatremia and polyuria. A second purpose is to illustrate a clinical example where the osmolality of the urine did not reflect the lack of action of ADH. A patient with ethanol intoxication seemed to have central diabetes insipidus on clinical grounds. However, the osmolality of the urine was 287 mosm/kg H2O, a value which made this diagnosis unlikely. Since the concentration of ethanol in plasma was 119 mmol/L, we suspected that the urine contained an appreciable quantity of alcohol; this might obscure the lack of action of ADH. A study was performed to document the quantitative relationship between the concentrations of ethanol in plasma and urine. The concentration of ethanol in the urine was approximately 1.4-fold greater than in plasma. Using this correction factor, the osmolality of the urine adjusted for ethanol in the patient was only 120 mosm/kg H2O, a value more consistent with the diagnosis of central diabetes insipidus.

Topics: Adult; Alcoholic Intoxication; Artifacts; Diabetes Insipidus; Diagnosis, Differential; Diuresis; Ethanol; False Negative Reactions; Female; Humans; Hypernatremia; Osmolar Concentration; Pituitary Gland, Posterior; Polyuria; Urinalysis; 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

We describe two sisters with chronic hypernatremia, lack of thirst, and inappropriate osmoregulated vasopressin secretion. Only one sister, who presented with microcephaly and developmental delay, showed signs of dysplasia of the midline structures (ie, septum pellucidum and corpus callosum) and a large intracranial cyst. Neither sister showed any signs of thirst, even when osmolality exceeded 337 mmol/kg. In both patients, the vasopressin secretion did not respond to either osmotic or nonosmotic stimuli or was suppressed by a water load. Plasma osmolality values returned to normal after treatment with forced hydration and a vasopressin analogue, desamino-D-arginine vasopressin. These findings indicate a severe defect in the hypothalamic osmoreceptors that control thirst and vasopressin secretion. To our knowledge, this is the first report of such a disorder in two sisters.

Topics: Aldosterone; Blood Urea Nitrogen; Female; Humans; Hypernatremia; Hypothalamus; Inappropriate ADH Syndrome; Infant; Osmolar Concentration; Renin; Sodium; Spasms, Infantile; Thirst; Vasopressins

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

We reported two infants with hydranencephaly and chronic hypernatremia. Their plasma sodium concentration gradually increased during the first week and remained between 150-160 mEq/L thereafter. They showed no signs of thirst. A water deprivation test demonstrated low urine osmolality and low plasma ADH concentration despite markedly elevated plasma osmolality in both cases. Urine was significantly concentrated when vasopressin was given. Thus, it was concluded that both thirst mechanism and ADH secretion were disturbed in these two cases. ADH producing cells, the thirst center and the osmoreceptor are all located in the hypothalamus. Radiographic measures showed dysplasia of the hypothalamus, providing the anatomical basis for their dysfunction.

Topics: Anencephaly; Chronic Disease; Female; Humans; Hydranencephaly; Hypernatremia; Infant, Newborn; Sodium; Vasopressins

Herein we will describe a case of chronic hypernatremic-hyperosmolar syndrome with cerebral localization of systemic sarcoidosis. Several determinations of plasma arginine vasopressin (p-AVP) at various plasma sodium levels were carried out in this patient. During the study p-AVP values varied between 2.6 and 9.5 pg/ml. A high percentage of them was related to plasma osmolality, pointing out that p-AVP secretion was osmotically mediated. This behavior is in contrast with the tendency of hypernatremic patients previously reported in the literature, in whom p-AVP values were inappropriately low for the corresponding degree of plasma osmolality, suggesting that vasopressin secretion was not influenced by osmotic stimulation. Furthermore, our case, unlike those previously described, showed high values of urinary osmolality. In conclusion, our patient represents, in essence, the 'middle' of the spectrum of the hypodipsic-hypernatremic syndrome, because she is to be inserted between the majority of patients who have little or no osmotically mediated AVP release and the case of a child, recently described, who had completely normal AVP secretion.

Topics: Arginine Vasopressin; Brain Diseases; Chronic Disease; Female; Humans; Hypernatremia; Middle Aged; Osmolar Concentration; Sarcoidosis; Syndrome; Thirst; Vasopressins

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

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

The authors describe a case of hypodipsia and severe hypernatremia most probably secondary to hydrocephalus in a 22-year-old man in the absence of abnormalities of ADH secretion or metabolism. The patient became hypernatremic only in situations when the decreased spontaneous fluid intake was insufficient to replace that lost caused by sweating or vomiting. Adequate hydration returned the sodium value to normal.

Topics: Adult; Humans; Hydrocephalus; Hypernatremia; Male; Thirst; Vasopressins; Water Deprivation

A case of a patient with the syndrome of chronic hypernatremia and hypodispia due to hypothalamic tumor was studied to evaluate the change of ADH response to plasma osmolality during the clinical course. A 23-year-old man was admitted for investigation of anorexia, hypodipsia and gait disturbance. Examination showed memory disturbance and generalized muscle weakness. Investigation showed marked hypernatremia (177 mEq/l) and hypopituitarism. Water loading test showed that ADH was not stimulated by hyperosmolality but continued to be secreted at a more or less constant level approximating normal basal state. CT scan revealed hypothalamic tumor. The tumor was suspected to be germinoma due to its radiosensitivity and high serum hCG level. After irradiation, the tumor lesion disappeared. ADH secretion came to be responsive to changes in osmolality but the response of the system was markedly reduced compared with the normal response, and hypodipsia and hypernatremia still remained. We conclude that the adipsia and complete destruction of the osmoreceptor in the patient caused marked hypernatremia and the destruction of ADH osmostat improved partially after irradiation. We believe it very useful for analyzing the disturbance of osmoregulatory system to evaluate the relationship of plasma ADH to plasma osmolality.

Topics: Adult; Dysgerminoma; Humans; Hypernatremia; Hypothalamic Neoplasms; Male; Osmolar Concentration; Thirst; Vasopressins

Topics: Atrial Natriuretic Factor; Clofibrate; Craniopharyngioma; Female; Humans; Hydrocortisone; Hypernatremia; Middle Aged; Pituitary Neoplasms; Postoperative Complications; Vasopressins

Dehydrated patients usually present with an elevated serum urea level, owing in part to increased renal reabsorption of urea mediated by antidiuretic hormone (ADH). We carried out a study to examine whether, during dehydration, the variations in the serum urea level could discriminate patients with central diabetes insipidus (CDI) from those with dehydration not due to CDI. We studied retrospectively 27 episodes of dehydration in 23 patients with CDI and 14 episodes in 14 patients without CDI. The mean serum urea level was 2.9 mmol/L in the CDI group and 15.4 mmol/L in the patients without CDI (p less than 0.001); the mean serum sodium level was 155 mmol/L in both groups. All the patients with CDI had a sodium/urea ratio greater than 24.2, whereas the ratio was less than 21.7 in all the patients without CDI. In the patients with CDI a positive correlation was found between the magnitude of diuresis and the percentage decrease in the serum urea level compared with the level before dehydration (p less than 0.001). In the patients with CDI the serum urea level returned to the level before dehydration after the administration of vasopressin; a striking increase in the clearance of urea, which exceeded the creatinine clearance, was observed during dehydration in the three patients in whom clearance studies were done. The results suggest that serum urea values can be used to distinguish patients dehydrated because of CDI from those with hypertonic dehydration but without ADH deficiency and that during dehydration the net reabsorption of urea is dependent on the renal action of ADH.

Topics: Adult; Creatinine; Dehydration; Diabetes Insipidus; Female; Fluid Therapy; Humans; Hypernatremia; Male; Middle Aged; Osmolar Concentration; Prospective Studies; Retrospective Studies; Urea; Vasopressins

We describe a patient with chronic hypernatraemia (plasma sodium 148-155 mmol/l) and partial nephrogenic diabetes insipidus who had received prolonged lithium treatment. Despite stopping the drug for one year the abnormalities remained. Infusion of hypertonic saline (NaCl 855 mmol/l) allowed the characterization of osmoregulation of thirst and vasopressin secretion. Linear regression analysis of plasma vasopressin and osmolality defined the function, pAVP = 0.27 (pOsm - 301), and analysis of thirst measured by a visual analogue scale and plasma osmolality, the function, thirst = 0.16 (pOsm - 302) where pAVP and pOsm represent plasma arginine vasopressin and osmolality respectively. The slopes of the regression lines which describe the sensitivity of the osmoreceptors were within the normal range, but both abscissal intercepts, which define the thresholds for vasopressin release and thirst, were markedly elevated in comparison to normal (upper limit less than 290 mOsm/kg). Other investigations of electrolytes, anterior pituitary function and high definition computed tomographic scanning of hypothalamo-pituitary region were all normal. We conclude that this patient's chronic hypernatraemia was due to resetting of the osmostats for both vasopressin release and thirst, a rarely described mechanism to account for hypernatraemia. Although it is probable that the partial nephrogenic diabetes insipidus was related to prolonged lithium therapy, the cause of the reset osmostats remains unclear.

Topics: Aged; Diabetes Insipidus; Female; Humans; Hypernatremia; Thirst; Vasopressins; Water-Electrolyte Balance

Drinking rapidly abolishes thirst and vasopressin secretion in dehydrated humans before major changes in plasma osmolality are observed. We studied the effects of drinking on plasma vasopressin and thirst in seven healthy volunteers rendered hypernatremic by the infusion of hypertonic (855 mmol/l) sodium chloride solution. Thirst was measured on a visual analogue scale (0-10 cm). Infusion of hypertonic saline caused linear increases in plasma osmolality (289 +/- 1 to 306 +/- 1 mosmol/kg, mean +/- SE, P less than 0.001), plasma vasopressin (0.6 +/- 0.2 to 6.4 +/- 1.9 pmol/l, P less than 0.001), and thirst (1.4 +/- 0.4 to 7.4 +/- 0.5 cm, P less than 0.001). Water was allowed 15 min after cessation of the infusion, and within 5 min of drinking both plasma vasopressin and thirst were significantly lower than postinfusion. After 20 min of drinking, plasma vasopressin had fallen from 6.5 +/- 0.9 to 1.3 +/- 0.3 pmol/l (P less than 0.001) and thirst from 7.7 +/- 0.5 to 1.0 +/- 0.2 cm (P less than 0.001) despite no significant change in plasma osmolality (306 +/- 0.9 to 304 +/- 0.8 mosmol/kg, P = 0.17), and the drinking of 1,200 +/- 60 ml of water, over 85% of the mean cumulative water intake in the 30-min drinking period. Control studies in the same subjects showed comparable rises in plasma vasopressin, plasma osmolality, and thirst during hypertonic saline infusion but no fall in any of these parameters during an equivalent 30-min period after the infusions, during which water was withheld.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Drinking; Humans; Hypernatremia; Male; Osmolar Concentration; Saline Solution, Hypertonic; Sodium; Thirst; Vasopressins

Topics: Aged; Humans; Hypernatremia; Male; Thirst; Vasopressins; Water-Electrolyte Imbalance

Patients with essential hypernatremia maintain urinary concentrating ability despite plasma hyperosmolality and low plasma vasopressin concentrations. We investigated renal sensitivity to ultralow dose vasopressin infusions in two patients with a syndrome of hypodipsia, hypernatremia with selective osmoreceptor dysfunction, early puberty, and aggressive behavior. The patients were water loaded until a hypotonic diuresis was established. Vasopressin was infused in stepwise increments from 0.4-12 fmol/kg X min. Both patients had increased renal sensitivity to vasopressin, achieving negative free water clearance at infusion rates of 0.4 and 4 fmol/kg X min (normal greater than or equal to 6). Treatment for 3 months with 1-desamino-8-D-arginine vasopressin (DDAVP) led to an improvement in behavior and the reporting, for the first time, of a sensation of thirst. After DDAVP therapy both patients had a reduction of their renal sensitivity to infused vasopressin. We conclude that untreated patients with essential hypernatremia have increased renal sensitivity to vasopressin which is reduced by DDAVP administration.

Topics: Adolescent; Adult; Deamino Arginine Vasopressin; Dose-Response Relationship, Drug; Drug Therapy, Combination; Humans; Hypernatremia; Kidney; Male; Osmolar Concentration; Vasopressins; Water-Electrolyte Balance

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

A case of hypodipsic hypernatremia in a 16-month-old Japanese boy is reported. Partial antidiuretic hormone deficiency was present. Computed tomography of the brain revealed absence of septum lucidum. No ophthalmological abnormality could be found. He had hyposmia, which has not been reported previously in association with hypernatremia due to hypodipsia. Forced fluid administration and nasal 1-deamino-8-d-arginine vasopressin treatment could maintain serum electrolyte levels within normal ranges. However, episodes of hypernatremia could not be completely avoided while he was treated with 1-deamino-8-d-arginine vasopressin and ad libitum oral fluid.

Topics: Central Nervous System; Diabetes Insipidus; Humans; Hypernatremia; Infant; Male; Olfactory Pathways; Septum Pellucidum; 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

A 17-year-old schizophrenic developed severe hypernatremia during a period of psychosis. The thirst-deficient abnormality that caused this hypernatremia resolved when his psychosis improved. The primary disorders causing a thirst deficiency leading to hypernatremia fall into three categories: lesions of the central nervous system, mineralocorticoid excess, and drug side effects. None of these disorders was found in our patient. We conclude that psychosis can severely impair the thirst mechanism directly.

Topics: Adolescent; Dehydration; Humans; Hypernatremia; Male; Osmolar Concentration; Schizophrenia; Thirst; Vasopressins

Topics: Brain; Brain Diseases; Calcinosis; Child, Preschool; Drinking Behavior; Humans; Hypernatremia; Male; Sodium; Thirst; Tomography, X-Ray Computed; Vasopressins; Water-Electrolyte Balance

Topics: Aged; Diabetes Insipidus; Female; Humans; Hypernatremia; Osmolar Concentration; Thirst; Vasopressins; Water-Electrolyte Balance

Hypernatraemic states are associated with an increased risk of thrombosis. To examine the relative contributions of sodium and vasopressin, we infused hypertonic saline in 11 male volunteers and measured the effect on factor VIII (FVIII), euglobulin clot lysis time (ELT) and fibrinopeptide A (FPA) generation. Samples were taken pre-infusion, hourly during a 3h infusion of 450 ml 6M saline and one hour after the infusion had stopped. Mean plasma osmolality (SEM) rose from 287(0.7) to 302(10) mOsm after 3h (p less than 0.01). Plasma vasopressin concentrations rose from 1.0(0.3) to 4(0.94) pg/ml over 3 hr (p 0.01). Plasminogen activator activity (10(6)/ELT2) rose from 65(10) to 372(55) units (p less than 0.001). There was a highly significant correlation between plasma osmolality and plasminogen activator activity (r = 0.5 p less than 0.0001). FPA generation time shortened from 7.2(0.4) to 5.4(0.6) min after 2h and 5.3(0.6) after 4h (n = 6). Values for FPA after 4 min incubation steadily increased from 5.8(1.2) to 14.3(4.6) pmol/ml during the infusion but differences failed to achieve statistical significance. FVIIIC (1 stage) remained constant at 75(5.5%) during the infusion. There was a small and statistically insignificant increase in FVIII RiCof after 3h and FVIII RAg decreased slightly. The results suggest that hypernatraemia and increasing plasma aVP concentrations produce changes in haemostatic function consistent with a hypercoaguable state. The mechanisms for the effect are unclear. These changes in haemostatic function might contribute to the thrombo-embolic complications of conditions such as hyperosmolar coma in diabetes mellitus or severe heatstroke in which degrees of hypernatraemia occur.

Topics: Factor VIII; Fibrinolysis; Humans; Hypernatremia; Kinetics; Male; Osmolar Concentration; Risk; Saline Solution, Hypertonic; Serum Globulins; Sodium Chloride; Thrombosis; Vasopressins

Topics: Adult; Aged; Body Weight; Diagnosis, Differential; Extracellular Space; Female; Glucose; Glycogen; Humans; Hypernatremia; Intracellular Fluid; Kidney Concentrating Ability; Male; Middle Aged; Vasopressins; Water Loss, Insensible

An infant with microcephaly and delayed development was found to have chronic asymptomatic hypernatremia. Computerized brain tomography disclosed dysplasia of the midline structures, septum pellucidum and corpus collosum. Evaluation revealed defective osmoregulation, hypothalamic hypothyroidism, and hypogonadotropinism. He showed no desire to drink at plasma osmolalities over 330 mOsm/kg. His plasma vasopressin levels (less than or equal to 1.4 pg/ml) were inappropriately low relative to his high levels of plasma osmolality (greater than or equal to 310 mOsm/kg), which might be accounted for by either deficient neurohypophyseal vasopressin stores or disturbance of the hypothalamic osmoreceptors governing vasopressin. The first possibility was ruled out by demonstrating normal vasopressin response (167 pg/ml) to nonosmotic (emetic) stimulation. Under baseline conditions, his urine was concentrated up to 747 mOsm/kg and urine volume was low. With water loading, maximal water diuresis developed (urine osmolality 68 mOsm/kg), but his plasma osmolality remained in the hyperosmolar range (312 mOsm/kg). Treatment with a vasopressin analogue, desamino-D-arginine vasopressin, and forced hydration restored plasma osmolality and plasma sodium to normal. These findings indicate a severe defect in the hypothalamic osmoreceptors controlling thirst and vasopressin secretion with normal vasopressin stores and preserved vasopressin responsiveness to nonosmotic stimuli. To our knowledge, this report provides the first documentation of selective osmoreceptor defect in conjunction with congenital dysplasia of midline brain structures.

Topics: Brain; Deamino Arginine Vasopressin; Dehydration; Developmental Disabilities; Humans; Hypernatremia; Infant; Male; Microcephaly; Osmolar Concentration; Thirst; Vasopressins

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

Topics: Adult; Body Fluids; Humans; Hypernatremia; Male; Posture; Sensory Receptor Cells; Vasopressins; Water-Electrolyte Imbalance

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

An adolescent boy with essential hypernatremia, absent corpus callosum, mental retardation, hypodipsia, and partial diabetes insipidus with "inappropriate" ADH regulation and secretion was studied regarding factors controlling ADH and neurophysin release. Persistent hyperosmolality was noted while on 100 mEq sodium intake daily. Endogenous vasopressin activity was demonstrated after prolonged water deprivation. Hypertonic saline infusion produced increased volumes but dilute urine. Aqueous pitressin increased urinary osmolality, decreased serum osmolality, urine flow rate, and free water clearance. Stable water diuresis was induced by water loading and on normal saline infusion. Nicotine-stimulated neurophysin remained unexpectedly low and below the level of detectability when sampled during the physiologic studies, whereas oestrogen-stimulated neurophysin was elevated during oestrogen stimulation, water loading, and orthostasis procedures. Plasma vasopressin was suppressed with water loading but remained suppressed 90 min after tilt table testing. These data indicate impairment of the osmoreceptor mechanism: however, since the patient had a normal response of oestrogen-stimulated neurophysin, that part of the neurohypophysis appears intact. Chlorpropamide was effective in alleviating the hyperosmolar state acutely and maintained normal osmolar concentrations during two years of therapy.

Topics: Adolescent; Chlorpropamide; Diabetes Insipidus; Diuresis; Electrolytes; Fluid Therapy; Humans; Hypernatremia; Intellectual Disability; Male; Neurophysins; Osmolar Concentration; Posture; Saline Solution, Hypertonic; Vasopressins; Water

A syndrome of chronic hypernatremia (range 148 to 161 mmoles/l) and partial hypopituitarism (growth hormone and gonadotropin deficiencies) is reported in a 27 year-old man with sarcoid hypothalamic involvement. The patient did not complain of thirst and spontaneous fluid intake was not sufficient to restore the serum sodium to normal. However, when larger amounts of water were given (50 ml/kg for 180 min), the plasma osmolality returned to normal values in 3 hours. Blood volume values were found subnormal on two occasions on free diet (63 and 74% of the theorical normal values) and plasma renin activity was elevated (22 ng/ml/hour). Plasma vasopressin (AVP) concentrations (range < 1 to 1.9 pg/ml) were inappropriately low for the degree of plasma osmolality and remained markedly subnormal when hypertonic saline was infused (NaCl 5%, 10 ml/min for 60 min). However, the secretory stores and hemodynamic control of AVP release were intact since a rise in plasma AVP to 10.8 pg/ml was observed after induction of arterial hypotension with sodium nitroprusside infusion. These results provide further direct evidence fo the dysfunction of the thirst mechanism and the osmotic contol of AVP release. They support the concept that osmoreceptor areas are anatomically distinct from the neurohypophyseal AVP secretory system and that neural inputs from baroreceptor and osmoreceptor cells are completely separated.

Topics: Adult; Blood Volume; Fluid Therapy; Humans; Hypernatremia; Hypopituitarism; Hypotension; Hypothalamus; Male; Nitroprusside; Osmolar Concentration; Renin; Sarcoidosis; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Aldosterone; Angiotensin II; Blood Pressure; Chronic Disease; Humans; Hypernatremia; Male; Middle Aged; Renin; Vasopressins

Topics: Humans; Hypernatremia; Thirst; Vasopressins

Topics: Adolescent; Adult; Child; Female; Humans; Hypernatremia; Male; Middle Aged; Muscular Dystrophies; Saline Solution, Hypertonic; Sodium; Vasopressins; Water

We have studied an infant (female) with a persisting hypernatremia and adipsia, examined for the first time at the age of five months. The funtional test carried out showed an insensibility of the osmoreceptors for very important changes in POsm. carryng with them a lack of response of the ADH. Neuroradiological studies demostrated hydrocephalia secondary to a stenosis of the aqueduct of Silvio. Treatment with chlorpropamide proved effective. The literature is being revised comparing out results with those of other authors.

Topics: Chlorpropamide; Dehydration; Diuresis; Female; Humans; Hydrocephalus; Hypernatremia; Hypothalamo-Hypophyseal System; Infant; Osmolar Concentration; Radiography; Saline Solution, Hypertonic; Vasopressins; Water-Electrolyte Balance

The pathogenesis of the rare hypernatremia, usually described in the literature as "neurogenic" or "essential" hypernatremia, consists of defective thirst mechanism either alone or in combination with impaired osmoregulation of ADH release. As etiology, disturbances of the neoplastic, vascular and degenerative type and malformations in the hypothalamic area are known. In patients with the hypodipsia-hypernatremia syndrome, dysfunction of the anterior pituitary lobe, obesity, abnormal regulation of body temperature, psychomotor retardation and episodic muscular weakness are frequently encountered as additional abnormalities. A 6-year-old patient is described with hypodipsia-hypernatremia syndrome manifest for 3 years. Besides hypernatremia, hypodipsia and the relative insensitivity of the osmoreceptors regulating ADH release, elevated body temperature, polyphagia and obesity, partial hypothalamic-hypophyseal dysfunction, lethargy and psychomotor retardation are the principal findings. An inflammatory lesion or one occupying an intracranial space was not demonstrable until now. Under forced water intake and hypocaloric diet the patient has progressed well with nearly complete normalization of the hypernatremia, body temperature and obesity.

Topics: Child; Diet, Reducing; Glomerular Filtration Rate; Humans; Hypernatremia; Hypothalamus; Kidney Concentrating Ability; Kidney Function Tests; Male; Pituitary Gland; Syndrome; Thirst; Vasopressins; Water; Water-Electrolyte Balance

A 49-year-old man was submitted to neurosurgery for a cranio-pharyngioma. The lesion, which appeared to involve the antero-inferior wall of the third ventricle, caused lack of appropriate antidiuretic hormone (ADH) release in response to hypernatraemia and plasma hyperosmolality. The probable mechanism of this hypothalamic syndrome is suggested.

Topics: Craniopharyngioma; Humans; Hypernatremia; Hypothalamus; Male; Middle Aged; Osmolar Concentration; Pituitary Neoplasms; Postoperative Complications; Potassium; Sodium; 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

Two patients ( 1 7/12-year-old and 1 11/12-year-old girls) with chronic hypernatremia were studied. Neuroradiological findings and mildine facial defects showed characteristic features of holoprosencephaly. Water deprivation tests showed clear evidence of antidiuretic hormone (ADH) secretion. The responses to hypertonic saline infusion and acute water loading were abnormal. In one case, the impaired osmotic regulation of ADH secretion was demonstrated by measuring urinary ADH by a radioimmunoassay. In this case, the volume regulation of ADH secretion seemed to be also incomplete since chronic water loading for a period of six days induced water retension.

Topics: Brain; Cerebral Angiography; Chronic Disease; Female; Humans; Hypernatremia; Infant; Osmolar Concentration; Saline Solution, Hypertonic; Tomography, X-Ray Computed; Vasopressins; Water

A 23-year-old man, diagnosed as having a pituitary adenoma at the age of 17 and received an operation 1 month ago showed a fluctuating hypernatremia and hypodipsia. The water deprivation, water load and hypertonic saline infusion tests were carried out. After a 14-hr water deprivation test, plasma osmolality was 310 mOsm/kg, plasma ADH was 1.5 microunits/ml, and urine osmolality was 591 mOsm/kg. On the water load test subsequently performed, the plasma osmolality decreased to 297 mOsm/kg, but the urine was still hypertonic. Infusion of 2.5% saline solution elicited paradoxically a marked diuresis and dilution of urine despite the elevàtion of plasma osmolality. On the treatment with carbamazepine and clofibrate, the urinary osmolality increased, the hypernatremia was normalized, and a marked natriuresis was elicited with a gain in body weight. These results suggested that the secretion of ADH is regulated by changes in blood volume rather than by the plasma osmolality in this patient. The hypernatremia may be explained as a disturbance or lack of osmoreceptor function for ADH release and the loss of thirst sensation, though the volume receptor still remains functioning for ADH secretion. Depletion of the extracellular fluid volume may be another contributing factor to the elevation of serum sodium level by enhancing the reabsorption of sodium from renal tubules.

Topics: Adult; Blood Volume; Carbamazepine; Clofibrate; Humans; Hypernatremia; Male; Osmolar Concentration; Perfusion; Pituitary Diseases; Saline Solution, Hypertonic; Vasopressins; Water Deprivation

In non-hydrated goats prolonged (3 h, 0.02 ml/min) intracerebroventricular (IVT) infusion of 0.35 M glycerol depressed the plasma vasopressin level during the entire infusion period which resulted in a conspicuous water diuresis outlasting the infusion by about 20 min. Since no compensatory drinking occurred during this sustained water diuresis it gradually induced pronounced dehydration (loss of greater than 1 liter of total body water causing 5% increase in plasma [Na+] and osmolality). The same degree of dehydration was in other experiments induced by water deprivation. It then caused a 5-fold increase in plasma vasopressin level. Corresponding IVT infusions of 0.35 M d-glucose depressed plasma vasopressin level only during the first half of the 3 h infusion period. Consequently, the resulting water diuresis was transient and subsided before the glucose infusion was finished. Plasma renin activity increased during the IVT glycerol infusion and during water deprivation, but was largely unaffected by IVT glucose. Both IVT glycerol and glucose decreased renal sodium excretion. The possibility is discussed that the pronounced ability of IVT glycerol to depress the vasopressin release and thirst is not only due to dilution induced reduction of CSF [Na+], but also to an influence of glycerol on choroidal and/or transependymal Na+-transporting mechanisms.

Topics: Animals; Blood; Dehydration; Diuresis; Female; Glucose; Glycerol; Goats; Hypernatremia; Injections, Intraventricular; Osmolar Concentration; Potassium; Sodium; Vasopressins; Water Deprivation

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

Two patients with hypodipsia and hypernatremia are described. The first patient, whose hypodipsia was of unknown cause, developed hypernatremia unless large volumes of fluid were urged upon him; upon treatment with chlorpropamide normal serum sodium levels were achieved with spontaneous fluid intake. The second patient had hypodipsia and diabetes insipidus resulting from a craniopharyngioma. Treatment with vasopressin and a prescribed daily water intake resulted in frequent hyper- and hyponatremia, but treatment with chlorpropramide yielded serum sodium values which were more often normal and less variable. In neither patient could the improved water regulation be attributed to an effect of chlorpropamide on renal water excretion. Possible mechanisms for the effect of chlorpropamide on thirst are discussed.

Topics: Adult; Chlorpropamide; Dehydration; Diabetes Insipidus; Humans; Hypernatremia; Male; Sodium; Thirst; Vasopressins

A 4-month old child presented with facial malformations and severe hypernatremia. Hypernatremia was secondary to diabetes insipidus due to a disorder of ADH secretion, associated with cerebral malformations. Clofibrate treatment was ineffective. However, after the patient was treated by a low osmotic residue diet, an increased water-intake and hydrochlorothiazide, natremia became normal and growth resumed.

Topics: Abnormalities, Multiple; Clofibrate; Diabetes Insipidus; Face; Humans; Hydrochlorothiazide; Hypernatremia; Infant; Limbic System; Male; Vasopressins

The authors report the case of 13 year old girl presenting with chronic hypernatremia. This case should be considered as either neurogenic or essential hypernatremia. Partial diabetes insipidus and hypodipsia hypernatremia. Partial diabetes insipidus and hypodipsia are the cause of chronic hypovolemia and a new homeostasis with an exceptionally high level of sodium (isoosmotic point 154 mEq/l). No cause was found and in particular, the search for a cerebral disease was until now proved negative.

Topics: Adolescent; Blood Volume; Chlorpropamide; Diabetes Insipidus; Female; Humans; Hydrochlorothiazide; Hypernatremia; Thirst; Vasopressins

Topics: Adolescent; Brain Neoplasms; Homeostasis; Humans; Hypernatremia; Male; Pineal Gland; Vasopressins; Water

A patient with the syndrome of chronic hypernatremia (serum Na+: mean = 154, range 139-184 mEq/l, n = 30) and hypodipsia due to a hypothalamic injury was studied to evaluate osmolar and baroreceptor control of arginine vasopressin (AVP) secretion. Resting plasma AVP levels measured by radioimmunoassay were inappropriately low for the degree of plasma hyperosmolality: range = less than 0.5-2.1 pg/ml, n = 10, with corresponding levels of plasma osmolality (P osM) greater than 300 m osmol/kg, suggesting either direct damage to the AVP synthesis and storage area or impaired afferent osmoreceptor function. Direct pituitary damage seemed unlikely, since anterior pituitary function was normal by standard testing. The existence of adequate neurohypophyseal stores of AVP was demonstrated by baroreceptor stimulation with the hypotensive agent trimethaphan (Arfonad): plasma AVP rising to 50.0 pg/ml during transient hypotension (BP = 70/0). Osmoreceptor function was evaluated during acute water loading followed by hypertonic saline infusion. During hypertonic saline infusion plasma AVP levels correlated with P osM (R = .87, P less than .01, n = 8), suggesting some residual osmotic regulation of AVP release. The osmotic threshold for AVP release (the x-axis intercept of the plasma AVP-P osM regression line) was not higher than normal. However, the AVP levels throughout this study remained markedly subnormal for the degree of plasma hyperosmolality (maximum plasma AVP = 1.9 PG/ML when P os M = 327 M OSMOL/KG). Since a substantial amount of AVP was released with baroreceptor stimulation, the inadequate rise in plasma AVP level with hyperosmolality indicates that afferent input from the osmoreceptor/thirst area of the hypothalamus is selectively impaired in this patient. These findings directly demonstrate a dissociation of osmoreceptor function from the AVP secretory apparatus in man.

Topics: Arginine Vasopressin; Humans; Hypernatremia; Hypertonic Solutions; Hypothalamus; Iatrogenic Disease; Male; Middle Aged; Pressoreceptors; Sodium Chloride; Trimethaphan; Vasopressins; Water-Electrolyte Balance

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

Topics: Adolescent; Adult; Brain Diseases; Diabetes Insipidus; Female; Humans; Hypernatremia; Kidney; Male; Middle Aged; Reference Values; Sodium; Vasopressins; Water-Electrolyte Balance

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: Chlorothiazide; Dehydration; Diabetes Insipidus; Fever of Unknown Origin; Humans; Hypernatremia; Infant, Newborn; Infant, Newborn, Diseases; Male; Renal Tubular Transport, Inborn Errors; Specific Gravity; Vasopressins

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 7-year-old girl twice developed severe hypernatremia (serum sodium values up to 194 mEq/l) without obvious cause. The ability of her kidneys to conserve water was normal, and increasing her plasma osmolality stimulated an appropriate ADH response. Unable to excrete a water load, her kidneys continued to conserve water even with a serum sodium concentration of 133 mEq/l. She was never thirsty and did not ingest sufficient fluid by choice. Although there was no demonstrable anatomic lesion, we postulate a localized defect of her thirst center. This may have modified release of ADH and resulted in an inability to dilute the urine by interrupting a pathway that could exist from the thirst center to the supraoptic nuclei. A therapeutic regimen based on these studies has prevented further hypernatremia.

Topics: Child; Child, Preschool; Drinking; Female; Glucose; Humans; Hypernatremia; Infusions, Parenteral; Recurrence; Saline Solution, Hypertonic; Thirst; Vasopressins; Water-Electrolyte Imbalance

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

Topics: Brain Diseases; Humans; Hypernatremia; Hypothalamus; Vasopressins; Water-Electrolyte Balance

This is a case report involving a 9 year old girl with a teratoma that infaced mainly the bilateral hypothalamus. The girl was observed for 14 months after partial surgical removal. During that time she showed aphagia, adipsia, hypopituitarism, and visual and psychiatric disturbances. Severe hypernatremia also was present, even though large amounts of 5% glucose solution without salt were given I.V. Food and water were given by nasal gastric gavage and later gavage via gastric fistula, but the hypernatremia remained unchanged. When pitressin or spironolacton (anti-aldosterone) were administered, remarkable effect on the hypernatremia couldn't be found. Upon autopsy it was discovered that the bilateral hypothalamus, left subthalamus and ventral part of the thalamus were invaded by teratoma. Comparing many similar clinical reports and manifestations of hypothalamic lesions in experimental animals, it is reasonable to assume that the mechanisms of hypernatremia were caused by the disturbances of ADH secretion, thirst centre and osmoreceptor in the hypothalamus.

Topics: Aldosterone; Cerebral Ventricle Neoplasms; Child; Female; Humans; Hypernatremia; Hypothalamus; Optic Chiasm; Optic Nerve; Teratoma; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Chlorpropamide; Diabetes Insipidus; Drinking; Female; Humans; Hydrochlorothiazide; Hypernatremia; Nicotine; Potassium; Sodium; Sodium Chloride; Spironolactone; Syndrome; Thirst; Urination; Vasopressins; Water Deprivation

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

A patient with ectopic pinealoma first presented with apparent anorexia nervosa and hypernatraemic coma. A history of diabetes insipidus two months previously was not known on admission to hospital. The diabetes insipidus was unmasked by the administration of steroids. Neuroendocrinal and neuropathological aspects of the case are discussed with reference to the march of symptoms due to the growth of the tumour. Histochemical evidence is presented supporting the similarity between ectopic pinealoma and seminoma which suggests that they may more properly be referred to as atypical teratomas.

Topics: Acid Phosphatase; Adult; Alkaline Phosphatase; Anorexia Nervosa; Brain Neoplasms; Coma; Diabetes Insipidus; Dihydrolipoamide Dehydrogenase; Dysgerminoma; Electron Transport Complex IV; Esterases; Female; Humans; Hydrocortisone; Hypernatremia; Hypothalamus; Male; Osmolar Concentration; Oxidoreductases; Pinealoma; Sodium; Testicular Neoplasms; Thyroxine; Tuberculosis; Vasopressins

Topics: Animals; Body Weight; Cats; Dehydration; Disease Models, Animal; Hypernatremia; Hypothalamus; Natriuresis; Osmolar Concentration; Potassium; Silver Nitrate; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Dehydration; Diet Therapy; Diuretics; Ethanol; Humans; Hypernatremia; Male; Muscular Diseases; Natriuresis; Osmolar Concentration; Paralysis; Potassium; Sodium; Vasopressins; Water Intoxication

Topics: Adult; Blood Glucose; Blood Urea Nitrogen; Blood Volume; Burns; Diabetes Complications; Diuresis; Female; Glycosuria; Humans; Hypernatremia; Infusions, Parenteral; Male; Middle Aged; Nitrogen; Osmolar Concentration; Sepsis; Vasopressins; Water-Electrolyte Balance

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: Adolescent; Aldosterone; Brain Neoplasms; Chlorothiazide; Humans; Hypernatremia; Male; Osmolar Concentration; Pituitary Gland; Prednisone; Renin; Teratoma; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Adult; Blood Urea Nitrogen; Brain Neoplasms; Chlorides; Craniopharyngioma; Diabetes Insipidus; Drinking Behavior; Dysgerminoma; Female; Humans; Hydrocortisone; Hypernatremia; Hypothalamus; Male; Middle Aged; Osmolar Concentration; Potassium; Sella Turcica; Sodium; Thirst; Thyroid Function Tests; Triiodothyronine; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Albumins; Body Water; Chronic Disease; Circadian Rhythm; Dehydration; Diabetes Insipidus; Glucose Tolerance Test; Humans; Hypernatremia; Hypogonadism; Hypothalamus; Intellectual Disability; Kidney Diseases; Male; Obesity; Polyuria; Renin; Sodium; Thirst; Vasopressins

Topics: Animals; Fluorides; Hydrogen-Ion Concentration; Hypernatremia; Kidney; Kidney Tubules; Male; Methoxyflurane; Microscopy, Electron; Polyuria; Rats; Rats, Inbred Strains; Urea; Vasopressins; Water-Electrolyte Balance

Topics: Brain Diseases; Carcinoma, Bronchogenic; Humans; Hypernatremia; Hyponatremia; Vasopressins

Topics: Arachnoid; Brain Diseases; Cerebral Ventricles; Cysts; Humans; Hydrocephalus; Hypernatremia; Hypothalamus; Male; Middle Aged; Thirst; 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: Abortion, Criminal; Abortion, Legal; Adult; Amniocentesis; Amnion; Amniotic Fluid; Female; Humans; Hydatidiform Mole; Hypernatremia; Hypertonic Solutions; Intestinal Perforation; Maternal Mortality; Oxytocin; Postoperative Complications; Potassium; Pregnancy; Punctures; Sodium; Surgical Wound Infection; Uterine Hemorrhage; Uterine Rupture; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Dehydration; Humans; Hypernatremia; Hypopituitarism; Hypothalamus; Male; Osmolar Concentration; Pinealoma; Thirst; Vasopressins

Topics: Aged; Chronic Disease; Dehydration; Female; Humans; Hydrochlorothiazide; Hypernatremia; Inflammation; Natriuresis; Pituitary Diseases; Pituitary Gland, Posterior; Sodium; Thirst; Vasopressins

Topics: Acetates; Acute Disease; Adult; Chlorides; Coma; Cortisone; Craniopharyngioma; Diabetes Insipidus; Diet Therapy; Electrocardiography; Humans; Hypernatremia; Hypokalemia; Male; Natriuresis; Osmolar Concentration; Paralysis; Pituitary Neoplasms; Postoperative Complications; Potassium; Sodium; Thirst; Thyroxine; Vasopressins

Topics: Electroencephalography; Hormones, Ectopic; Humans; Hypernatremia; Hypokalemia; Hyponatremia; Metabolic Diseases; Penicillins; Uremia; Vasopressins

Topics: Adult; Aged; Chronic Disease; Diabetes Insipidus; Female; Humans; Hypernatremia; Vasopressins

Topics: Aldosterone; Angiotensin II; Humans; Hydrocortisone; Hypernatremia; Hyponatremia; Natriuresis; Vasopressins; Water-Electrolyte Balance

Topics: Chlorpropamide; Creatinine; Cyclic AMP; Dehydration; Diuresis; Female; Humans; Hydrochlorothiazide; Hypernatremia; Hypothalamus; Insulin; Insulin Secretion; Islets of Langerhans; Kidney; Middle Aged; Osmolar Concentration; Sodium; Thirst; Tolbutamide; Vasopressins; Water; Water-Electrolyte Balance

Topics: Blood Urea Nitrogen; Craniocerebral Trauma; Hematocrit; Humans; Hyperkalemia; Hypernatremia; Hypokalemia; Hyponatremia; Natriuresis; Osmosis; Potassium; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Child; Dehydration; Female; Hormones; Humans; Hypernatremia; Hypothalamus; Pinealoma; Polyuria; Thirst; Vasopressins

Topics: Aldosterone; Extracellular Space; Humans; Hyperkalemia; Hypernatremia; Hyponatremia; Potassium; Preoperative Care; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Blood Urea Nitrogen; Blood Volume; Creatinine; Diagnosis, Differential; Ethanol; Extracellular Space; Female; Humans; Hypernatremia; Infusions, Parenteral; Nitrogen; Potassium; Urea; Vasopressins; Water-Electrolyte Balance

Topics: Adenoma, Chromophobe; Chronic Disease; Dehydration; Diuresis; Humans; Hydrocortisone; Hypernatremia; Male; Mannitol; Middle Aged; Pituitary Gland, Posterior; Potassium; Sodium; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Dehydration; Diabetes Insipidus; Diagnosis, Differential; Diuresis; Glomerular Filtration Rate; Humans; Hypernatremia; Hypothalamus; Kidney; Mammals; Physiology, Comparative; Polyuria; Thirst; Vasopressins; Water; Water-Electrolyte Balance

Topics: Aged; Female; Humans; Hydrocortisone; Hypernatremia; Male; Methylprednisolone; Middle Aged; Pituitary Gland; Sepsis; Shock, Septic; Spironolactone; Vasopressins

Topics: Animals; Homeostasis; Humans; Hypernatremia; Lung Neoplasms; Male; Middle Aged; Rabbits; Rats; Vasopressins

Topics: Angiotensin II; Animals; Atropine; Blood Pressure; Ergotamine; Female; Heart; Hypernatremia; Hypertension; Injections, Intravenous; Male; Oxytocin; Peptides; Rats; Sodium Chloride; Vagotomy; Vasopressins

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Child; Child, Preschool; Diabetes Insipidus; Diuresis; Female; Glucuronidase; Humans; Hypernatremia; Kidney Function Tests; Lysine; Male; Vasopressins

Topics: Acetazolamide; Child; Dehydration; Diet Therapy; Humans; Hypernatremia; Hypothalamus; Male; Mercaptopurine; Potassium; Thirst; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Child; Dehydration; Drug Therapy; Humans; Hypernatremia; Hypothalamus; Hypothyroidism; Metabolism; Neoplasms; Neurosurgery; Pinealoma; Pituitary-Adrenal Function Tests; Prednisone; Thirst; Triiodothyronine; Vasopressins; Water-Electrolyte Balance

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: Anti-Allergic Agents; Arginine Vasopressin; Biomedical Research; Estrogens; Female; Histamine H1 Antagonists; Humans; Hyperaldosteronism; Hypernatremia; Premenstrual Syndrome; Progesterone; Progestins; Toxicology; Vasopressins; Water-Electrolyte Balance

Topics: Adrenal Cortex Hormones; Biological Transport; Desoxycorticosterone; Dogs; Hypernatremia; Hypertonic Solutions; Inulin; Kidney Function Tests; Kidney Glomerulus; Kidney Tubules; Natriuresis; p-Aminohippuric Acid; Pharmacology; Research; Sodium; Sodium Chloride; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Dehydration; Diabetes Insipidus; Fetal Diseases; Humans; Hypernatremia; Infant; Infant Nutrition Disorders; Measles; Vasopressins

Topics: Child; Child Behavior Disorders; Diabetes Insipidus; Fever; Humans; Hypernatremia; Infant; Mental Disorders; Povidone; Vasopressins

Topics: Aldosterone; Arginine Vasopressin; Edetic Acid; Electrolytes; Hormones; Humans; Hypernatremia; Sodium; Vasopressins; Water

Topics: Aldosterone; Animals; Arginine Vasopressin; Hypernatremia; Oxytocin; Potassium; Rats; Sodium; Vasopressins