pituitrin and Polyuria

Vasopressin has become an important vasopressor drug while treating a critically ill patient to maintain adequate mean arterial pressure. Diabetes insipidus (DI) is a rare syndrome characterized by the excretion of a large volume of diluted urine, inappropriate for water homeostasis. We noticed that several COVID19 patients developed excessive polyuria suggestive of DI, with a concomitant plasma sodium-level increase and/or low urine osmolality. We noticed a temporal relationship between vasopressin treatment cessation and polyuria periods. We reviewed those cases to better describe this phenomenon.. We retrospectively collected COVID19 ECMO patients' (from July 6, 2020, to November 30, 2021) data from the electronic medical records. By examining urine output, urine osmolality (if applicable), plasma sodium level, and plasma osmolality, we set DI diagnosis. We described the clinical course of DI episodes and compared baseline characteristics between patients who developed DI and those who did not.. Out of 37 patients, 12 had 18 episodes of DI. These patients were 7 years younger and had lower severity scores (APACHE-II and SOFA). Mortality difference was not seen between groups. 17 episodes occurred after vasopressin discontinuation; 14 episodes were treated with vasopressin reinstitution. DI lasted for a median of 21 h, with a median increase of 14 mEq/L of sodium.. Temporary DI prevalence after vasopressin discontinuation in COVID19 ECMO patients might be higher than previously described for vasopressin-treated patients.

Topics: COVID-19; Critical Illness; Diabetes Insipidus; Humans; Polyuria; Retrospective Studies; Sodium; Vasopressins

Diabetes insipidus (DI) is a disorder characterized by a high hypotonic urinary output of more than 50ml per kg body weight per 24 hours, with associated polydipsia of more than 3 liters a day [1,2]. Central DI results from inadequate secretion and usually deficient synthesis of Arginine vasopressin (AVP) in the hypothalamus or pituitary gland. Besides central DI further underlying etiologies of DI can be due to other primary forms (renal origin) or secondary forms of polyuria (resulting from primary polydipsia). All these forms belong to the Polyuria Polydipsia Syndrom (PPS). In most cases central and nephrogenic DI are acquired, but there are also congenital forms caused by genetic mutations of the AVP gene (central DI) [3] or by mutations in the gene for the AVP V2R or the AQP2 water channel (nephrogenic DI) [4]. Primary polydipsia (PP) as secondary form of polyuria includes an excessive intake of large amounts of fluid leading to polyuria in the presence of intact AVP secretion and appropriate antidiuretic renal response. Differentiation between the three mentioned entities is difficult [5], especially in patients with Primary polydipsia or partial, mild forms of DI [1,6], but different tests for differential diagnosis, most recently based on measurement of copeptin, and a thorough medical history mostly lead to the correct diagnosis. This is important since treatment strategies vary and application of the wrong treatment can be dangerous [7]. Treatment of central DI consists of fluid management and drug therapy with the synthetic AVP analogue Desmopressin (DDAVP), that is used as nasal or oral preparation in most cases. Main side effect can be dilutional hyponatremia [8]. In this review we will focus on central diabetes insipidus and describe the prevalence, the clinical manifestations, the etiology as well as the differential diagnosis and management of central diabetes insipidus in the out- and inpatient setting.

Topics: Adult; Antidiuretic Agents; Aquaporin 2; Child; Deamino Arginine Vasopressin; Diabetes Insipidus; Diagnosis, Differential; Glycopeptides; Humans; Mutation; Neurophysins; Pituitary Gland; Polydipsia; Polyuria; Protein Precursors; Vasopressins

Nocturnal enuresis is the involuntary pass of urine during sleep beyond the age of 5 years. It is a common condition in childhood and has an impact on the child's well-being. Research into the pathophysiology of the condition in the last decades has led to a paradigm shift, and enuresis is no longer considered a psychiatric disorder but rather a maturation defect with a somatic background. An excess urine production during sleep is a common finding in children with enuresis and disturbances in the circadian rhythm of arginine-vasopressin (AVP) is found in the majority of children with nocturnal polyuria. Children with enuresis and nocturnal polyuria lack the physiologic increase in AVP levels during sleep and treatment with the AVP analogue desmopressin can restore this rhythm and lead to dry nights. The reasons for this aberrant circadian AVP rhythm are not established. Furthermore, not all children with enuresis and nocturnal polyuria can be successfully treated with desmopressin suggesting that factors beyond renal water handling can be implicated such as natriuresis, hypercalciuria, and sleep-disordered breathing. The advances in the research of the genetic background of the condition may shed further light on the enuresis pathophysiology.

Topics: Arginine; Arginine Vasopressin; Child; Child, Preschool; Circadian Rhythm; Deamino Arginine Vasopressin; Humans; Nocturnal Enuresis; Polyuria; 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

The two main differential diagnoses of central diabetes insipidus are nephrogenic diabetes insipidus and primary polydipsia. Reliable distinction between those entities is essential as treatment differs substantially with the wrong treatment potentially leading to serious complications. Past diagnostic measures using the indirect water deprivation test had several pitfalls, resulting in a low diagnostic accuracy. With the introduction of copeptin, a stable and reliable surrogate marker for arginine vasopressin, diagnosis of diabetes insipidus was new evaluated. While unstimulated basal copeptin measurement reliably diagnoses nephrogenic diabetes insipidus, a stimulation test is needed to differentiate patients with central diabetes insipidus from patients with primary polydipsia. Stimulation can either be achieved through hypertonic saline infusion or arginine infusion. While the former showed high diagnostic accuracy and superiority over the indirect water deprivation test in a recent validation study, the diagnostic accuracy for arginine-stimulated copeptin was slightly lower, but superior in test tolerance. In summary of the recent findings, a new copeptin based diagnostic algorithm is proposed for the reliable diagnosis of diabetes insipidus.

Topics: Biomarkers; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Diagnosis, Differential; Diagnostic Techniques, Endocrine; Humans; Neurophysins; Polyuria; Protein Precursors; Vasopressins

Most cases of acquired central diabetes insipidus are caused by destruction of the neurohypophysis by: 1) anatomic lesions that destroy the vasopressin neurons by pressure or infiltration, 2) damage to the vasopressin neurons by surgery or head trauma, and 3) autoimmune destruction of the vasopressin neurons. Because the vasopressin neurons are located in the hypothalamus, lesions confined to the sella turcica generally do not cause diabetes insipidus because the posterior pituitary is simply the site of the axon terminals that secrete vasopressin into the bloodstream. In addition, the capacity of the neurohypophysis to synthesize vasopressin is greatly in excess of the body's needs, and destruction of 80-90% of the hypothalamic vasopressin neurons is required to produce diabetes insipidus. As a result, even large lesions in the sellar and suprasellar area generally are not associated with impaired water homeostasis until they are surgically resected. Regardless of the etiology of central diabetes insipidus, deficient or absent vasopressin secretion causes impaired urine concentration with resultant polyuria. In most cases, secondary polydipsia is able to maintain water homeostasis at the expense of frequent thirst and drinking. However, destruction of the osmoreceptors in the anterior hypothalamus that regulate vasopressin neuronal activity causes a loss of thirst as well as vasopressin section, leading to severe chronic dehydration and hyperosmolality. Vasopressin deficiency also leads to down-regulation of the synthesis of aquaporin-2 water channels in the kidney collecting duct principal cells, causing a secondary nephrogenic diabetes insipidus. As a result, several days of vasopressin administration are required to achieve maximal urine concentration in patients with CDI. Consequently, the presentation of patients with central diabetes insipidus can vary greatly, depending on the size and location of the lesion, the magnitude of trauma to the neurohypophysis, the degree of destruction of the vasopressin neurons, and the presence of other hormonal deficits from damage to the anterior pituitary.

Topics: Aquaporin 2; Brain Injuries, Traumatic; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Homeostasis; Humans; Neurophysins; Pituitary Diseases; Pituitary Gland, Posterior; Polydipsia; Polyuria; Protein Precursors; Vasopressins; Water-Electrolyte Balance

As a rare hereditary disease, congenital nephrogenic diabetes insipidus (NDI) is clinically characterized by polyuria with hyposthenuria and polydipsia. NDI results from collecting duct principal cell hyporesponsiveness or insensitivity to the antidiuretic action of arginine vasopressin (AVP). The principal cell-specific water channel aquaporin-2 (AQP2) plays an essential role in water reabsorption along osmotic gradients. The capacity to accumulate AQP2 in the apical plasma membrane in response to decreased fluid volume or increased plasma osmolality is critically regulated by the antidiuretic hormone AVP and its receptor 2 (AVPR2). Mutations in

Topics: Aquaporin 2; Diabetes Insipidus, Nephrogenic; Humans; Mutation; Neurophysins; Polyuria; Protein Interaction Maps; Protein Precursors; Protein Processing, Post-Translational; Protein Transport; Receptors, Vasopressin; Vasopressins

Diabetes insipidus (DI), be it from central or nephrogenic origin, must be differentiated from secondary forms of hypotonic polyuria such as primary polydipsia. Differentiation is crucial since wrong treatment can have deleterious consequences. Since decades, the gold standard for differentiation has been the water deprivation test, which has limitations leading to an overall unsatisfying diagnostic accuracy. Furthermore, it is cumbersome for patients with a long test duration. Clinical signs and symptoms and MRI characteristics overlap between patients with DI and primary polydipsia. The direct test including vasopressin (AVP) measurement upon osmotic stimulation was meant to overcome these limitations, but failed to enter clinical practice mainly due to technical constraints of the AVP assay. Copeptin is secreted in equimolar amount to AVP but can easily be measured with a sandwich immunoassay. A high correlation between copeptin and AVP has been shown. Accordingly, copeptin mirrors the amount of AVP in the circulation and has led to a 'revival' of the direct test in the differential diagnosis of DI. We have shown that a baseline copeptin, without prior thirsting, unequivocally identifies patients with nephrogenic DI. In contrast, for the differentiation between central DI and primary polydipsia, a stimulated copeptin level of 4.9 pmol/L upon hypertonic saline infusion differentiates these two entities with a high diagnostic accuracy and is superior to the water deprivation test. Close sodium monitoring during the test is a prerequisite. Further new test methods are currently evaluated and might provide an even simpler way of differential diagnosis in the future.

Topics: Awards and Prizes; Diabetes Insipidus, Neurogenic; Diagnosis, Differential; Glycopeptides; Humans; Polydipsia; Polyuria; Saline Solution, Hypertonic; Syndrome; Vasopressins

Enuresis was historically viewed as a primarily psychiatric disorder, but this understanding has changed dramatically since the end of the last century, when it became clear that somatic factors, such as nocturnal polyuria as a result of vasopressin deficiency, nocturnal detrusor overactivity and high arousal thresholds, all play a crucial role in enuresis pathogenesis. It has also become clear that enuresis is inherited in the majority of cases, although the correlation between genotype and enuretic phenotype is not straightforward. The standard view of enuresis as being the result of either (i) nocturnal polyuria and high arousal thresholds; or (ii) nocturnal detrusor overactivity and high arousal thresholds has become well-established, but further research now complicates the picture. First, psychological/psychiatric problems are overrepresented in enuresis, and might in a minority of cases have a causal or aggravating role. Second, nocturnal polyuria is not always linked to vasopressin deficiency. Third, nocturnal detrusor overactivity is in itself pathogenetically heterogeneous, and could be linked to constipation. Fourth, the sleep of enuretic children might be "deep," but possibly also disturbed (by obstructed airways or a distended or contracting bladder). These children might have high arousal thresholds because of the enuresis instead of the other way around. The same might possibly be said about nocturnal polyuria. Taking these new insights into account, a new model of enuresis pathogenesis is presented, which is more complicated but hopefully also more true than the standard consensus.

Topics: Adult; Antidiuretic Agents; Arousal; Central Nervous System; Child; Constipation; Deamino Arginine Vasopressin; Enuresis; Humans; Polyuria; Sleep; Urinary Bladder, Overactive; Vasopressins

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

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

Water excretion is regulated in large part through the regulation of osmotic water permeability of the renal collecting duct epithelium. Water permeability is controlled by vasopressin through regulation of the water channel, aquaporin-2 (AQP2). Two processes contribute: (1) regulation of AQP2 trafficking to the apical plasma membrane; and (2) regulation of the total amount of the AQP2 protein in the cells. Regulation of AQP2 abundance is defective in several water-balance disorders, including many polyuric disorders and the syndrome of inappropriate antidiuresis. Here we review vasopressin signaling in the renal collecting duct that is relevant to the two modes of water permeability regulation.

Topics: Animals; Aquaporin 2; beta Catenin; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Heart Failure; Humans; Inappropriate ADH Syndrome; Kidney Tubules, Collecting; Liver Cirrhosis; Mice; Myosin-Light-Chain Kinase; Nephrotic Syndrome; Permeability; Phosphoproteins; Phosphorylation; Polyuria; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-jun; Rats; Signal Transduction; Transcription Factor AP-1; Transcription Factors; Vasopressins

Aquaporin-2 (AQP2), the vasopressin-regulated water channel of the renal collecting duct, is dysregulated in numerous disorders of water balance in people and animals, including those associated with polyuria (urinary tract obstruction, hypokalemia, inflammation, and lithium toxicity) and with dilutional hyponatremia (syndrome of inappropriate antidiuresis, congestive heart failure, cirrhosis). Normal regulation of AQP2 by vasopressin involves 2 independent regulatory mechanisms: (1) short-term regulation of AQP2 trafficking to and from the apical plasma membrane, and (2) long-term regulation of the total abundance of the AQP2 protein in the cells. Most disorders of water balance are the result of dysregulation of processes that regulate the total abundance of AQP2 in collecting duct cells. In general, the level of AQP2 in a collecting duct cell is determined by a balance between production via translation of AQP2 mRNA and removal via degradation or secretion into the urine in exosomes. AQP2 abundance increases in response to vasopressin chiefly due to increased translation subsequent to increases in AQP2 mRNA. Vasopressin-mediated regulation of AQP2 gene transcription is poorly understood, although several transcription factor-binding elements in the 5' flanking region of the AQP2 gene have been identified, and candidate transcription factors corresponding to these elements have been discovered in proteomics studies. Here, we review progress in this area and discuss elements of vasopressin signaling in the collecting duct that may impinge on regulation of AQP2 in health and in the context of examples of polyuric diseases.

Topics: Animals; Aquaporin 2; Humans; Kidney Tubules, Collecting; Polyuria; Signal Transduction; Vasopressins; Water-Electrolyte Imbalance

Over the past two decades, the genetic and molecular basis of familial forms of diabetes insipidus has been elucidated. Diabetes insipidus is a clinical syndrome characterized by the excretion of abnormally large volumes of diluted urine (polyuria) and increased fluid intake (polydipsia). The most common type of diabetes insipidus is caused by lack of the antidiuretic hormone arginine vasopressin (vasopressin), which is produced in the hypothalamus and secreted by the neurohypophysis. This type of diabetes insipidus is referred to here as neurohypophyseal diabetes insipidus. The syndrome can also result from resistance to the antidiuretic effects of vasopressin on the kidney, either at the level of the vasopressin 2 receptor or the aquaporin 2 water channel (which mediates the re-absorption of water from urine), and is referred to as renal or nephrogenic diabetes insipidus. Differentiation between these two types of diabetes insipidus and primary polydipsia can be difficult owing to the existence of partial as well as complete forms of vasopressin deficiency or resistance. Seven different familial forms of diabetes insipidus are known to exist. The clinical presentation, genetic basis and cellular mechanisms responsible for them vary considerably. This information has led to improved methods of differential diagnosis and could provide the basis of new forms of therapy.

Topics: Animals; Aquaporin 2; Arginine Vasopressin; Deamino Arginine Vasopressin; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Diagnosis, Differential; Female; Humans; Male; Mutation; Phenotype; Polydipsia; Polyuria; Receptors, Vasopressin; Vasopressins

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

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

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

Beyond polyuria following psychogenic polydipsia, in a more narrow sense, this condition may be classified into impaired water re-absorption (i) due to tubular injury or (ii) relative or absolute loss of function of antidiuretic hormone (ADH). Tubular injury may be caused by different toxins affecting the ascending Henle loop as hypercalciuria, drugs and antibiotics as tubular necrosis. ADH deficiency, either absolute or relative, occurs with central or peripheral diabetes insipidus, which is based on synthesis failure or loss of peripheral efficacy of ADH due to receptor malfunction. Diagnosis of polyuria rests upon a thirst challenge in conjunction with laboratory studies of osmolality in serum and urine, which discloses the non-function of the hypothalamic-renal axis. Administration of ADH may differentiate between central and peripheral diabetes insipidus.

Topics: Humans; Kidney Diseases; Polyuria; Practice Guidelines as Topic; Practice Patterns, Physicians'; Vasopressins

Polyuria and polydipsia (PUPD) occur frequently in dogs and may be caused by a variety of endocrine, metabolic, and renal disturbances. The studies described in this PhD Thesis, which was defended in January 2004 in Utrecht, investigated the role of the antidiuretic hormone vasopressin (VP) in the pathogenesis of different forms of canine polyuria. Experiments in healthy dogs demonstrated that the ranges of urine specific gravity and urine osmolality are much larger than previously thought. A water deprivation test is not required in all polyuric dogs, because serial measurements of urine osmolality may already lead to the diagnosis of primary polydipsia, in some cases. In dogs with primary polydipsia a wide variation in VP responses to hypertonic stimulation can be found, including a hyperresponse, a hyporesponse, and a non-linear response. The significance of the VP response to hypertonic saline infusion as the 'gold standard' for a diagnosis of canine polyuria is discussed. In the dog, VP is secreted in a pulsatile fashion with a wide variation in the number of VP pulses, VP pulse duration, and VP pulse amplitude and height. The occurrence of spontaneous VP pulses may severely hamper the interpretation of the curve describing the relationship between plasma osmolality and plasma VP concentration during osmotic stimulation. A radioimmunoassay to measure the VP-dependent water channel aquaporin-2 (AQP2) in urine was developed in dogs. In healthy dogs, urinary AQP2 excretion closely reflects changes in collecting duct exposure to VP. Measurement of urinary AQP2 excretion in polyuric dogs may be helpful to distinguish between central diabetes insipidus, nephrogenic diabetes insipidus, and primary polydipsia.

Topics: Animals; Area Under Curve; Diagnosis, Differential; Dog Diseases; Dogs; Osmolar Concentration; Periodicity; Polyuria; Radioimmunoassay; Vasopressins; Water-Electrolyte Imbalance

Topics: Adolescent; Adult; Body Water; Child; Child, Preschool; Deamino Arginine Vasopressin; Diabetes Insipidus; Drinking; Homeostasis; Humans; Infant; Magnetic Resonance Imaging; Polyuria; Renal Agents; Vasopressins

Intracellular dehydration is the major risk in case of a polyuropolydipsic syndrome. Excepting osmotic polyuria, prognosis depends on a possibly progressive functional anomaly of the hypothalamopituitary axis.. Polyuropolydipsia occurs when antidiuretic hormone (ADH) secretion is absent (central diabetes insipidis), the kidney does not respond to ADH (nephrogenic diabetes insipidus) or in case of physiological inhibition of ADH secretion (primary polydipsia).. Dynamic explorations are associated with radioimmunoassay of ADH. They are particularly useful in case of atypical diabetes insipidus and include the water restriction test and a study of the sensitivity to exogenous ADH (dDAVP). The results orient the etiologic diagnosis and allow an evaluation of the fluid intake required as a function of the maximal concentrating capacity of the kidneys.. Treatment is based on ADH analogs (dDAVP). The aim is to obtain a constant antidiuretic effect without hyponatremia or escape. In case of partial central diabetes insipidus, a non-hormone treatment using compounds which increase vasopressin release or its effect on the kidney can be proposed.

Topics: Diagnosis, Differential; Drinking; Humans; Osmolar Concentration; Polyuria; Syndrome; Thirst; Vasopressins

Aquaporins are proteins that mediate transmembrane water transport in a variety of tissues including the kidney. Vasopressin plays an important role in regulation of water metabolism, and under normal conditions the kidney collecting duct is extremely sensitive to vasopressin. Vasopressin stimulates the synthesis of aquaporin 2 (AQP2) in kidney collecting duct principal cells. Studies in Brattle Boro rats which are vasopressin deficient, revealed low levels of AQP2 in association with extreme polyuria. After vasopressin treatment for 5 days AQP2 levels increased threefold. Using rat models with nephrogenic diabetes insipidus (NDI) we have demonstrated that AQP2 expression is down regulated in association with polyuria, suggesting that reduced levels of AQP2 may be a general factor in acquired forms of NDI from a variety of reasons. The polyuria and urinary concentrating defects associated with an abnormal nightly-increase in AVP in patients with nocturnal enuresis may partly be due to a lack of vasopressin-mediated AQP2 expression since treatment with desmopressin in these patients have normalised their nocturnal urine production.

Topics: Animals; Aquaporin 2; Aquaporin 6; Aquaporins; Biological Transport; Cell Membrane; Diabetes Insipidus, Nephrogenic; Disease Models, Animal; Enuresis; Humans; Ion Channels; Polyuria; Rats; Rats, Brattleboro; Urinary Bladder; Vasopressins; Water-Electrolyte Balance

Topics: Diagnosis, Differential; Humans; Pituitary Function Tests; Pituitary Gland, Posterior; Polyuria; Saline Solution, Hypertonic; Vasopressins

Topics: Diabetes Insipidus; Diagnosis, Differential; Humans; Inappropriate ADH Syndrome; Pituitary Function Tests; Pituitary Gland, Posterior; Polyuria; Vasopressins; Water; Water Deprivation

Topics: Diagnosis, Differential; Humans; Nicotine; Pituitary Function Tests; Pituitary Gland, Posterior; Polyuria; Saline Solution, Hypertonic; Vasopressins; Water Deprivation

Diabetes insipidus, characterized by the excretion of copious volumes of unconcentrated urine, results from a deficiency in the action of the antidiuretic hormone arginine vasopressin and can be caused by any of four fundamentally different defects, including impaired secretion (neurohypophyseal diabetes insipidus), impaired renal response (nephrogenic diabetes insipidus), excessive fluid intake (primary polydipsia), or increased metabolism of the hormone (gestational diabetes insipidus). Differentiation between their causes, pathophysiology, and treatment methods is essential for effective management and is best achieved by a combination of hormonal, clinical, and neuroradiologic observations. Understanding of the genetic forms has advanced greatly and may soon lead to improved methods of prevention, diagnosis, and treatment.

Topics: Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diagnosis, Differential; Female; Humans; Male; Osmolar Concentration; Polyuria; Pregnancy; Vasopressins

The role played by antidiuretic hormone in enuresis remains controversial. As a symptomatic treatment, desmopressin (DDAVP) has already proved to be a useful addition to the measures applied against this condition.

Topics: Adolescent; Child; Child, Preschool; Deamino Arginine Vasopressin; Double-Blind Method; Enuresis; Humans; Polyuria; Vasopressins

Topics: Animals; Calcium; Humans; Hypercalcemia; Kidney; Kidney Concentrating Ability; Kidney Medulla; Polyuria; Renal Circulation; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Digestive System; Growth; Hydrogen-Ion Concentration; Kidney; Kidney Tubules, Proximal; Lithium; Natriuresis; Nephritis, Interstitial; Polyuria; Potassium; Rats; Urine; Vasopressins

Topics: Acid-Base Equilibrium; Glomerular Filtration Rate; Humans; Kidney; Kidney Diseases; Kidney Tubules; Kinetics; Lithium; Mental Disorders; Polyuria; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Disease Models, Animal; Epithelium; Humans; Kidney Tubules, Collecting; Lithium; Models, Biological; Osmolar Concentration; Polyuria; Rabbits; Rats; Vasopressins

Topics: Anti-Inflammatory Agents; Chlorpropamide; Diabetes Insipidus; Female; Furosemide; Humans; Inappropriate ADH Syndrome; Male; Polyuria; Vasopressins

Topics: Diuresis; Humans; Inappropriate ADH Syndrome; Kidney; Osmolar Concentration; Polyuria; Vasopressins

Topics: Diabetes Insipidus; Endocrine System Diseases; Female; Humans; Kidney Diseases; Male; Neurophysins; Osmolar Concentration; Oxytocin; Pituitary Function Tests; Polyuria; Radioimmunoassay; Vasopressins

Topics: Animals; Blood Volume; Diabetes Insipidus; Dog Diseases; Dogs; Humans; Kidney Concentrating Ability; Polyuria; Rats; Specific Gravity; Thirst; Vasopressins; Water Deprivation

The authors present a brief review of the problem of diabetes insipidus in neurosurgical patients, with particular emphasis on the differential diagnosis of postoperative and posttraumatic polyuria and the management of diabetes insipidus in these periods. A listing of drugs currently used in its treatment is given.

Topics: Administration, Intranasal; Benzothiadiazines; Brain Injuries; Carbamazepine; Chlorpropamide; Deamino Arginine Vasopressin; Diabetes Insipidus; Diabetes Mellitus; Diagnosis, Differential; Diuretics; Humans; Hypothalamo-Hypophyseal System; Lypressin; Methods; Polyuria; Postoperative Complications; Sodium Chloride Symporter Inhibitors; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Cyclic AMP; Diabetes Insipidus; Humans; Kidney Diseases; Kidney Medulla; Lithium; Polyuria; Serous Membrane; Sodium; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Biological Assay; Blood; Blood Pressure; Blood Volume; Dehydration; Diabetes Insipidus; Humans; Kidney Concentrating Ability; Osmolar Concentration; Polyuria; Posture; Radioimmunoassay; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Body Weight; Dehydration; Diabetes Insipidus; Diagnosis, Differential; Humans; Hypertonic Solutions; Injections, Intramuscular; Injections, Intravenous; Isotonic Solutions; Nicotine; Polyuria; Smoking; Sodium Chloride; Sulfonylurea Compounds; Thirst; Vasopressins

Topics: Circadian Rhythm; Humans; Hydrocortisone; Male; Middle Aged; Polyuria; Urination; Vasopressins; Water; Water Movements

Topics: Aged; Diuresis; Drainage; Humans; Infant; Kidney; Male; Middle Aged; Natriuresis; Polyuria; Postoperative Complications; Prostatic Hyperplasia; Prostatic Neoplasms; Ureteral Calculi; Ureteral Obstruction; Urinary Bladder Neck Obstruction; Urologic Diseases; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Adult; Aged; Animals; Arginine; Child; Dehydration; Diabetes Insipidus; Female; Humans; Hyperaldosteronism; Hypertonic Solutions; Hypocalcemia; Kidney Failure, Chronic; Kidney Transplantation; Kidney Tubules; Male; Middle Aged; Nicotine; Osmolar Concentration; Polyuria; Sex Factors; Sodium Chloride; Thirst; Time Factors; Urine; Urologic Diseases; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Adrenergic Uptake Inhibitors; Adult; Antidepressive Agents, Tricyclic; Circadian Rhythm; Deamino Arginine Vasopressin; Enuresis; Humans; Imipramine; Polyuria; Renal Agents; Treatment Outcome; Urination; Vasopressins

The effect of lithium on the urine concentrating response to antidiuretic hormone (ADH) and the excretion of ADH has been studied in rats and man. The maximum urine osmolarity following 18 h dehydration and Pitressin (5 u) was decreased in three out of four patients during lithium treatment compared to their response to the same test in the absence of lithium. In a fifth patient, tested only during lithium treatment, the urine remained hypotonic to plasma throughout this test. Lithium increased the excretion of ADH in non-polyuric patients from 9-22 mu/24 h in the absence of lithium to 36-202 mu/24 - during lithium treatment. In four patients with lithium-induced polyuria, a diuretic acting on the distal tubules, clorexolone, reduced the polyuria. Lithium increased urine volume and the excretion of ADH in four rats receiving lithium in their diet. The response to exogenous ADH was decreased during lithium administration.

Topics: Animals; Clinical Trials as Topic; Deamino Arginine Vasopressin; Dose-Response Relationship, Drug; Humans; Kidney Concentrating Ability; Lithium; Polyuria; Psychotic Disorders; Rats; Vasopressins

Topics: Adult; Child; Child, Preschool; Clinical Trials as Topic; Clofibrate; Diabetes Insipidus; Diuresis; Drug Synergism; Female; Gonadotropins, Pituitary; Growth Hormone; Humans; Male; Middle Aged; Osmolar Concentration; Pituitary Gland; Placebos; Polyuria; Thyroid Gland; Time Factors; Vasopressins

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

Nocturnal polyuria (NP) due to a suppressed vasopressin circadian rhythm is a well-documented pathogenetic mechanism in enuresis, mainly studied in monosymptomatic enuresis. A substantial percentage of patients do not respond to desmopressin. This suggests that NP may not only be related to vasopressin, but that other kidney components play a role. Solute handling and osmotic excretion have been investigated in the past, especially in refractory patients. Nevertheless, data in treatment-naïve populations with information on timing overnight are sparse. This study aims to investigate the diuresis and solute excretion in treatment-naïve patients with or without NP, with emphasis on circadian rhythms.. Retrospective analysis of 403 treatment-naïve children 5-18 years with severe enuresis (> 8 nights/2 weeks). Circadian rhythms were evaluated by a 24-h urine collection in 8 timed portions (4 day, 4 nighttime) at in-home settings. Urine volume, osmolality, and creatinine were measured. Patients were subdivided into three groups according to nocturnal diuresis (ND) and Expected Bladder Capacity (EBCage) ratio: (a) < 100%, (b) 100-129%, (c) > 130%.. All groups maintained circadian rhythm for diuresis and diuresis rates. Patients with higher ND (100-129% and > 130% EBCage) had higher daytime volumes and less pronounced circadian rhythm. In the ND group > 130% EBCage, the ND rate was higher during the first night collection and osmotic excretion was significantly higher overnight.. Overall 24-h fluid intake (reflected by 24-h diuresis) and nutritional intake (24-h osmotic excretion) might play a role in enuresis. Increased diuresis rate early in the night can be important in some patients, whereas the total night volume can be important in others. A higher resolution version of the Graphical abstract is available as Supplementary Information.

Topics: Child; Circadian Rhythm; Deamino Arginine Vasopressin; Humans; Nocturnal Enuresis; Polyuria; Retrospective Studies; Vasopressins; Water

Ureteral obstruction is marked by disappearance of the vasopressin-dependent water channel aquaporin-2 (AQP2) in the renal collecting duct and polyuria upon reversal. Most studies of unilateral ureteral obstruction (UUO) models have examined late time points, obscuring the early signals that trigger loss of AQP2.. We performed RNA-Seq on microdissected rat cortical collecting ducts (CCDs) to identify early signaling pathways after establishment of UUO.. Vasopressin V2 receptor (AVPR2) mRNA was decreased 3 hours after UUO, identifying one cause of AQP2 loss. Collecting duct principal cell differentiation markers were lost, including many not regulated by vasopressin. Immediate early genes in CCDs were widely induced 3 hours after UUO, including. Immediately after establishment of UUO, collecting ducts manifest a stunned state with broad disappearance of mRNAs. Within 3 hours, there is upregulation of immediate early and inflammatory genes and disappearance of the V2 vasopressin receptor, resulting in loss of AQP2 (confirmed by lipopolysaccharide administration). The inflammatory response seen rapidly after UUO establishment may be relevant to both UUO-induced polyuria and long-term development of fibrosis in UUO kidneys.

Topics: Animals; Aquaporin 2; Kidney; Kidney Tubules, Collecting; Polyuria; Rats; RNA, Messenger; Ureteral Obstruction; Vasopressins

Familial neurohypophyseal diabetes insipidus (FNDI) is a rare disorder characterized by childhood-onset progressive polyuria and polydipsia due to mutations in the arginine vasopressin (AVP) gene. The aim of the study was to describe the clinical and molecular characteristics of families with neurohypophyseal diabetes insipidus.. Five Portuguese families with autosomal dominant FNDI underwent sequencing of the AVP gene and the identified mutations were functionally characterized by in vitro studies.. Three novel and two recurrent heterozygous mutations were identified in the AVP gene. These consisted of one initiation codon mutation in the signal peptide coding region (c.2T > C, p.Met1?), three missense mutations in the neurophysin II (NPII) coding region (c.154T > C, p.Cys52Arg; c.289C > G, p.Arg97Gly; and c.293G > C, p.Cys98Ser), and one nonsense mutation in the NPII coding region (c.343G > T, p.Glu115Ter). In vitro transfection of neuronal cells with expression vectors containing each mutation showed that the mutations resulted in intracellular retention of the vasopressin prohormone. Patients showed progressive symptoms of polyuria and polydipsia, but with wide variability in severity and age at onset. No clear genotype-phenotype correlation was observed.. The intracellular accumulation of mutant vasopressin precursors supports the role of cellular toxicity of the mutant proteins in the etiology of the disorder and explains the progressive onset of the disorder. These findings further expand the AVP mutational spectrum in FNDI and contribute to the understanding of the molecular pathogenic mechanisms involved in FNDI.

Topics: Arginine Vasopressin; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Humans; Mutation; Neurophysins; Pedigree; Polydipsia; Polyuria; Vasopressins

Central diabetes insipidus (CDI) is characterized by polyuria and polydipsia caused by impairment of arginine vasopressin (AVP) secretion. In this study, we evaluated plasma AVP concentrations during a hypertonic saline infusion test using a new AVP radioimmunoassay (RIA) which is now available in Japan. Thirteen control subjects, mostly with hypothalamo-pituitary disease but without CDI, and 13 patients with CDI were enrolled in the study. Whether or not subjects had CDI was determined based on the totality of clinical data, which included urine volumes and osmolality. Regression analysis of plasma AVP and serum Na concentrations revealed that the gradient was significantly lower in the CDI group than in the control group. The area under the receiver-operating-characteristic (ROC) curve was 0.99, and the <0.1 gradient cut-off values for the simple regression line to distinguish CDI from control had a 100% sensitivity and a 77% specificity. The ROC analysis with estimated plasma AVP concentrations at a serum Na concentration of 149 mEq/L showed that the area under the ROC curve was 1.0 and the <1.0 pg/mL cut-off values of plasma AVP had a 99% sensitivity and a 95% specificity. We conclude that measurement of AVP by RIA during a hypertonic saline infusion test can differentiate patients with CDI from those without CDI with a high degree of accuracy. Further investigation is required to confirm whether the cut-off values shown in this study are also applicable to a diagnosis of partial CDI or a differential diagnosis between CDI and primary polydipsia.

Topics: Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Female; Humans; Male; Middle Aged; Polyuria; Radioimmunoassay; Saline Solution, Hypertonic; Sodium; Vasopressins

Urinary dysfunction is a common complaint following spinal cord injury (SCI) and is a leading issue for individuals with SCI that impacts their quality of life. One urinary complication that has received little attention is SCI-induced polyuria, even though individuals with SCI will significantly restrict their fluid intake to decrease urine production, leading to sequelae of medical complications. Understanding the mechanisms instigating the development of polyuria will allow us to target interventions that may alleviate polyuria symptoms, leading to significant improvements in the quality of life and urinary health of individuals with SCI. In a rat SCI contusion model, an increase in the amount of urine excreted over a 24-h period ( P ≤ 0.001) was found at 2 wk postinjury. The urine excreted was more dilute with decreased urinary creatinine and specific gravity ( P ≤ 0.001). Several factors important in fluid balance regulation, vasopressin (AVP), natriuretic peptides, and corticosterone (CORT), also changed significantly postinjury. AVP levels decreased ( P = 0.042), whereas atrial natriuretic peptide (ANP) and CORT increased ( P = 0.005 and P = 0.031, respectively) at 2 wk postinjury. There was also a positive correlation between the increase in ANP and urine volume postinjury ( P = 0.033). The changes in AVP, ANP, and CORT are conducive to producing polyuria, and the timing of these changes coincides with the development of SCI-induced polyuria. This study identifies several therapeutic targets that could be used to ameliorate polyuria symptoms and improve quality of life in individuals with SCI.

Topics: Animals; Disease Models, Animal; Male; Motor Activity; Natriuretic Peptides; Polyuria; Rats, Wistar; Recovery of Function; Spinal Cord Injuries; Vasopressins

Aquaporin-2 (AQP2) is a water channel protein expressed in principal cells (PCs) of the kidney collecting ducts (CDs) and plays a critical role in mediating water reabsorption and urine concentration. AQP2 undergoes both regulated trafficking mediated by vasopressin (VP) and constitutive recycling, which is independent of VP. For both pathways, actin cytoskeletal dynamics is a key determinant of AQP2 trafficking. We report here that manganese chloride (MnCl

Topics: Actin Cytoskeleton; Actins; Animals; Aquaporin 2; Chlorides; Kidney Concentrating Ability; Kidney Tubules, Collecting; LLC-PK1 Cells; Male; Manganese Compounds; Mice, Inbred C57BL; Phosphorylation; Polymerization; Polyuria; Protein Transport; rho GTP-Binding Proteins; rhoA GTP-Binding Protein; Signal Transduction; Swine; Vasopressins

The water deprivation test (WDT) is widely used for the differential diagnosis of the polyuria-polydipsia syndrome (PPS). However, it is inconvenient and may not always be precise in differentiating partial forms of diabetes insipidus (DI) from primary polydipsia (PP). The aim of this study was to evaluate the results of a combined outpatient and inpatient overnight WDT protocol that included an overnight unsupervised period concerning its feasibility and safety.. We performed a retrospective analysis of clinical data and laboratory results of 52 patients with PPS undergoing WDT at a single center.. PP was the most frequent diagnosis, followed by complete central DI (cCDI), partial central DI (pCDI), and nephrogenic DI (NDI). Over 90% of the patients showed an expected increase in serum osmolality at the end of the dehydration period. There were no reports of complications during the overnight deprivation period. Post-dehydration urine osmolality and urine-to-serum osmolality ratio significantly differentiated all the groups ( P<.05), except for cCDI and NDI, which could be differentiated by basal and post-dehydration vasopressin (AVP) levels ( P<.05 for both). Although these measurements were useful for differentiating patients according to their allocation groups, results from WDT and direct AVP levels may often require a comprehensive diagnostic approach, particularly in the challenging groups of PP and pCDI.. A combined outpatient and inpatient overnight WDT protocol is safe and feasible when the test is performed with special care at experienced centers. Newer diagnostic tools are expected to improve the accuracy of PPS diagnosis.. AQP2 = aquaporin-2; AVP = vasopressin; CDI = central diabetes insipidus; cCDI = complete central diabetes insipidus; DDAVP = desmopressin; DI = diabetes insipidus; IQR = interquartile range; MRI = magnetic resonance imaging; Na

Topics: Adolescent; Adult; Aged; Ambulatory Care; Child; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Female; Hospitalization; Humans; Male; Middle Aged; Neurophysins; Osmolar Concentration; Polydipsia; Polydipsia, Psychogenic; Polyuria; Protein Precursors; Retrospective Studies; Syndrome; Vasopressins; Water Deprivation; Young Adult

Diabetes insipidus (DI) and primary polydipsia (PP) are characterised by polyuria and polydipsia. It is crucial to differentiate between these two disorders since the treatment is different. The aim of this study was to evaluate the diagnostic value of the short and an extended variant of the water deprivation test (WDT) and of measuring urinary vasopressin (AVP) in patients with polyuria and polydipsia.. A retrospective, single-centre study based on WDTs performed between 2004 and 2014 including 104 consecutive patients with the polyuria-polydipsia syndrome. During a strict water deprivation, weight, urinary osmolality, urinary vasopressin and specific gravity were collected until one of the following was reached: i) >3% weight reduction, ii) Urinary specific gravity >1.020 or, urinary osmolality >800 mOsm/L, iii) Intolerable adverse symptoms such as excessive thirst.. Out of 104 patients (67 women, 37 men), 21 (20%) were diagnosed with DI and 83 (80%) with PP. The median (interquartile range; range) test duration was 14 hours (10-16; 3-36) in patients with DI and 18 hours (14-24; 7-48) in patients with PP (P=0.011). Of those diagnosed with PP, 22 (26%) did not reach urinary specific gravity >1.020 nor urine osmolality >800 mOsm/L. Urine AVP did not overlap between patients with PP and patients with central DI.. The short WDT is of limited value in the diagnostic work-up of polydipsia and polyuria and a partial DI may have been missed in every fourth patient diagnosed with PP. Urinary AVP has excellent potential in discriminating PP from central DI.

Topics: Adult; Diabetes Insipidus; Female; Humans; Male; Middle Aged; Neurophysins; Polydipsia; Polydipsia, Psychogenic; Polyuria; Predictive Value of Tests; Protein Precursors; Retrospective Studies; Syndrome; Vasopressins; Water Deprivation

Mammalian class IX myosin Myo9a is a single-headed, actin-dependent motor protein with Rho GTPase-activating protein activity that negatively regulates Rho GTPase signaling. Myo9a is abundantly expressed in ciliated epithelial cells of several organs. In mice, genetic deletion of Myo9a leads to the formation of hydrocephalus. Whether Myo9a also has essential functions in the epithelia of other organs of the body has not been explored. In the present study, we report that Myo9a-deficient mice develop bilateral renal disease, characterized by dilation of proximal tubules, calyceal dilation, and thinning of the parenchyma and fibrosis. These structural changes are accompanied by polyuria (with normal vasopressin levels) and low-molecular-weight proteinuria. Immunohistochemistry revealed that Myo9a is localized to the circumferential F-actin belt of proximal tubule cells. In kidneys lacking Myo9a, the multiligand binding receptor megalin and its ligand albumin accumulated at the luminal surface of Myo9a-deficient proximal tubular cells, suggesting that endocytosis is dysregulated. In addition, we found, surprisingly, that levels of murine diaphanous-related formin-1, a Rho effector, were decreased in Myo9a-deficient kidneys as well as in Myo9a knockdown LLC-PK1 cells. In summary, deletion of the Rho GTPase-activating protein Myo9a in mice causes proximal tubular dilation and fibrosis, and we speculate that downregulation of murine diaphanous-related formin-1 and impaired protein reabsorption contribute to the pathophysiology.

Topics: Albumins; Animals; Carrier Proteins; Cells, Cultured; Endocytosis; Formins; GTPase-Activating Proteins; Hydronephrosis; Kidney Tubules; LLC-PK1 Cells; Mice; Mice, Inbred C57BL; Mice, Knockout; Myosins; Nephrons; Polyuria; rho-Associated Kinases; Swine; Vasopressins

Topics: Humans; Male; Natriuretic Peptide, Brain; Nocturia; Polyuria; Sleep Apnea, Obstructive; Vasopressins

Topics: Cardiac Surgical Procedures; Child, Preschool; Female; Heart Septal Defects; Humans; Polyuria; Substance Withdrawal Syndrome; Transposition of Great Vessels; Urodynamics; Vasoconstrictor Agents; Vasopressins

To investigate the impact of obstructive sleep apnea syndrome (OSAS) on night-time secretion of brain natriuretic peptide (BNP) and antidiuretic hormone (ADH) in older men with nocturia accompanied by nocturnal polyuria.. One hundred six men with nocturia aged ≥ 60 years underwent full-night polysomnography to determine whether they had OSAS. Blood count, standard chemistry panel, BNP, urinary ADH, urinary creatinine (u-Cre), and urinary osmolarity were measured at 6:00 AM, and a frequency volume chart was recorded on the same day that polysomnography was performed.. We evaluated 83 patients after excluding 18 with mild OSAS and 5 with nocturnal polyuria index <0.35. Participants with OSAS had higher apnea-hypopnea index (P < .0001) than those without OSAS. Body mass index and systolic blood pressure were higher in OSAS patients than those in the control group. BNP was higher in the OSAS patients than in the control patients (48.6 ± 41.4 vs 30.7 ± 31.5; P = .0006). On urinalysis, OSAS patients showed higher urinary sodium and u-Cre secretion than controls (24.7 ± 11.3 vs 16.2 ± 5.1; P <.0001). Urine osmolarity was also higher in OSAS patients than in the control patients (616 ± 172 vs 516 ± 174; P = .0285). There was no significant difference in urinary ADH and u-Cre (6.7 ± 10.4 vs 6.8 ± 7.8; P = .3617) between the 2 groups.. Our results indicated that older men with nocturnal polyuria and OSAS did not compensate their fluid imbalance presented with decreased secretion of ADH but increased BNP level.

Topics: Aged; Aged, 80 and over; Circadian Rhythm; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Nocturia; Polyuria; Sleep Apnea, Obstructive; Vasopressins

Topics: Humans; Male; Natriuretic Peptide, Brain; Nocturia; Polyuria; Sleep Apnea, Obstructive; Vasopressins

Topics: Humans; Male; Natriuretic Peptide, Brain; Nocturia; Polyuria; Sleep Apnea, Obstructive; Vasopressins

Central diabetes insipidus (CDI) is caused by deficient secretion of antidiuretic hormone (ADH) due to different conditions that can affect the hypothalamic neurons. It results in an inability to retain normal quantities of free water, which leads to polyuria, including at night, and polydipsia. In adults, it is mostly due to the "idiopathic" form or present after pituitary surgery or a traumatic brain injury. In rare cases, an underlying systemic disease is found. The diagnosis of CDI is based on the water deprivation test. Pituitary MRI and specific clinical and biological work-up are recommended to precise etiology. Treatment of choice is desmopressin, a synthetic analogue of the endogenous ADH hormone. A multidisciplinary team generally provides management and monitoring of CDI.

Topics: Adult; Antidiuretic Agents; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Humans; Magnetic Resonance Imaging; Patient Care Team; Polydipsia; Polyuria; Vasopressins; Water Deprivation

Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI), a disorder caused by mutations in the vasopressin (AVP)-neurophysin II (NPII) gene, manifests gradually during early childhood with progressive polyuria and polydipsia. Patients are usually treated with synthetic AVP analog. If unlimited access to water is provided, prognosis is usually good even in the absence of specific treatment. In this study, we describe three families with adFNDI, in which growth failure was a prominent complaint, on the clinical and molecular level.. Histories from affected and unaffected family members were taken. Height and weight of index patients were recorded longitudinally. Patients underwent water deprivation tests, magnetic resonance imaging, and genetic analysis. One mutant was studied by heterologous expression in cell culture.. A total of ten affected individuals were studied. In two of the three pedigrees, a novel mutation in the AVP-NPII gene was found. The index children in each pedigree showed growth retardation, which was the reason for referral in two. In these cases, water intake was tightly restricted by the parents in an attempt to overcome suspected psychogenic polydipsia and to improve appetite. Once the children were treated by hormone replacement, they rapidly caught up to normal weight and height.. Genetic testing and appropriate parent counseling should be enforced in adFNDI families to ensure adequate treatment and avoid chronic water deprivation, which causes failure to thrive.

Topics: Child; Child, Preschool; Diabetes Insipidus, Neurogenic; Female; Growth Disorders; Humans; Infant; Magnetic Resonance Imaging; Male; Mutation; Neurophysins; Pedigree; Polyuria; Vasopressins; Water Deprivation

Topics: Adult; Blood Gas Analysis; Diabetes Insipidus; Female; Fluid Therapy; Humans; Osmolar Concentration; Perioperative Care; Pituitary Gland; Pituitary Neoplasms; Polyuria; Postoperative Complications; Sodium; Vasopressins; Water-Electrolyte Imbalance

Topics: Child, Preschool; Diabetes Insipidus, Nephrogenic; Humans; Hydronephrosis; Male; Mutation; Neurophysins; Polyuria; Protein Precursors; Vasopressins

To evaluate the relationship between leg edema, nocturnal urine volume (NUV), and the secretion of antidiuretic hormone (ADH) during the night, and to investigate the principal factors affecting nocturnal polyuria in older men.. A total of 74 male inpatients more than 50 years of age were enrolled in this study. Blood count, standard chemistry panel, brain natriuretic peptide (BNP), urinary ADH (u-ADH), urinary creatinine (u-Cre), and urinary osmolarity were measured at 6:00 am. Keeping a frequency volume chart, bioelectric impedance analysis was performed at 5 pm. Leg edema was measured as an edema ratio, using the following formula: extracellular water [L)/(extracellular water [L) + intracellular water [L)) in legs.. A total of 66 patients were evaluated. NUV had a significant positive correlation with leg edema (r = 0.32, P = .008), negative correlation with u-ADH/u-Cre (r = -0.37, P = .003) but not BNP. Leg edema had a significant positive correlation with the level of BNP (r = 0.33, P = .012) and negative correlation with u-ADH/u-Cre (r = -0.4, P = .001). However a partial correlation showed that there was no significant correlation between NUV and leg edema. A multivariate logistic model showed that only u-ADH/u-Cre was an independent predictive variable of nocturnal polyuria.. This study suggested that leg edema influenced nocturnal urine volume with an associated decrease in ADH secretion but not directly. ADH secretion during the night was the principal factor affecting NP in older men.

Topics: Aged; Blood Pressure; Edema; Heart Failure; Humans; Leg; Male; Middle Aged; Natriuretic Peptide, Brain; Nocturia; Osmolar Concentration; Polyuria; Vasopressins

To investigate the effects of Yiniao Recipe, a compound traditional Chinese herbal medicine, on contents of serum antidiuretic hormone, and plasma cyclic adenosine monophosphate and cyclic guanosine monophosphate in rats with kidney-yang deficiency.. Forty male Wistar rats were randomly divided into blank control group, untreated group, desmopressin (Minirin) group, low-dose Yiniao Recipe group and high-dose Yiniao Recipe group, with 8 rats in each group. Rats in the blank control group were injected with 0.2 mL normal saline, and rats in the other groups were given intramuscular injection of hydrocortisone 25 mg/kg, 1 time daily for 21 consecutive days; from the 8th day of injection, rats were given double distilled water, Minirin, and high- and low-dose Yiniao Recipe respectively for 30 days. Before and after treatment, 24-hour urine volume was observed, and serum antidiuretic hormone (AVP) as well as plasma cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) contents were detected by enzyme-linked immunosorbent assay. The cAMP/cGMP ratio and morphological changes in renal tissues were also observed.. Compared with blank control group, 24-hour urine volume, serum AVP content and cAMP/cGMP ratio in the untreated group were decreased; compared with the untreated group, Minirin and Yiniao Recipe at low and high doses reduced 24-hour urine volume and increased serum AVP content and cAMP/cGMP ratio significantly (P<0.05 or P<0.01). There were no obvious pathological changes in renal tissue in all groups.. Yiniao Recipe may reduce 24-hour urine volume by increasing serum AVP content and regulating the ratio of cAMP to cGMP in kidney-yang deficiency rats.

Topics: Animals; Cyclic AMP; Cyclic GMP; Drugs, Chinese Herbal; Male; Phytotherapy; Polyuria; Rats; Rats, Wistar; Vasopressins; Yang Deficiency

A 19-year-old girl presented at our emergency room with hypokalemic periodic paralysis. She had a thyrotoxic goiter and had experienced three paralytic attacks during the previous 2 years on occasions when she stopped taking antithyroid drugs. In addition to thyrotoxic periodic paralysis (TPP), she had metabolic acidosis, urinary potassium loss, polyuria and polydipsia. Her reduced ability to acidify urine during spontaneous metabolic acidosis was confirmed by detection of coexisting distal renal tubular acidosis (RTA). The polyuria and polydipsia were caused by nephrogenic diabetes insipidus, which was diagnosed using the water deprivation test and vasopressin administration. Her recurrent and frequent paralytic attacks may have been the combined effects of thyrotoxicosis and RTA. Although the paralytic attack did not recur after improving the thyroid function, mild acidosis and nephrogenic DI have been remained subsequently. Patients with TPP, especially females with atypical metabolic features, should be investigated for possible precipitating factors.

Topics: Acidosis, Renal Tubular; Adult; Antithyroid Agents; Diabetes Insipidus, Nephrogenic; Female; Goiter; Humans; Hypokalemic Periodic Paralysis; Medication Adherence; Polyuria; Propylthiouracil; Recurrence; Thyrotoxicosis; Vasopressins; Water Deprivation

Polyuria is a symptom that appears in association with diabetes mellitus. Because sustained polyuria causes serious dehydration, it is believed that the body has a compensating mechanism to alleviate dehydration. In the present study, the role of renal aquaporin 2 (AQP2) in the compensating mechanism was investigated in KKAy mice, a type 2 diabetes model.. The renal AQP2 expression levels in KKAy mice aged between 5 and 24 weeks were determined using Western blotting. The hypothalamic vasopressin mRNA expression levels also were measured by real-time RT-PCR. Insulin was subcutaneously administered to 11-week-old KKAy mice twice a day for 7 days. After insulin treatment, the renal AQP2 protein expression and the hypothalamic vasopressin mRNA expression were measured.. The urinary volumes of 5- and 12-week-old KKAy mice were 1.5 ± 0.3 mL and 9.5 ± 1.2 mL, respectively. The inner medullary AQP2 protein expression of 12-week-old KKAy mice was approximately 2.5-fold higher than that of 5-week-old KKAy mice. The hypothalamic vasopressin mRNA expression of 12-week-old KKAy mice was approximately twice that of 5-week-old KKAy mice. Insulin treatment in KKAy mice resulted in a significant reduction in the plasma glucose level, urinary volume, and inner medullary AQP2 protein and hypothalamic vasopressin mRNA expression.. The present study demonstrated that AQP2 is a renal functional molecule of vasopressin that controls urinary volume and that AQP2 in the kidney increases to alleviate dehydration due to type 2 diabetes with polyuria.

Topics: Animals; Aquaporin 2; Blood Glucose; Blotting, Western; Dehydration; Diabetes Mellitus, Type 2; Disease Models, Animal; Gene Expression Regulation; Hypoglycemic Agents; Insulin; Male; Mice; Polyuria; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Vasopressins

Diabetes insipidus is an ancient disease considered under the rubric of diabetes, the Greek descriptive term for polyuria, which was unrecognized even after the sweetness of urine was reported as a characteristic of diabetes mellitus in the 17th century. It would be another century before diabetes insipidus was identified from the insipid rather than saccharine taste of urine in cases of polyuria. After its increased recognition, pathologic observations and experimental studies connected diabetes insipidus to the pituitary gland in the opening decades of the 20th century. Simultaneously, posterior pituitary lobe extracts were shown to be vasoconstrictive (vasopressin) and antidiuretic (antidiuretic hormone). As vasopressin was purified and synthesized and its assay became available, it was shown to be released in response to both osmotic and volume stimuli that are integrated in the hypothalamus, and vasopressin thereby was essential to maintaining internal water balance. The antidiuretic properties of vasopressin to treat the rare cases of diabetes insipidus were of limited clinical utility until its vasoconstrictive effects were resuscitated in the 1970s, with the consequent increasing wider use of vasopressin for the treatment of compromised hemodynamic states. In addition, the discovery of antidiuretic hormone receptor blockers has led to their increasing use in managing hypo-osmolar states.

Topics: Diabetes Insipidus; History, 15th Century; History, 16th Century; History, 17th Century; History, 18th Century; History, 19th Century; History, 20th Century; History, 21st Century; History, Ancient; History, Medieval; Humans; Hypothalamus; Pituitary Gland; Polyuria; Vasopressins; Water-Electrolyte Balance

To identify the relationship between nocturnal AVP deficiency, nocturnal polyuria (NP), and low urinary osmolality in children suffering of primary monosymptomatic nocturnal enuresis (NE).. The study included 50 children (28 males and 22 females) with primary monosymptomatic NE and 30 non enuretic children of the same age group (controls). Night samples of blood and urine were obtained for AVP, blood osmolality, and urine osmolality. In addition, volume frequency charts, arousal threshold, and urodynamics were performed for these children.. Twenty eight (56%) of the enuretic children were considered to have NP. Mean AVP level was 44.80 +/- 8.19 and 32.49 +/- 18.25 pg/ml while mean urine osmolality was 865.07 +/- 158.66 mOsm/kg and 700.06 +/- 84.42 mOsm/kg in controls and enuretic group respectively. These differences were highly significant. No significant difference was found between the controls and enuretics without NP. On the other hand, nocturnal AVP and urine osmolality were significantly lower in enuretics with NP when compared to both controls and enuretics without NP. Blood osmolality did not reach statistically significant difference between subgroups. Arousal threshold was significantly higher in enuretic children irrespective to NP. The timing for NE episodes were predominantly late in the night in NE children without NP while patients suffering of NE with NP typically experienced multiple incidents each night.. We have shown that low nocturnal AVP and urine osmolality may play a role in the pathophysiology of enuretics with NP. This abnormality doesn't occur as an isolated disease as these children suffer from arousal defect as well.

Topics: Adolescent; Case-Control Studies; Child; Circadian Rhythm; Diagnostic Techniques, Urological; Female; Humans; Male; Neurophysins; Nocturnal Enuresis; Osmolar Concentration; Polyuria; Predictive Value of Tests; Protein Precursors; ROC Curve; Sensitivity and Specificity; Sleep Arousal Disorders; Urodynamics; Vasopressins

Angiotensin II plays an important role in the regulation of blood pressure, body salt and fluid balance, and urine concentration. Mice with deletion of the AT(1a) receptor develop polyuria and urine concentration defects. We studied the mechanisms of these urine concentration defects by treating wild-type and AT(1a)-knockout mice with arginine vasopressin (AVP) for 2 weeks, controlling their water intake, or giving them an osmotic diuretic (sucrose) in order to determine whether central or nephrogenic mechanisms were involved. Under basal conditions, AT(1a)-knockout mice were hypotensive, had lower plasma AVP, and excreted more urine with a markedly reduced osmolality compared with wild-type mice. However, basal glomerular filtration rates were similar in both strains of mice. We isolated total lysate and membrane proteins from the inner medulla of wild-type and mutant mouse kidneys, and found that the amounts of aquaporin 2 (AQP2), adenylyl cyclases III and V/VI, and phosphorylated MAP kinases ERK 1/2 proteins were all reduced in the inner medulla of the knockout mice. Infusion of AVP raised plasma levels and blood pressure proportionally in both strains, but polyuria persisted and urine osmolality remained significantly lower in the knockout mice. Although AVP increased urine osmolality slightly in water-deprived knockout mice, this was well below the basal osmolality of wild-type mice. The diuretic response to the hyperosmotic sucrose was also impaired in the knockout mice. Neither AVP nor water rationing restored the levels of the inner medullary signaling proteins and membrane AQP2 proteins in the knockout mice. We suggest that AT(1a) receptor deletion causes polyuria and urine concentration defects by decreasing basal AVP release and impairing AVP-induced receptor signaling in the inner medulla.

Topics: Animals; Antidiuretic Agents; Aquaporin 2; Arginine Vasopressin; Hypotension; Kidney Concentrating Ability; Kidney Medulla; Mice; Mice, Knockout; Polyuria; Receptor, Angiotensin, Type 1; Receptors, Vasopressin; Vasopressins

Topics: Adult; Antidiuretic Agents; Cardiac Surgical Procedures; Humans; Hypotension; Male; Polyuria; Postoperative Complications; Substance Withdrawal Syndrome; Vasopressins

To explore the influence of obstructive sleep apnea hypopnea syndrome (OSAHS) in children on the secretion of antidiuretic hormone (ADH).. Thirty pediatric patients with OSAHS were examined with polysomnography (PSG) and urinary volume was recorded during sleep, and vein blood was sampled in deep sleep to detect the level of ADH in serum using radioimmunoassay technique, which were performed before and after adenotonsillectomy. Among twenty heath children were also detected the secretion of ADH as normal controls.. After surgery, apnea-hypopnea index (AHI) decreased (from 17.4 +/- 2.6 to 3.3 +/- 1.4, t = 27.68, P < 0.001), lowest SaO2 increased (from 0.783 +/- 0.134 to 0.954 +/- 0.062, t = 6.45, P < 0.001). The level of ADH in OSAHS patients (63.1 +/- 35.2) ng/L was much lower than that in health children (85.1 +/- 22.2) ng/L (t = 2.75, P < 0.01). The serum ADH level in postoperative patients (83.1 +/- 21.2) ng/L was increased significantly compared with that of preoperative (t = 2.56, P < 0.05), and no statistical difference versus that of health children (t = 0.17, P > 0.05). Nycturia volume of preoperative OSAHS children (492 +/- 90) ml was significant higher than that of postoperative (332 +/- 56) ml or normal controls (346 +/- 62) ml (t was 7.85 and 6.43, both P < 0.001). There was no significance in nycturia volume between postoperative group and control group (t = 0.77, P > 0.05).. After adenotonsillectomy in children with OSAHS caused by adenotonsillar hypertrophy, the sleep pattern and ADH secretion could become normal.

Topics: Adenoidectomy; Case-Control Studies; Child; Female; Humans; Male; Polysomnography; Polyuria; Sleep Apnea, Obstructive; Tonsillectomy; Vasopressins

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

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

To investigate the clinical feature, treatment and prognosis of both the mother and the fetus with gestational diabetes insipidus.. A total of 7 cases of gestational diabetes insipidus collected in the First Affiliated Hospital of Wenzhou Medical College, Wenzhou Combination of Traditional Chinese Medicine with Western Medicine Hospital, and Zhejiang Taizhou Hospital from June 1993 to June 2006 were analyzed retrospectively.. Seven cases symptoms all characterized by excessive thirst polydipsia and polyuria. The average 24 h urinary output was between 11 L to 13 L and manifested of hypobaricuria. After effective treatment (three cases were treated with 1-deamino-8-D-arginine vasopressin, another three patients were managed with hydrochlorothiazide, and the last one was cured with antisterone), seven patients with gestational diabetes insipidus did not have any severe consequences. Their symptoms of excessive thirst, polyuria, and polydypsia disappeared from 7 days to 3 months after parturition. Urinary volume returned to normal standard of 1000-2000 ml during 24 hours. Specific gravity of urine recovered normally between a range 1.015-1.025 and serum sodium recovered between 135-147 mmol/L. The average duration of illness was 52 days. Eight newborn infants survived. Two of them were sent to neonatal intensive care unit for treatment. One was because of premature delivery caused by antepartum eclampsia, and the other case was one of the twins who had hydronephrosis. The baby of the first case left hospital after 3 weeks' treatment. The latter one's symptom disappeared 2 weeks after delivery. No obvious symptom was discovered among all the babies through follow-up telephone calls 42 days after childbirth.. Gestational diabetes insipidus is a rare endocrinopathy complicating pregnancy. This disorder is characterized by excessive thirst, polydypsia, polyuria, hypobaric urine and electrolyte disturbances usually manifesting in the third trimester of pregnancy or puerperium. This is a transient syndrome. The first treatment of choice in patients with gestational diabetes insipidus is 1-deamino-8-D-arginine vasopressin and the second-choice is hydrochlorothiazide. Early diagnosis and appropriate management of the disease may reduce the hazard for both the mother and the fetus during perinatal period.

Topics: Adult; Deamino Arginine Vasopressin; Diabetes Insipidus; Female; Humans; Hydrochlorothiazide; Infant, Newborn; Polyuria; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Prognosis; Retrospective Studies; Sodium; Vasopressins; Young Adult

Diabetes insipidus (DI) is a rare clinical condition, which is usually caused by neurohypophyseal or pituitary stalk infiltration in cancer patients.. we present a 62-year old metastatic breast cancer woman with DI. She admitted to the hospital because of nausea, vomiting, polyuria and polydipsia, while she was on no cytotoxic medication. She had no electrolyte imbalance except mild hypernatremia. The CT scan of the brain yielded a suspicious area in pituitary gland. A pituitary stalk metastasis was found on magnetic resonance imaging (MRI) of pituitary. Water deprivation test was compatible with DI. A clinical response to nasal vasopressin was achieved.. Cancer patients who have symptoms such as nausea, vomiting, polyuria and polydipsia while they are not on chemotherapy should be evaluated for not only metabolic complications like hypercalcemia but also posterior pituitary or stalk metastasis MRI could be the choice of imaging for pituitary metastasis.

Topics: Administration, Intranasal; Breast Neoplasms; Diabetes Insipidus; Female; Humans; Magnetic Resonance Imaging; Nausea; Pituitary Neoplasms; Polyuria; Thirst; Vasopressins; Vomiting

Monosymptomatic nocturnal enuresis is frequently associated with nocturnal polyuria and low urinary osmolality during the night. Initial studies found decreased vasopressin levels associated with low urinary osmolality overnight. Together with the documented desmopressin response, this was suggestive of a primary role for vasopressin in the pathogenesis of enuresis in the absence of bladder dysfunction. Recent studies no longer confirm this primary role of vasopressin. Other pathogenetic factors such as disordered renal sodium handling, hypercalciuria, increased prostaglandins and/or osmotic excretion might have a role. So far, little attention has been given to abnormalities in the circadian rhythm of glomerular filtration rate. We evaluated the circadian rhythm of glomerular filtration rate and diuresis in children with desmopressin resistant monosymptomatic nocturnal enuresis and nocturnal polyuria.. We evaluated 15 children (9 boys) 9 to 14 years old with monosymptomatic nocturnal enuresis and nocturnal polyuria resistant to desmopressin treatment. The control group consisted of 25 children (12 boys) 9 to 16 years old with monosymptomatic nocturnal enuresis without nocturnal polyuria.. Compared to the control population, children with nocturnal polyuria lost their circadian rhythm not only for diuresis and sodium excretion but also for glomerular filtration rate.. Patients with monosymptomatic nocturnal enuresis and nocturnal polyuria lack a normal circadian rhythm for diuresis and sodium excretion, and the circadian rhythm of glomerular filtration rate is absent. This absence of circadian rhythm of glomerular filtration rate and/or sodium handling cannot be explained by a primary role of vasopressin, but rather by a disorder in circadian rhythm of renal glomerular and/or tubular functions.

Topics: Adolescent; Case-Control Studies; Child; Circadian Rhythm; Deamino Arginine Vasopressin; Diuresis; Drug Resistance; Female; Glomerular Filtration Rate; Humans; Male; Nocturnal Enuresis; Osmolar Concentration; Polyuria; Prospective Studies; Reference Values; Severity of Illness Index; Sodium; Statistics, Nonparametric; Urodynamics; Vasopressins

A 39-year-old man was hospitalized after divalproate self-poisoning. He presented coma requiring tracheal intubation and mechanical ventilation at 11 hours and central diabetes insipidus. Serum valproic acid concentration was 590 mg/l at 30 hours. Progressive improvement occurred after hydratation and administration of vasopressin.

Topics: Adult; Bipolar Disorder; Coma; Diabetes Insipidus; Fluid Therapy; Humans; Intubation, Intratracheal; Male; Poisoning; Polyuria; Respiration, Artificial; Suicide, Attempted; Valproic Acid; Vasopressins

Up to 21% of severe cases of malaria tropica are associated with polyuria and are life-threatening. We describe a 39-yr-old man with malaria tropica who developed disseminated intravascular coagulation, polyuria, and a pituitary lesion. Empiric treatment with vasopressin improved the polyuria. This is the first case of malaria tropica in which central diabetes insipidus has been documented.

Topics: Adrenal Insufficiency; Adult; Diabetes Insipidus, Neurogenic; Disseminated Intravascular Coagulation; Humans; Hydrocortisone; Magnetic Resonance Imaging; Malaria, Falciparum; Male; Natriuresis; Pituitary Gland, Posterior; Polyuria; Pulmonary Embolism; Renal Insufficiency; Vasopressins

Prostaglandins have an important role in renal salt and water reabsorption. PGE2 is the main kidney prostaglandin and is thought to be mainly produced in the kidney inner medulla (IM). There are indications that PGE2 synthesis in nephrogenic (NDI) and central (CDI) diabetes insipidus is altered. We hypothesize that the expression of the major PGE2 synthesis enzymes cyclooxygenases 1 and 2 (COX-1, COX-2) and membrane-associated PGE2 synthase (mPGES) is altered in the kidneys of rats with NDI and CDI. Wistar rats treated with lithium for 4 wk were used as the NDI model. One-half of the NDI model rats were additionally dehydrated for 48 h. Brattleboro (BB) rats that lack endogenous antidiuretic hormone were used as the CDI model. Expression and localization of COX-1, COX-2, and mPGES in IM, inner stripe of outer medulla (ISOM), and cortex were determined by immunoblotting and immunohistochemistry. In lithium-induced NDI, expression of COX-1, COX-2, and mPGES was markedly decreased in IM. In ISOM and cortex, COX-1 expression was marginally reduced and mPGES expression was unaltered. COX-2 expression was undetected in ISOM and marginally increased in cortex. Consistent with this, the density of COX-2-expressing cells in macula densa was significantly increased, indicating differential regulation of COX-2 in IM and cortex. Dehydration of NDI rats resulted in a marked increase in COX-2 immunolabeling in IM interstitial cells, and there was no significant change in COX-1 and mPGES expression in any kidney zone. Treatment of DDAVP in BB rats for 6 days resulted in a markedly increased expression of COX-1, COX-2, and mPGES in IM. In the cortex, there were no changes in the expression of COX-1 and mPGES, whereas COX-2 expression was decreased. These results identify markedly reduced expression of COX-1, COX-2, and mPGES in IM in lithium-induced NDI. Furthermore, there were major changes in the expression of COX-1, COX-2, and mPGES in rats with CDI.

Topics: Animals; Cyclooxygenase 1; Cyclooxygenase 2; Deamino Arginine Vasopressin; Dehydration; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Dinoprostone; Intramolecular Oxidoreductases; Kidney Concentrating Ability; Kidney Cortex; Kidney Medulla; Lithium; Male; Membrane Proteins; Polyuria; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Brattleboro; Rats, Wistar; Renal Agents; Vasopressins; Water Deprivation

Topics: Diabetes Insipidus; Female; Humans; Incidence; Polyuria; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Pregnancy Trimester, Third; Prognosis; Risk Assessment; Vasopressins

Transient diabetes insipidus may rarely present during late pregnancy and/or the immediate puerperium, and if unrecognized, may cause neurologic injury and threaten the lives of mother and fetus. However, when recognized early and treatment is initiated with desmopressin acetate, an analog of vasopressin that is resistant to vasopressinase, water loss in the urine is eliminated and complications may be abrogated. This report aims to increase the awareness of this disorder and describes appropriate treatment.. Two cases of diabetes insipidus, believed to be due to excess vasopressinase, are presented to demonstrate the clinical features, pathogenesis, and treatment of this syndrome.. Awareness of the syndrome of transient diabetes insipidus may lead to early diagnosis and appropriate treatment that will reduce the risks of maternal and fetal morbidity.

Topics: Adult; Deamino Arginine Vasopressin; Diabetes Insipidus; Female; Follow-Up Studies; Humans; Maternal Age; Polyuria; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Pregnancy Trimester, Third; Risk Assessment; Treatment Outcome; Vasopressins

The present study aims to evaluate the effect of desmopressin treatment on urine output, density and glomerular filtration rate (GFR) in patients with posterior urethral valve (PUV) and the factors affecting the response to this treatment.. A total of 68 PUV patients who were followed-up after valve ablation were examined with the fluid intake, urine output and GFR. Sixteen patients who were polyuric (a urine output more than 30 ml/kg/day) and had hypoosmolar urine (urinary density of 1015 or lower) included in the study. Blood chemistry and serum ADH level were studied. Following 5 days of observation, patients were given DDAVP perorally with a dosage of 0.4 mg/day, two equal doses per day. After 7 days and after a 3 month period of treatment, voiding characteristics, day-time and night-time urine densities and also GFR have been re-evaluated.. The mean age was 6.8 years (range 2 to 11 years). The mean age at valve ablation was 20.7 months (range 5 months to 6 years). The mean daily urine output during first week and at the third month of the treatment had decreased significantly (p=0.004 and p=0.006). There was increase in night-time and day-time urine density in 10 patients (62%) and in 13 patients (81%) respectively at the third month evaluation. Increments in urine density were statistically significant for the third month evaluation. Nine (56%) patients had ADH levels within normal (<7 pcg/ml) levels and 7 patients had higher levels. There was no statistically significant difference between pretreatment and posttreatment micturation characteristics. However patients with voiding dysfunction responded better to DDAVP treatment.. Desmopressin treatment improves polyuria in PUV patients. The responses are better particularly in PUV patients with significant bladder dysfunction. This supports the harmful role of polyuria on bladder dysfunction. The DDAVP treatment improves the day-time and night-time in PUV patients. Combination of DDAVP treatment with overnight catheterization may be a good alternative that needs to be evaluated by further prospective randomized studies.

Topics: Antidiuretic Agents; Child; Child, Preschool; Deamino Arginine Vasopressin; Follow-Up Studies; Glomerular Filtration Rate; Humans; Infant; Male; Polyuria; Urination Disorders; Urine; Urodynamics; Vasopressins

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

Autosomal dominant neurohypophyseal diabetes insipidus (ADNDI) is a defect in free water conservation caused by mutations in the single gene that encodes both vasopressin (VP) and its binding protein, neurophysin II (NP II). Most of the human mutations in this gene have been in the portion encoding the NP molecule; the resultant abnormal gene products are believed to cause cellular toxicity as improperly folded precursor molecules accumulate in the endoplasmic reticulum. We identified a new American kindred with ADNDI and found a novel mutation in the VP molecule. A 78-yr-old man was noted to have hypotonic polyuria and plasma hyperosmolarity; the urinary concentration defect was reversed by administration of VP. His symptomatology dated to childhood, and his family history was consistent with autosomal transmission of the polyuric syndrome, with affected members in three generations, including several females. Affected individuals were found to be heterozygous for a 3-bp deletion in exon 1 of arginine VP (AVP)-NP II, predicting a deletion of phenylalanine 3 (known to be critical for receptor binding) in the VP nonapeptide. Neuro 2A cells stably transfected with the mutant AVP-NP construct showed increased rates of apoptosis as assessed by flow cytometric methods. These observations support the concept that cellular toxicity of abnormal AVP-NP gene products underlies the development of ADNDI, and the data further demonstrate that mutations affecting the AVP moiety can result in initiation of these pathological processes.

Topics: Aged; Apoptosis; Base Sequence; Diabetes Insipidus, Neurogenic; Flow Cytometry; Gene Deletion; Genes, Dominant; Heterozygote; Humans; Male; Molecular Sequence Data; Mutation; Neurophysins; Pedigree; Polyuria; Protein Precursors; Vasopressins

We verify the sodium fraction excretion rate (FE Na) and potassium fraction excretion (FE K) rates in monosymptomatic nocturnal enuresis. We also correlate FE Na and FE K to urinary osmolality, nocturnal polyuria and vasopressin in the same population.. A total of 438 children 6 to 15 years old (mean age 9.7) presenting with monosymptomatic nocturnal enuresis were recruited from different centers. Inclusion criteria were 3 or greater wet nights a week, no daytime incontinence and no treatment in the previous 2 months. Exclusion criteria were cardiopathy, endocrinopathy, psychiatric problems and urinary tract abnormalities. Micturition chart, diurnal (8 am to 8 pm) and nocturnal (8 pm to 8 am) urine collection, including separate diuresis volumes, (Na, K and Ca) electrolytes and osmolality were evaluated, as well as serum electrolytes, creatinine and nocturnal (4 am) vasopressin. Diurnal and nocturnal FE K and FE Na were calculated. ANOVA test, chi-square test, Student's t test and Pearson correlation test were used for statistical analysis.. : Nocturnal polyuria (diurnal to nocturnal diuresis ratio less than 1) was found in 273 children (62.3%, group 1 and nocturnal urine volumes were normal in 165 with enuresis (37.7%, group 2). Nocturnal FE Na was abnormal in 179 children (40.8%), including 118 in group 1 (43.2%) and 61 in group 2 (36.9%) (chi-square not significant). FE Na was also increased in nocturnal versus daytime diuresis (Student's t test p <0.001). In group 1 nocturnal FE Na correlated with nocturnal diuresis (Pearson correlation p = 0.003, r = +0.175), while daytime FE Na and nocturnal FE Na correlated with diurnal diuresis (Pearson correlation p = 0.001, r = +0.225 and Pearson correlation p = 0.001, r = +0.209, respectively). In group 2 nocturnal FE Na did not correlate with diuresis (Pearson correlation p = 0.103, r = +0.128) but correlated with vasopressin values (Pearson correlation p = 0.042, r = -0.205). Urine osmolality was reduced in 140 children (31.9%) and correlated with nocturnal diuresis (Pearson correlation p = 0.003, r = -0.321). Vasopressin was decreased in 332 children (75.8%, 62.6% in group 1 and 13.2% in group 2). No significant difference was found between sexes and age of enuretic subgroups.. Nocturnal FE Na correlates with nocturnal diuresis, whereas daytime FE Na does not. FE K in daytime and nighttime diuresis does not statistically differ in nocturnal polyuric and nonpolyuric enuretic groups. Osmolality correlates with nocturnal diuresis, and vasopressin at 4 am was lower in the nocturnal polyuric group. The hypothesis of a subset of enuretic patients presenting with nocturnal polyuria associated with high nocturnal natriuria and low vasopressin values has been confirmed.

Topics: Adolescent; Child; Enuresis; Female; Humans; Male; Osmolar Concentration; Polyuria; Potassium; Sodium; Vasopressins

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

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

We determined in older adults whether frequent nighttime voiding is associated with urine overproduction at night or nocturnal polyuria (NP) and whether NP is associated with abnormalities of arginine vasopressin (AVP) blood levels and/or renal responsiveness to AVP.. We used a convenience sample of adults 65 years and older in home and general clinical research center settings. A total of 45 participants completed the 3-day general clinical research center stay. We used 7-day voiding diaries to determine which participants had 2 or greater nighttime voids and NP, defined as 35% or greater of 24-hour urine output at night. Abnormalities in AVP release and secretion were determined by water deprivation testing and by twice daily blood AVP measurement.. There was a strong positive association between the number of nighttime voids and the proportion of urine produced at night (r = 0.6, p <0.001). There was no association between NP and AVP blood levels or action. Participants with and without NP had similar maximum urine osmolality following water deprivation and exogenous AVP administration (mean 549 mOsm, range 422 to 713 and 547 mOsm, range 353 to 692, respectively).. We found no association between NP and AVP abnormalities in this sample of older adults. Study participants had low maximal urine osmolality in response to fluid deprivation and exogenous vasopressin administration irrespective of whether they were identified as having NP.

Topics: Aged; Arginine Vasopressin; Deamino Arginine Vasopressin; Female; Humans; Male; Osmolar Concentration; Polyuria; Urine; Vasopressins; Water Deprivation

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

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

Topics: Adult; Blood Chemical Analysis; Diabetes Insipidus; Drinking Behavior; Female; Follow-Up Studies; Humans; Infant, Newborn; Liver Function Tests; Polyuria; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Pregnancy Trimester, Third; Risk Assessment; Thirst; Twins; Urinalysis; Vasopressins

The apical Na+-H+ exchanger NHE3 plays an important role in fluid reabsorption in the proximal tubule. However, whether its deletion alters the salt and water transport in the distal nephron remains unknown. To answer these questions, wild-type (Nhe3+/+) and NHE3 null mice (Nhe3-/-) were placed in metabolic cages and their water balance and urine osmolality were examined. Nhe3-/- mice demonstrated a significant polydipsia (P < 0.03) and polyuria (P < 0.04), with a lower urine osmolality (P < 0.003) as compared to Nhe3+/+ mice. Northern hybridization and immunoblotting studies indicated that the mRNA expression and protein abundance of the collecting duct (CD) water channel AQP2 decreased by 52 % (P < 0.0003) and 73 % (P < 0.003) in the cortex, and by 53 % and 54 % (P < 0.002) in the inner medulla (IM) of Nhe3-/- vs. Nhe3+/+ mice. The expression of AQP2 in the outer medulla (OM) remained unchanged. Further, the mRNA expression and protein abundance of the medullary thick ascending limb (mTAL) apical Na+-K+-2Cl- cotransporter (NKCC2) decreased by 52 % (P < 0.02) and 44 % (P < 0.01), respectively, in the OM of Nhe3-/- vs. Nhe3+/+ mice. The circulating plasma levels of vasopressin as well as the mRNA expression of vasopressin prohormone were significantly increased in Nhe3-/- vs. Nhe3+/+ mice (P < 0.05). Studies in mice treated with acetazolamide indicated that increased bicarbonate and fluid delivery to distal nephron did not alter the expression of NKCC2 in mTAL and decreased AQP2 protein only in OM but not in the cortex or IM. In conclusion, mice lacking the apical NHE3 have impairment in their water balance and urine osmolality, which correlates with the downregulation of AQP2 expression. These defects occur despite increased circulating levels of vasopressin. We propose that an ADH-independent mechanism is responsible for the downregulation of AQP2 and the resulting polyuria in NHE3 null mice.

Topics: Acetazolamide; Animals; Aquaporin 1; Aquaporin 2; Aquaporins; Blotting, Northern; Blotting, Western; Down-Regulation; Drinking; Gene Expression; Heterozygote; Homozygote; Hydrogen-Ion Concentration; Kidney; Kidney Cortex; Kidney Medulla; Mice; Mice, Knockout; Osmolar Concentration; Polyuria; Sodium; Sodium-Hydrogen Exchanger 3; Sodium-Hydrogen Exchangers; Sodium-Potassium-Chloride Symporters; Sodium-Potassium-Exchanging ATPase; Solute Carrier Family 12, Member 1; Urine; Vasopressins

Desmopressin may not be effective for nocturnal enuresis associated with polyuria and hypercalciuria. Nighttime hypercalciuria in an enuretic population from 5 centers and its correlation with nighttime polyuria were verified.. A total of 450 enuretic patients (278 males, 172 females, mean age 9.7 years) were evaluated with 72-hour micturition charts, urinalysis, serum creatinine and osmolarity, diurnal and nocturnal electrolytes with fractional Na+ and K+ urinary excretion, and nocturnal (4 a.m.) plasma vasopressin. Creatinine electrolytes and osmolarity were measured in daytime (8 a.m. to 8 p.m.) and nighttime (8 p.m. to 8 a.m.) urine volumes. Patients were divided into group 1 with nocturnal polyuria and group 2 without nocturnal polyuria. Hypercalciuria was defined as urinary calcium-to-urinary creatinine ratio greater than 0.21. Statistic evaluation was performed using chi-square, Pearson correlation and ANOVA tests.. Nighttime polyuria was demonstrated in 292 bedwetters (65% group 1). Nocturnal hypercalciuria was present in 179 of the 450 children (39.7%), including 125 in group 1 (42.8%) and 54 in group 2 (34.2%), which was statistically significant (chi-square p = 0.008, Pearson correlation test r = 0.157). Daytime calciuria was not statistically modified in either group (group 1 p = 0.054, group 2 p = 0.56). Adrenocorticotropic hormone (ADH) was normal in 18.5% and low in 81.5% of enuretics with nocturnal hypercalciuria. ADH levels and nocturnal hypercalciuria significantly correlated (p = 0.003, r = 0.148). Conversely, the group 2 patients had normal ADH levels.. Nocturnal hypercalciuria has a pivotal role in nocturnal enuresis, as it is significantly associated with low ADH levels and nocturnal polyuria. A new classification of nocturnal enuresis subtypes based on nighttime calciuria levels is mandatory to address treatment properly.

Topics: Adolescent; Adrenocorticotropic Hormone; Calcium; Child; Circadian Rhythm; Creatinine; Deamino Arginine Vasopressin; Diagnosis, Differential; Electrolytes; Enuresis; Female; Humans; Male; Polyuria; 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

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

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

A water deprivation test or a hypertonic saline infusion test with the measurement of plasma osmolality and plasma vasopressin are the gold standard tests in the differential diagnosis of polyuric syndromes. Because commercially available vasopressin kits are too insensitive for this approach, and the concentration of vasopressin in urine is much higher than in plasma, urinary vasopressin measurements may be an alternative to the more difficult plasma vasopressin measurement.. The diagnostic value of the measurement of urinary vasopressin with a rather insensitive commercially available vasopressin kit was compared with plasma vasopressin measurement by a highly sensitive radioimmunoassay (RIA).. Thirteen normal subjects and 27 patients with polyuria/polydipsia were examined by an 8-h fluid deprivation test. In all blood samples (0800 h, 1200 h, 1400 h and 1600 h) and in all urine collections (2-hourly fractions), osmolality as well as vasopressin were measured.. Using plasma vasopressin measurement with a highly sensitive RIA as gold standard test, nine patients were classified as having primary polydipsia, whereas 18 had partial or complete cranial diabetes insipidus. Whereas the substitution of plasma vasopressin measurement by urinary vasopressin measurement alone did not provide 100% separation between both groups, the product of urinary vasopressin and urinary osmolality related to plasma osmolality completely separated the patients with primary polydipsia from those with diabetes insipidus. Urinary measurement of vasopressin and osmolality alone, which was recommended as a noninvasive diagnostic procedure in children, was too insensitive for exact differential diagnosis in our adult patients.. The simultaneous measurement of plasma vasopressin and plasma osmolality in a dehydration test is the most powerful diagnostic tool in the differential diagnosis of polyuria/polydipsia. However, if highly sensitive assays for plasma vasopressin measurements are not available, the measurement of urinary vasopressin with commercially available, less sensitive RIAs may be a diagnostic alternative, which showed nearly the same sensitivity as plasma vasopressin measurement in our study population.

Topics: Adult; Aged; Case-Control Studies; Deamino Arginine Vasopressin; Diabetes Insipidus; Diagnosis, Differential; Drinking; Female; Humans; Male; Middle Aged; Osmolar Concentration; Polyuria; Predictive Value of Tests; Radioimmunoassay; Vasopressins

In a 10-year-old castrated male shorthaired German pointer polyuria was associated with slight hypokalemia, hypophosphatemia and alkalosis, as well as elevated plasma concentrations of a glucocorticoid-inducible iso-enzyme of alkaline phosphatase. Repeated measurements of urinary corticoids and normal suppressibility of the hypothalamus-pituitary-adrenocorticial axis excluded glucocorticoid excess. Urine osmolality (Uosm) did not increase during administration of the vasopressin analogue desmopressin. At the time water deprivation had caused Uosm to rise from 300 to 788 mOsm/kg, there was also plasma hypertonicity. During hypertonic saline infusion the osmotic threshold for vasopressin release was increased. The combination of elevated plasma aldosterone concentrations and unmeasurably low plasma renin activity pointed to primary hyperaldosteronism. As initially computed tomography (CT) did not reveal an adrenocortical lesion, the dog was treated with the aldosterone antagonist spironolactone. This caused Uosm to rise in a dose-dependent manner. However, well-concentrated urine was only achieved with doses that gave rise to adverse effects. Once repeated CT, using 2-mm-thick slices, had revealed a small nodule in the cranial pole of the left adrenal, unilateral adrenalectomy was performed which resolved the polyuria completely. Also the plasma concentrations of kalium, aldosterone and renin activity returned to within their respective reference ranges. The adrenocortical nodule had the histological characteristics of an aldosteronoma, with the non-affected zona glomerulosa being atrophic.In this dog with primary hyperaldosteronism the polyuria was characterized by vasopressin resistance and increased osmotic threshold of vasopressin release, similar to the polyuria of glucocorticoid excess. The possibility is discussed that the polyuria of glucocorticoid excess is actually a mineralocorticoid effect.

Topics: Adrenalectomy; Aldosterone; Animals; Dog Diseases; Dogs; Hyperaldosteronism; Male; Osmolar Concentration; Polyuria; Renin; Saline Solution, Hypertonic; Urine; Vasopressins

The mechanisms underlying the prevention of age-related polyuria by chronic food restriction were investigated in female WAG/Rij rats. The decreased osmolality of renal papilla observed in senescent rats was not corrected by food restriction. A reduced urea content in the inner medulla of senescent rats, fed ad libitum or food-restricted, was suggested by the marked decrease in expression of UT-A1 and UT-B1 urea transporters. Aquaporin-2 (AQP2) downregulation in the inner medulla of senescent rats was partially prevented by food restriction. Both AQP2 and the phosphorylated form of AQP2 (p-AQP2), the presence of which was diffuse within the cytoplasm of collecting duct principal cells in normally fed senescent rats, were preferentially targeted at the apical region of the cells in food-restricted senescent animals. Plasma vasopressin (AVP) was similar in 10- and 30-mo-old rats fed ad libitum, but was doubled in food-restricted 30-mo-old rats. This study indicates that 1) kidney aging is associated with a marked decrease in AQP2, UT-A1, and UT-B1 expression in the inner medulla and a reduced papillary osmolality; and 2) the prevention of age-related polyuria by chronic food restriction occurs through an improved recruitment of AQP2 and p-AQP2 to the apical membrane in inner medulla principal cells, permitted by increased plasma AVP concentration.

Topics: Aging; Animals; Aquaporin 2; Aquaporin 6; Aquaporins; Carrier Proteins; Cell Polarity; Eating; Female; Kidney; Kidney Medulla; Kidney Tubules; Membrane Glycoproteins; Membrane Transport Proteins; Osmolar Concentration; Phosphorylation; Polyuria; Protein Transport; Rats; Urea Transporters; Urine; Vasopressins; Water-Electrolyte Imbalance

The mechanisms underlying age-related polyuria were investigated in 10- and 30-mo-old female WAG/Rij rats. Urinary volume and osmolality were 3.9 +/- 0.3 ml/24 h and 2,511 +/- 54 mosmol/kgH(2)O in adult rats and 12.8 +/- 0.8 ml/24 h and 1,042 +/- 44 mosmol/kgH(2)O in senescent animals. Vasopressin V(2) receptor mRNA did not significantly differ between 10 and 30 mo, and [(3)H]vasopressin binding sites in membrane papilla were reduced by 30%. The cAMP content of the papilla was unchanged with age, whereas papillary osmolality was significantly lowered in senescent animals. The expression of aquaporin-1 (AQP1) and -4 was mostly unaltered from 10 to 30 mo. In contrast, aquaporin-2 (AQP2) and -3 (AQP3) expression was downregulated by 80 and 50%, respectively, and AQP2 was markedly redistributed into the intracellular compartment, in inner medulla of senescent animals, but not in renal cortex. These results indicate that age-related polyuria is associated with a downregulation of AQP2 and AQP3 expression in the medullary collecting duct, which is independent of vasopressin-mediated cAMP accumulation.

Topics: Aging; Animals; Aquaporin 2; Aquaporin 3; Aquaporin 6; Aquaporins; Binding Sites; Body Weight; Cell Membrane; Cyclic AMP; Down-Regulation; Drinking; Eating; Female; Fluorescent Antibody Technique, Indirect; Kidney; Kidney Medulla; Kidney Tubules; Osmolar Concentration; Polyuria; Rats; Rats, Inbred Strains; Receptors, Vasopressin; RNA, Messenger; Vasopressins

Cisplatin (CP)-induced polyuria in rats is attributed to decreased medullary hypertonicity and/or an end-organ resistance to vasopressin. However, the roles of renal aquaporins (AQPs) have not yet been explored.. Male Sprague-Dawley rats (230 to 245 g) received either a single injection of CP (5 mg/kg, N = 4) or saline (N = 4) intraperitoneally five days before sacrifice. Urine, blood, and kidney samples were analyzed.. Platinum accumulated in the cortex and outer medulla of CP-treated rats (39.05 +/- 7.50 and 36.48 +/- 12.44 microg/g vs. 2.52 +/- 0.43 and 1.87 +/- 0.84 microg/g dry tissue in controls, respectively). Histologically, tubular damage and decreased AQP1 immunolabeling were detected in the S3 segment of proximal tubules. CP treatment caused 4.4- and 4.8-fold increases, respectively, in blood urea nitrogen and urine volume, and a 4. 4-fold decrease in urine osmolality. Immunoblots showed that AQP2 and AQP3 were significantly reduced to 33 +/- 10% (P < 0.001) and 69 +/- 11% (P < 0.05), respectively, in the inner medulla of CP-treated rats. Immunocytochemical analysis showed a decrease in AQP2 labeling in the inner medulla of CP-treated rats. Northern hybridization revealed a 33 +/- 11% (P < 0.002) decrease in AQP2 mRNA expression in the inner medulla of CP-treated rats. AQP1 protein expression levels were modestly (67 +/- 7%, P = 0.057) and significantly (53 +/- 13%, P < 0.007) decreased in outer and inner medullae, respectively, of CP-treated rats.. CP-induced polyuria in rats is associated with a significant decrease in the expression of collecting duct (AQP2 and AQP3) and proximal nephron and microvascular (AQP1) water channels in the inner medulla.

Topics: Animals; Antineoplastic Agents; Aquaporin 1; Aquaporin 2; Aquaporin 3; Aquaporin 6; Aquaporins; Blood Urea Nitrogen; Blotting, Northern; Body Weight; Cisplatin; Disease Models, Animal; Gene Expression; Immunoblotting; Kidney Tubules, Collecting; Kidney Tubules, Proximal; Male; Platinum; Polyuria; Rats; Rats, Sprague-Dawley; RNA, Messenger; Urinalysis; Vasopressins

Early morning urine osmolality was tested in two urinary specimens, one taken immediately upon awakening and the other approximately 30 min thereafter, in 52 enuretic and 15 non-enuretic children. In a follow-up study, using the same study population, urine osmolality and volume were measured sequentially at 3-h intervals at 19.00, 22.00, 01.00, 04.00 and 07.00 h. Thereafter, all enuretics were treated by intranasal DDAVP for a 6-month period. There were no differences in urinary osmolality between enuretic and non-enuretic children when comparing the two early morning specimens. Nor were there any differences between groups in urine osmolalities at 19.00, 01.00 and 07.00 h. In contrast, at 04.00 h, urine osmolality was significantly lower in 17 of 52 enuretics [designated as ADH-negative (ADH-)] compared to the remaining enuretics [designated as ADH-positive (ADH+)] and non-enuretic children (610 +/- 251 vs 995 +/- 195 and 1089 +/- 195 mosmol/kg H2O, respectively, p < 0.05). This decreased osmolality was paralleled by an increase in urine production during the time period 01.00-04.00 (83 +/- 24 vs 52 +/- 18 and 45 +/- 22 ml, respectively, p < 0.05). At the end of the 6-month period of DDAVP treatment, the percentage response was similar between the ADH- and ADH+ enuretics (79% vs 75%). However, the time taken to achieve a response was quicker in the ADH- subjects. These data suggest the existence of a subgroup of enuretics whose underlying pathophysiology is the development of nocturnal polyuria probably due to a relative night-time ADH deficiency. Nocturnal sequential monitoring of urinary osmolality, as described above, allows identification of this subgroup.

Topics: Child; Circadian Rhythm; Deamino Arginine Vasopressin; Enuresis; Female; Humans; Male; Osmolar Concentration; Polyuria; Renal Agents; Time Factors; Urination Disorders; Urine; Vasopressins

Healthy individuals have a nocturnal decrease in urine output due to increased plasma antidiuretic hormone levels at night. This does not occur in spinal cord injury and most patients experience nocturnal polyuria, which triggers dysreflexic crises secondary to urinary bladder overdistension, and interferes with patients' sleep due to the need for extra catheterization.. To evaluate the diurnal variation in ADH level, urinary output, and plasma and urine osmolality in SCI patients with regard to their level of injury and in comparison with age- and sex-matched healthy individuals.. Sixteen ASIA-A spinal cord-injured patients, eight with paraplegia, eight with tetraplegia, and eight healthy individuals, were evaluated for urinary output, urine and serum osmolality, and antidiuretic hormone levels during day and night hours.. Absence of diurnal variation in urinary output and antidiuretic hormone secretion was detected in both paraplegic and tetraplegic patients, while antidiuretic hormone levels rose significantly at night in the control group.. Antidiuretic hormone levels should be monitored both day and night in spinal cord injury patients, with severe nocturnal polyuria. Treatment with desaminocystein-D-arginine vasopressin can be attempted when conservative measures fail to control nocturnal polyuria, especially in patients who are on an intermittent catheterization program.

Topics: Adult; Analysis of Variance; Blood Proteins; Case-Control Studies; Circadian Rhythm; Female; Humans; Male; Osmolar Concentration; Polyuria; Radioimmunoassay; Spinal Cord Injuries; Statistics, Nonparametric; Vasopressins

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

Although disorders of ADH secretion associated with meningitis are usually consistent with the Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH), central diabetes insipidus (DI) is an exceptional complication of meningitis. Transient DI as a complication of Escherichia coli (E. coli) meningitis due to ventriculoperitoneal shunt in an 18-month-old boy is presented. Blood and spinal fluid cultures yielded E. coli, sensitive to cefotaxime. The DI arose on the day 3 after admission and continued to the day 20. Treatment comprised cefotaxime, dexamethasone, fluid adjustment and vasopressin. The course of our case supports that in cases of bacterial meningitis, initial fluid restriction may occasionally result in dangerous conditions. Therefore, all children with bacterial meningitis should be followed closely not only in terms of SIADH but also DI. To our knowledge this is the first transient DI associated with E. coli-caused meningitis case reported.

Topics: Dandy-Walker Syndrome; Deamino Arginine Vasopressin; Diabetes Insipidus; Escherichia coli Infections; Humans; Infant; Male; Meningitis, Bacterial; Polyuria; Radioimmunoassay; Renal Agents; Tomography, X-Ray Computed; Vasopressins; Ventriculoperitoneal Shunt

The syndrome of polyuria and polydipsia is practically identical in three very different disorders (central diabetes insipidus, nephrogenic diabetes insipidus, primary polydipsia). In congenital nephrogenic diabetes insipidus both the thirst mechanism and the production of the antidiuretic hormone are intact, but the hormone is ineffective in the kidney. The acquired form of the disease is caused most frequently by tubulointerstitial and urinary tract obstructive disorders as well as among the several drugs, lithium. In the differential-diagnosis the results of determinations related to the nomograms of normal interrelationships between osmolality and vasopressin in urine and plasma are used, besides the classical Carter-Robbins and indirect dehydration (Miller) tests. It has been postulated recently that in many cases the resistancy toward vasopressin is not absolute and these partially vasopressin sensitive patients can be treated successfully by thiazide, and potassium sparing compounds, antiprostaglandin pain killers (non-steroid antiinflammatory drugs) and first of all dDAVP as well as combinations of these preparations.

Topics: Diabetes Insipidus, Nephrogenic; Drug Resistance; Female; Humans; In Vitro Techniques; Polyuria; Renal Agents; Thirst; Vasopressins

To examine the involvement of vasopressin and dehydration in the regulation of aquaporin-2 (AQP2) expression in rat kidney, we investigated the effects of treatment for 60 h with the specific V2-receptor antagonist OPC-31260 (OPC), alone and in conjunction with dehydration for the last 12 h. Changes in AQP2 protein and mRNA expression in kidney inner medulla were determined by Western and Northern blotting, and AQP2 distribution was analyzed by immunocytochemistry and immunoelectron microscopy. Treatment with OPC increased urine output fourfold, with a reciprocal decrease in urine osmolality. AQP2 expression decreased to 52 +/- 11% of control levels (n = 12, P < 0.05), and AQP2 was found predominantly in intracellular vesicles in collecting duct principal cells. This is consistent with efficient blockade of the vasopressin-induced AQP2 delivery to the plasma membrane and with the observed increased diuresis. Consistent with this, AQP2 mRNA levels were also reduced in response to prolonged OPC treatment (30 +/- 10% of control levels, n = 9). Five days of treatment with furosemide, despite producing even greater polyuria than OPC, was not associated with downregulation of AQP2 levels, demonstrating that AQP2 downregulation is not secondary to increased urine flow rate or loss of medullary hypertonicity. During 12-h thirsting in the continued presence of OPC, urine output dropped dramatically, to levels not significantly different from that seen in (nonthirsted) control animals. In parallel with this, AQP2 levels rose to control levels. Control experiments confirmed continued effective receptor blockade. These results indicate that the V2-receptor antagonist causes a modest decrease in AQP2 expression that is not a consequence of increased urine flow rate or washout of medullary hypertonicity. However, this decrease is much less marked than that seen in some forms of acquired nephrogenic diabetes insipidus. In conjunction with the effects of thirsting, this suggests that modulation of AQP2 expression is mediated partly, but not exclusively, via V2 receptors.

Topics: Animals; Aquaporin 2; Aquaporin 6; Aquaporins; Benzazepines; Dehydration; Diuresis; Diuretics; Furosemide; Gene Expression; Immunohistochemistry; Ion Channels; Kidney Medulla; Male; Microscopy, Immunoelectron; Polyuria; Rats; Rats, Wistar; RNA, Messenger; Vasopressins; Water Deprivation

We report a case of central diabetes insipidus with spontaneous remission 8 months after clinical beginning of the disease. A 20 years-old man developed polydipsia and polyuria in October 1994. A water deprivation study showed a defect in the urine concentrating function, which was corrected by vasopressine. A Magnetic Resonance imaging of the skull revealed a thickening of the pituitary stalk. His condition was well controlled by nasal DDAVP administration and 6 months later patient reduced spontaneously medication dose without clinical worsening. 8 months after clinical beginning, patient has become completely free from the need for medication to control clinical symptoms and urine concentrating function, as demonstrated by a re-evaluation study with water deprivation. A control Magnetic Resonance showed the regression of stalk enlargement. The clinical and radiological features of this case are discussed.

Topics: Adult; Brain; Diabetes Insipidus; Humans; Magnetic Resonance Imaging; Male; Polyuria; Remission, Spontaneous; Renal Agents; Vasopressins

We have recently reported a large cluster of patients with nephrogenic diabetes insipidus (NDI) due to an autosomal recessive aquaporin-2 (AQP-2) early-stop codon. This paper describes the clinical manifestations and evaluation of therapeutic approaches to this new entity.. Nine patients with an AQP-2 mutation were studied. Urine osmolality was measured in five patients before and at 3 x 30 min intervals after desmopressin given in increasing doses of 5-100 micrograms. Urinary prostaglandins PGE2 and 6-keto PGF1 alpha, were extracted from 24-h urine samples and estimated by radioimmunoassays. Eight NDI patients were given a combination of a low-sodium diet and hydrochlorothiazide. Four to 11 weeks later, ibuprofen was added, and the patients were retested within the following 4-9 weeks.. Urine osmolality remained unchanged after supra-pharmacological doses of desmopressin, at 60-70 mOsm/kg. Urinary PGE2 in control subjects was 0.74 +/- 0.1 microgram/g creatinine (mean +/- SD) compared to 5.0 +/- 2.6 micrograms/g creatinine in AQP-2 deficient patients (P < 0.05). Urinary 6-keto PGF1 alpha, was 0.20 +/- 0.03 microgram/g creatinine in controls and 0.75 +/- 0.31 microgram/g creatinine in AQP-2 deficiency (P < 0.05). Urinary volumes decreased by a mean 31% on a low-salt diet and hydrochlorothiazide, and by a mean of 38% on the combination therapy. Plasma osmolality decreased by a mean 15 mOsm/kg on the low-salt diet and hydrochlorothiazide, and by 22 mOsm/kg on the combination therapy. Urinary osmolality increased from a mean 80 mOsm/kg to 96 mOsm/kg on the low-salt diet and hydrochlorothiazide, and to 146 mOsm/kg on the combination therapy.. AQP-2 deficiency in these patients with an early-stop codon is associated with complete unresponsiveness of the collecting duct to vasopressin, implying an indispensable role for AQP-2 in vasopressin antidiuresis. Urinary PGE2 and 6-keto PGF1 alpha are elevated, the former being extremely high, apparently due to the extreme vasopressin unresponsiveness. Combination therapy with a combination of a low-salt diet, thiazide and non-steroidal anti-inflammatory drug is partially effective.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Anti-Inflammatory Agents, Non-Steroidal; Aquaporin 2; Aquaporin 6; Aquaporins; Child; Child, Preschool; Combined Modality Therapy; Deamino Arginine Vasopressin; Diabetes Insipidus, Nephrogenic; Diet, Sodium-Restricted; Dinoprostone; Diuretics; Dose-Response Relationship, Drug; Drug Therapy, Combination; Female; Humans; Hydrochlorothiazide; Ibuprofen; Infant; Male; Osmolar Concentration; Polyuria; Vasopressins

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

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

To establish baseline ADH levels in spinal cord injury patients and to evaluate whether spinal cord patients have attenuation of diurnal variation of ADH similar to children with enuresis and elderly with nocturnal polyuria.. Twenty-seven healthy quadriplegic patients, ASIA impairment scale A, were evaluated for serum ADH levels at night and during the day.. Evaluation of whether bladder overdistention caused by attenuation of diurnal variation of ADH is responsible for the episodes of autonomic dysreflexia and recurrent urinary tract infections in spinal cord injury patients who are on intermittent catheterization for bladder management.. A lack of diurnal variation of ADH in the subject population.. A trial of desaminocystein-D-arginine vasopressin (DDAVP) should be considered for patients with established attenuation of the diurnal variation ADH.

Topics: Adult; Aged; Circadian Rhythm; Humans; Male; Middle Aged; Osmolar Concentration; Polyuria; Spinal Cord Injuries; Urinary Catheterization; Vasopressins

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

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

Plasma immunoreactive vasopressin (iAVP) was studied by RIA in a patient suffering from polyuria during chronic treatment with lithium. The combined use of two antisera specific for different regions of the AVP molecule allowed us to detect circulating forms which are modified in the acyclic tripeptide portion. In this lithium-treated patient, iAVP was abnormally low with respect to plasma osmolality. However, iAVP increased during hypertonic saline infusion, probably through an osmosensitive mechanism. A remarkable finding was that contrary to the observations made in healthy subjects and in another patient with diabetes insipidus, iAVP measured with the antiserum specific for the acyclic portion of the AVP molecule was below the values measured with the antiserum specific for the hexapeptide ring. This unusual immunoreactivity profile suggests that the plasma of this polyuric lithium-treated patient contains vasopressin-like peptides which differ from arginine vasopressin in the structure of the C-terminal tripeptide tail.

Topics: Female; Humans; Lithium; Middle Aged; Peptides; Polyuria; Radioimmunoassay; Vasopressins

Polyuria after release of bilateral ureteral obstruction (BUO) is frequently seen in patients with urological disorders. In this study, we examined the effect of BUO and release of BUO on the expression of the vasopressin-regulated water channel aquaporin-2 (AQP-2) in rat kidney. Ureters were obstructed for 24 h in all experiments, and BUO was either not released or released for 24 or 48 h or 7 days. Each group of experimental rats were matched with sham-operated controls. One kidney was used for membrane fractionation and immunoblotting, whereas the contralateral was fixed for immunocytochemistry. Immunoblotting demonstrated a significant reduction in AQP-2 expression in inner medullar during 24 h of BUO to 26 +/- 8% (P < 0.001). Release of BUO was associated with immediate onset of a predominant osmotic-dependent polyuria. Forty-eight hours after release of BUO, the reduction in AQP-2 expression persisted (19 +/- 8%, P < 0.001), concurrent with a marked nonosmotic postobstructive polyuria, as determined by a significant reduction in free-water clearance (-50 +/- 7 vs. -85 +/- 10 microliters.min-1.kg-1, P < 0.05). Immunofluorescence and immunoelectron microscopy confirmed the reduced levels of AQP-2 in collecting duct principal cells. Seven days after release, the renal excretion of water and electrolytes had almost normalized. However, the downregulation of AQP-2 was not partly reversed (49 +/- 14%, P < 0.001), and, consistent with this, the urinary concentrating capacity was significantly reduced 7 days after release to a 18-h period of thirst. This strongly suggests that the persistent downregulation of AQP-2 is the cause of the slow recovery in concentration capacity. In conclusion, BUO and release of BUO were associated with a marked reduction in expression of AQP-2, coincident with the development and maintenance of postobstructive polyuria. Thus reduced AQP-2 levels may represent an important factor in the slow recovery from postobstructive diuresis.

Topics: Animals; Aquaporin 2; Aquaporin 6; Aquaporins; Fluorescent Antibody Technique; Immunoenzyme Techniques; Ion Channels; Kidney; Male; Microscopy, Immunoelectron; Polyuria; Rats; Rats, Wistar; Tissue Distribution; Ureteral Obstruction; Vasopressins

In five members of three generations in a family studied in 1972, 3 nephrological disorders occurred concurrently: distal renal tubular acidosis (dRTA), polycystic kidney and nephrogenic diabetes insipidus (with the exception of a five-year-old child in whom polycystic kidney was not detectable--yet?). Chromosoma studies revealed an increased rate of the occurrence of variations. The youngest patient was reinvestigated in 1993; the other four affected members of the family were already not alive. 7 offsprings in two generations of the 3 healthy members of the third "patient generation" were healthy. The autosomal dominant way of inheritance characteristic to both dRTA and polycystic kidney disease was obvious in this family. On the other hand the same degree of the concentrating defect found both in the patients of the familial dRTA and in 11 control patients with non familial (acquired) dRTA suggested that the nephrogenic diabetes insipidus as an acquired disorder was associated with the two congenital abnormalities. The clinical picture of the combined disease was dominated by the symptoms of polydipsia and polyuria. The vasopressin resistance with a variation in the degree interindividually seemed to be responsible for the nephrogenic diabetes insipidus. Functional insufficiency of the loop of Henle was excluded on the basis of normal responses to a "loop diuretic".

Topics: Acidosis, Renal Tubular; Adolescent; Adult; Aged; Child; Child, Preschool; Diabetes Insipidus, Nephrogenic; Drinking; Female; Humans; Male; Middle Aged; Nephrocalcinosis; Pedigree; Polycystic Kidney, Autosomal Dominant; Polyuria; Radiography; Vasopressins

Chronic cervical spinal cord injury is characterized by defects in sodium and water homeostasis and defects of adaptive hormonal responses. The plasma osmolality is maintained in a relatively narrow range, the lower limit of which is determined by osmotic threshold for vasopressin release and the upper limit by the third threshold. Antidiuretic hormone as an important mediator of fluid and electrolyte balance was well investigated in able bodied children comparing children with normal voiding pattern and children with enuresis. The normal subjects were found to have higher plasma ADH at night, not detected in the group with enuresis. The findings were similar in elderly patients with increased diuresis at night, suggesting an important role of ADH in nocturnal decrease of urine output. Investigators studied the effect of rapid tilt on plasma ADH in tetraplegic compared with normal subjects, but there are no data available in the literature regarding ADH and its effects on water and electrolyte balance in healthy tetraplegic subjects with a normal lifestyle. We decided to undertake a pilot study to attempt to establish baseline ADH levels in this subject group, to better understand and manage tetraplegic patients with water and electrolyte dysregulation. Our preliminary data suggest that these individuals lack the normal diurnal variation of ADH, a phenomenon similar to that demonstrated in enuretic children and elderly, and furthermore appear to have generally depressed ADH levels.

Topics: Adult; Aged; Circadian Rhythm; Humans; Male; Middle Aged; Osmolar Concentration; Polyuria; Spinal Cord Injuries; Vasopressins

Topics: Central Nervous System; Child; Child, Preschool; Circadian Rhythm; Deamino Arginine Vasopressin; Enuresis; Humans; Polyuria; Renal Agents; Treatment Failure; Urination; Urodynamics; Vasopressins

1. Tsukuba hypertensive mice (THM) carry both human renin and angiotensinogen genes, and develop hypertension. The animal has high levels of renin activity and angiotensin II concentration in the plasma. 2. Urinary excretion in THM was greater than in the control animal, non-transgenic C57BL/6j. THM showed a greater amount of daily water intake. The osmolality of 24 h urine was lower than that of the control animal. 3. When water was deprived for 12 h and then loaded with 0.25 mL/10 g bodyweight, the osmolality of urine at the first 0-3 h period was the same in THM and control, but significantly lower in THM at the following 3-6 h period, indicating that the urine concentrating activity is insufficient in THM compared with the control animal. 4. Urinary excretion of vasopressin was significantly higher in THM. Plasma aldosterone concentration and urinary excretion of aldosterone were also higher in THM. Plasma potassium level was significantly low. 5. The mechanism underlying the pathophysiology of polyuria is not totally explained; however, hypokalaemia, which was probably the result of hyperaldosteronism, may be at least partially involved, since hypokalaemia is considered to be a factor hampering the action of vasopressin for concentration of urine at the site of the collecting duct of the kidney.

Topics: Aldosterone; Angiotensinogen; Animals; Electrolytes; Humans; Hyperaldosteronism; Hypertension; Kidney Concentrating Ability; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Polyuria; Rats; Renin; Vasopressins

Topics: Adrenocorticotropic Hormone; Corticotropin-Releasing Hormone; Cushing Syndrome; Cytokines; Humans; Inappropriate ADH Syndrome; Interleukin-6; Polyuria; Vasopressins

We report on two healthy white men who sustained high-voltage electrical burns and were transferred to our regional burn center for specialized care. Within 24 hours of admission, both patients developed clinical signs and laboratory evidence of diabetes insipidus. With appropriate treatment, no sequelae occurred and their endocrinopathy spontaneously resolved. Diabetes insipidus following traumatic events is not uncommon; however, it has never been reported following an electrical injury.

Topics: Adult; Burns, Electric; Diabetes Insipidus; Diagnosis, Differential; Hand Injuries; Humans; Male; Polyuria; Vasopressins

Cisplatin is an antineoplastic agent. Several nephrotoxic effects are associated with its use including chronic and acute renal failure, renal magnesium wasting, and polyuria. We have investigated polyuria in groups of rats treated with cisplatin at doses of 2.5 and 5 mg/kg body weight given once weekly for 3 weeks to determine possible mechanisms of this impairment. After cisplatin administration, glomerular filtration rate was reduced and significant increases in sodium and water loss were also seen. These changes were associated with decreases in urinary cAMP. Inner medullary collecting duct (IMCD) cells were removed from these animals and were stimulated with graded doses of vasopressin. Cells from cisplatin-treated rats showed an impaired response in cAMP generation to vasopressin stimulation as compared to cells from normal animals. To determine more precisely the site of impairment, the adenylate cyclase complex of the IMCD cells was further studied with forskolin and NaF. Forskolin was used to probe the catalytic unit activating adenylate cyclase, and NaF the guanine nucleotide regulatory protein (G protein). In response to forskolin, cells from cisplatin-treated rats and normal rats responded similarly in generating cAMP. However, following NaF, the cAMP response was blunted in the cells from the cisplatin rats. These results suggested that the catalytic unit was not injured by cisplatin (forskolin study) but the G protein was (NaF). In conclusion, the present study suggests that the polyuria seen following cisplatin administration is associated with an end-organ resistance to vasopressin manifested by reduced cAMP generation, secondary in part or whole to a defect at the level of the G protein.

Topics: Animals; Cisplatin; Colforsin; Cyclic AMP; Dose-Response Relationship, Drug; Glomerular Filtration Rate; GTP-Binding Proteins; Kidney; Male; Neoplasms, Experimental; Polyuria; Rats; Rats, Wistar; Sodium Fluoride; Vasopressins

A 67-year-old patient with Shy-Drager syndrome (SDS), exhibited nocturnal polyuria associated with abnormal circadian rhythm of antidiuretic hormone (ADH) secretion and nocturnal polyuria. The patient excreted a larger volume of urine during the nighttime compared to that in the daytime. The specific gravity of urine at night was lower than that during the day. In contrast to normal circadian rhythm of ADH, the patient's plasma concentration of ADH was increased in the daytime. The present study raised the possibility that an altered circadian rhythm of plasma ADH secretion might be considered a result of the neurodegenerative changes involving the hypothalamus.

Topics: Aged; Circadian Rhythm; Humans; Male; Polyuria; Shy-Drager Syndrome; Specific Gravity; Urine; Vasopressins

The role of vasopressin and Henle's loop transport in age-related polyuria and decrease in urine osmolality was investigated in female WAG/Rij rats free of kidney disease. In these animals, urine osmolality dropped from 2000 mosmol/kg H2O to 1000-1200 mosmol/kg H2O between 10 and 30 months, and urinary volume increased in proportion. Vasopressin concentration measured in plasma withdrawn from conscious, unrestrained, chronically catheterized rats was not significantly different in 10, 20 and 30-month-old animals (mean values 2.5 +/- 0.7, 2.2 +/- 0.2 and 2.0 +/- 0.3 pg/ml (n = 8), respectively). This suggests an impaired responsiveness of old kidney to antidiuretic hormone. The possible involvement of Henle's loop in this defect was studied by micropuncture. Paired collections of tubular fluid were done in the early distal and late proximal convolutions of the same cortical nephrons. Single nephron filtration rates did not significantly differ with age. Tubular fluid osmolalities in the early distal convolution were 165 +/- 13, 178 +/- 9 and 160 +/- 11 (n = 14) mosmol/kg H2O in 10-, 20- and 30-month-old rats, indicating similar diluting capacity of the cortical thick ascending limb. The amount of sodium transported from lumen to peritubular space by Henle's loop was also unchanged with age as were water, calcium, magnesium and potassium reabsorptions. These data indicate that the age-related decrease in urine osmolality is not related to either a significant reduced vasopressin plasma concentration or an increased single glomerular filtration rate or a reduced transport capacity of Henle's loop of the cortical nephron. Rather they suggest an impaired response to vasopressin of other segments of the nephron that is, the medullary thick ascending limb of Henle's loop and/or the collecting duct.

Topics: Aging; Animals; Female; Glomerular Filtration Rate; Kidney Concentrating Ability; Kidney Cortex; Loop of Henle; Nephrons; Osmolar Concentration; Polyuria; Rats; 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

The mechanism of polyuria associated with paroxysmal supraventricular tachycardia (SVT) was investigated in 8 patients. SVT was induced artificially and sustained for 60 minutes. Urine and blood samples were collected every 30 minutes. During the latter half of SVT, urine flow increased twofold in the control subjects before SVT. Urinary sodium excretion increased significantly (p less than 0.01) within 30 minutes after SVT. Urinary excretion of antidiuretic hormone (ADH) decreased (p less than 0.01) during the latter half of SVT and increased (p less than 0.01) after SVT, respectively. Plasma level of ADH did not change during SVT but increased (p less than 0.05) after SVT. The concentration of plasma atrial natriuretic polypeptide (ANP) increased significantly (p less than 0.05) before SVT ended. Urinary excretion of prostaglandin E2 increased significantly (p less than 0.05) after termination of SVT. The percent changes in the urinary excretion of prostaglandin E2 were correlated (r = 0.713, p less than 0.001) with those of ADH. There was also a correlation (r = 0.6, p less than 0.001) between the percent changes in the urinary excretion of prostaglandin E2 and those of sodium. Their findings suggest that the polyuria during SVT is attributed mainly to the inhibition of ADH release and that the natriuresis after SVT is due not only to the increased ANP but also to the increased renal prostaglandin E2 probably stimulated by ADH.

Topics: Adult; Atrial Natriuretic Factor; Blood Pressure; Dinoprostone; Female; Heart Rate; Humans; Kidney; Male; Middle Aged; Natriuresis; Osmolar Concentration; Polyuria; Tachycardia, Paroxysmal; Tachycardia, Supraventricular; Vasopressins

Topics: Body Water; Dehydration; Diabetes Insipidus; Diuretics; Drinking; Feedback; Glomerular Filtration Rate; Homeostasis; Humans; Inappropriate ADH Syndrome; Polyuria; Vasopressins; Water Intoxication

Transient polyuria and polydipsia during pregnancy are rare, and their cause is not entirely clear. Possible explanations include the exacerbation of preexisting abnormalities in the secretion or action of vasopressin and abnormally large increases in plasma vasopressinase activity.. We studied two women in whom overt polyuria and polydipsia developed during the third trimester of pregnancy and disappeared after delivery. The secretion and action of vasopressin were studied both when the women had polyuria and polydipsia and later, when their water intake and urine volume were normal.. One patient had partial nephrogenic diabetes insipidus. She had little increase in urine osmolality in response to water deprivation, hypertonic-saline infusion, and vasopressin injection and no response to desmopressin acetate (1-deamino-8-D-arginine vasopressin) during the immediate postpartum period. Her basal and stimulated plasma vasopressin concentrations were high (16.5 to 203.4 pmol per liter) before and during hypertonic-saline infusion 30 months post partum. The other patient had partial neurogenic diabetes insipidus. She had subnormal basal plasma vasopressin concentrations, a subnormal increase in the plasma vasopressin level and a subnormal decrease in urine flow in response to the administration of vasopressin, and a normal response to desmopressin. After pregnancy, when her urine volume was normal, she had no increase in plasma vasopressin in response to hypertonic-saline infusion, but she had a normal rise in the plasma vasopressin level and a normal renal response to vasopressin administration.. Pregnancy may unmask subclinical forms of both nephrogenic and neurogenic diabetes insipidus. This exacerbation may result from both increased vasopressinase activity and diminished renal responsiveness to vasopressin.

Topics: Adult; Deamino Arginine Vasopressin; Diabetes Insipidus; Female; Humans; Hypertonic Solutions; Osmolar Concentration; Polyuria; Pregnancy; Pregnancy Complications; Pregnancy Trimester, Third; Thirst; Vasopressins

To examine a possible role for atrial natriuretic peptide (ANP) in water and sodium metabolism disturbances associated with abnormal vasopressin (AVP) secretion, we measured plasma ANP concentrations in 15 patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and in 17 patients with central diabetes insipidus (DI). The mean plasma ANP concentration (30.2 +/- 10.4 pmol/L) in SIADH patients who had hyponatremia, plasma hypoosmolality, hyperosmolar urinary compared to plasma sodium levels, and increased plasma AVP levels relative to plasma osmolality was significantly higher than that in normal subjects (12.6 +/- 4.9 pmol/L), although there was a considerable individual variation in plasma ANP ranging from normal to clearly elevated levels (15.1-47.0 pmol/L). When hyponatremia was corrected by water restriction or demeclocycline administration, plasma ANP levels decreased significantly and fell into the normal range (12.5 +/- 4.3 pmol/L). DI patients who complained of polyuria and polydipsia and had hypoosmolar urine, normal or elevated plasma sodium concentrations, and decreased plasma AVP levels relative to plasma osmolality, on the other hand, had a significantly lower mean plasma ANP level (7.6 +/- 2.9 pmol/L) than normal subjects. There was, again, a considerable overlap between plasma ANP levels in individual DI patients (4.2-13.9 pmol/L) and those in normal subjects. Treatment with 1-desamino-8-D-arginine vasopressin resulted in a significant increase in the mean plasma ANP level (18.6 +/- 8.0 pmol/L). There were no significant correlations between plasma ANP and AVP levels in either group of patients. The results indicate that ANP secretion is modulated by changes in plasma volume consequent to abnormal AVP secretion, which may have a pathophysiological significance in maintaining volume homeostasis.

Topics: Adolescent; Adult; Aged; Atrial Natriuretic Factor; Blood Volume; Deamino Arginine Vasopressin; Demeclocycline; Diabetes Insipidus; Female; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Polyuria; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Diabetes Insipidus; Diabetes Mellitus; Diagnosis, Differential; Diuresis; Humans; Hypothalamo-Hypophyseal System; Polyuria; Syndrome; Thirst; Vasopressins

Topics: Adult; Creatinine; Diabetes Insipidus; Drinking; Female; Humans; Indomethacin; Kidney Concentrating Ability; Lithium; Lithium Carbonate; Male; Middle Aged; Osmolar Concentration; Polyuria; Urodynamics; Vasopressins; Water Deprivation

The effects of cisplatin (5 mg/kg BW given intraperitoneally) on renal concentration mechanism were evaluated initially by clearance studies in rats 5-7 days after cisplatin administration and compared to normal rats. During hypotonic saline infusion, cisplatin rats showed a lower inulin clearance (0.56 +/- 0.07 vs. 1.12 +/- 0.09 ml/min/100 g BW, p less than 0.01), a higher fractional distal delivery (CNa + CH2O/Cin) (36.3 +/- 4.4 vs. 22.8 +/- 4.5%, p less than 0.05), and lower CH2O/CNa + CH2O (33.6 +/- 5.8 vs. 56.5 +/- 5.0%, p less than 0.01). During hypertonic saline infusion the TcH2O/Cosm was lower in cisplatin (18.3 +/- 1.1%) than in normal rats (33.4 +/- 3.5%, p less than 0.01). These results suggest a defect in NaCl transport in the thick ascending limb of Henle and proximal tubule. In order to characterize these tubular defects, we measured Na-K-ATPase activity (microM Pi/mg protein/h). In the renal cortex of cisplatin rats the ATPase activity was lower (18.1 +/- 3.2) than in normal rats (33.4 +/- 6.4, p less than 0.05), also in the inner strip of the outer medulla of cisplatin rats Na-K-ATPase was reduced (26.0 +/- 5.7) when compared with normal rats (67.3 +/- 9.2, p less than 0.01), presumably representing a decrease in enzyme activity in the thick ascending limb.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Cisplatin; Diuresis; Kidney Concentrating Ability; Kidney Tubules; Male; Polyuria; Rats; Sodium-Potassium-Exchanging ATPase; Vasopressins

In two dogs with pituitary-dependent hyperadrenocorticism, adrenocorticolysis with o.p'-DDD led to the disappearance of the signs and symptoms except for the polyuria. After a modified water-deprivation test the osmoregulation of vasopressin release was studied by hypertonic saline infusion. In both dogs the hypertonicity, thus induced, resulted in very minimal responses of the vasopressin secretion.

Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Animals; Dog Diseases; Dogs; Male; Osmolar Concentration; Polyuria; Recurrence; Vasopressins; Water Deprivation

The authors discuss about five cases of diabetes insipidus observed in patients affected by traumatic cervical spine fractures and/or dislocations, without either evident lesions of the cerebral structures at CT scan examination, or important craniocerebral trauma. In all patients polyuria and hyperthermia arose some days after the traumatic accident and regressed spontaneously or after exogeneous vasopressin administration. Vasopressin urinary levels confirmed the presence of a true diabetes insipidus, the origin of which is in largely obscure. A central medullary vasopressin mediated pathway, demonstrated only in experimental animals, may be responsible for such a finding.

Topics: Adolescent; Adult; Cervical Vertebrae; Diabetes Insipidus; Female; Fever; Fractures, Bone; Humans; Hypothalamo-Hypophyseal System; Joint Dislocations; Male; Polyuria; Radiography; Spinal Cord Injuries; Syndrome; Vasopressins

Acute cerebral compression by a supra- and infratentorial balloon produced a triphasic pattern of diuresis. The 1st phase was characterized by polyuria associated with five fold increase of plasma (p) antidiuretic hormone (ADH) concentration, decreased urine osmolality in spite of natriuresis and blood pressure elevation. The 2nd phase was characterized by oliguria, a decrease of pADH and reduced urine Na+ concentration, whereas urine osmolality transiently increased. At this stage there was respiratory arrest and fall of blood pressure. The final stage was diabetes insipidus (DI), when EEG activity had disappeared. An increase of serum osmolality mainly occurred during the last DI phase. Serum Na+ concentration fluctuated slightly during the whole period of diuresis. These results present evidence, that the diuresis pattern reflects the hypothalamo-hypophyseal antidiuretic system (HHAS) reaction to acute intracranial pressure (ICP) increase with the vegetative symptoms of cerebral shock.

Topics: Animals; Anuria; Cats; Diabetes Insipidus; Hypothalamo-Hypophyseal System; Oliguria; Osmolar Concentration; Polyuria; Pseudotumor Cerebri; Vasopressins; Water-Electrolyte Balance

The involvement of prostaglandin E2 (PGE2), adenosine 3',5'-cyclic monophosphate (cAMP), and vasopressin in lithium-induced polyuria was investigated in rats. Administration of LiCl (4 mmol/kg body wt) for 7 days induced a marked polyuria with a significant excretion of urinary PGE2. Administration of indomethacin (IND, 5 mg/kg body wt) for 4 days to lithium-induced diabetes insipidus (LiDI) rats diminished urine volume by 80% and urinary PGE2 by 85%. The in vitro data of the intact rat kidney showed that lithium stimulated arginine vasopressin (AVP)-induced PGE2 production and suggested that PGE2 suppressed cAMP synthesis in rat renal medulla. The AVP-induced PGE2 synthesis was greater and the AVP-stimulated cAMP production lower in the LiDI rat kidney in vitro. Interference of the vasopressin-associated cAMP system and the increased PGE2 synthesis in the kidney may be involved in the development of LiDI. The reduced cAMP production in the LiDI rat kidney might be partly due to the increased PGE2 synthesis. In LiDI rats plasma vasopressin increased, whereas AVP concentration in the hypothalamus and the neurohypophysis significantly decreased. It is postulated that lithium stimulates vasopressin release from the central nervous system and that elevated plasma vasopressin potentiates PGE2 production in the kidney synergistically with lithium.

Topics: 1-Methyl-3-isobutylxanthine; Animals; Arginine Vasopressin; Chlorides; Cyclic AMP; Dinoprostone; Kidney Medulla; Lithium; Lithium Chloride; Male; Polyuria; Prostaglandins E; Rats; Rats, Inbred Strains; Vasopressins

Topics: Adult; Atrial Natriuretic Factor; Dinoprostone; Female; Humans; Male; Middle Aged; Polyuria; Tachycardia, Supraventricular; Vasopressins

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

Topics: Diabetes Insipidus; Humans; Polyuria; Vasopressins; Water-Electrolyte Imbalance

Topics: Adult; Diabetes Insipidus; Humans; Hyperaldosteronism; Male; Polyuria; Thirst; Vasopressins

1. Cisplatin [6 mg/kg body weight, in 0.9% (w/v) NaCl] was injected intraperitoneally as a single dose to two groups of rats (Fischer 344 strain). Two further groups of rats, injected intraperitoneally with an equivalent volume of 0.9% (w/v) NaCl, were used as controls. The cisplatin-treated rats developed a pronounced polyuria which did not recover during an 18 week observation period. 2. After 21 weeks, one group of the cisplatin-treated animals received a 6 h infusion of 2.5% D-glucose. Vasopressin (60 mu-units min-1 100 g-1 body weight) was incorporated into the infusate for the final 2 h. A control group of animals received an identical infusion. One week later the other group of cisplatin-treated rats received a 6 h infusion of 0.9% (w/v) NaCl. Indomethacin was incorporated into the infusate for 15 min, at 3 h 52.5 min, to deliver a dose of 10 mg/kg body weight. A control group again received an identical infusion. 3. Cisplatin did not impair the antidiuretic effect of vasopressin, but it reduced the natriuretic effect of vasopressin, and also impaired the ability of the animals to produce concentrated urine. 4. Cisplatin did not alter basal PGE2 excretion, or the reduction in PGE2 excretion induced by indomethacin. However, the urine flow in the cisplatin-treated group did not fall after indomethacin, whereas there was a fall in urine flow in the control group.

Topics: Animals; Cisplatin; Dinoprostone; Indomethacin; Kidney; Male; Osmolar Concentration; Polyuria; Potassium; Prostaglandins E; Rats; Sodium; Vasopressins

We examined the release of vasopressin and the renal response to exogenous vasopressin before and during desoxycorticosterone acetate (DOCA) administration in the dog. As treatment with DOCA produced potassium loss, urine volume increased, urinary osmolality decreased, and urinary PGE2 tended to increase. The increase in urine volume was accompanied by increases in serum sodium, in plasma osmolality and in plasma arginine vasopressin. The threshold for vasopressin release measured during polyuria was higher than control but the rate of vasopressin release was unchanged. The DOCA-induced polyuria was not affected by treatment with vasopressin which further increased plasma vasopressin. Treatment with indomethacin which corrected the increase in urinary PGE2 excretion but not the hypokalemia, restored the renal responsiveness to vasopressin, decreased the secretion of vasopressin, and corrected the polyuria and the hypernatremia. These findings suggest that DOCA-induced polyuria is attributable to a decrease in renal responsiveness to vasopressin which may be mediated in part by an increase in the renal synthesis of prostaglandins.

Topics: Animals; Body Water; Desoxycorticosterone; Diabetes Insipidus; Dinoprostone; Dogs; Female; Polyuria; Potassium; Prostaglandins E; Vasopressins

Hypertonic saline test is indispensable for the evaluation of posterior pituitary function. However the test is not simple, including water loading, urine sampling and at least 45 min of hypertonic saline infusion, mostly because the test relies on urinary osmolality as an index of ADH secretion. The object of this study is try to simplify the test by directly measuring plasma ADH concentration before and after 10 min of hypertonic saline infusion. Intravenous infusion of hypertonic saline (5% NaCl, 0.24 ml/kg/min, for 10 min) was performed on normal subjects, patients with diabetes insipidus and patients with renal failure under chronic hemodialysis. Venous blood samples were obtained seriously including just before and after 10 min of the infusion. ADH was extracted from plasma using Sep-Pak C18 column and assayed by specific RIA. Minimum sensitivity of the assay was 0.25 pg/ml. The hypertonic saline infusion resulted in an increase of plasma osmolality by about 8 mOsm/kg H2O and plasma sodium concentration by 4 mEq/l. Plasma ADH increased from 0.77 +/- 0.09 to 3.42 +/- 0.73 pg/ml (m +/- SE, n = 8, p less than 0.01) in normal subjects of ad lib. water drinking and from 0.55 +/- 0.33 to 2.34 +/- 0.33 (m +/- SE, n = 4, p less than 0.05) in water loaded normal subjects (20 ml/kg of water, 60 min before hypertonic saline infusion).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Diagnosis, Differential; Humans; Pituitary Function Tests; Polyuria; Saline Solution, Hypertonic; Sodium Chloride; Vasopressins

A basal value of antidiuretic activity (ADA) of the plasma was determined in 79 HFRS patients and stimulated activity using the insulin tolerance test in 24 persons. A decrease in the plasma ADA was observed in the acute period of disease. The insulin tolerance test did not cause a statistically significant increment of the plasma ADA in the HFRS patients.

Topics: Adolescent; Adult; Convalescence; Hemorrhagic Fever with Renal Syndrome; Humans; Hypothalamo-Hypophyseal System; Insulin; Middle Aged; Oliguria; Polyuria; Time Factors; Vasopressins

Injection of a synthetic progesterone, medroxyprogesterone acetate (MPA or Depo-ProveraR), a widely used contraceptive, into Chinese hamsters (Cricetulus griseus) induced a profound polyuria with daily output of dilute urine equal to about 50% body weight of the hamster. However, relatively normal ability for renal urine concentration was demonstrated by administration of exogenous vasopressin. Body weight did not increase during onset of MPA-induced polyuria or during interval of vasopressin-induced oliguria, suggesting that primary polydipsia was not etiologic. Administration of this steroid to Chinese hamsters was nontoxic, although these polyuric animals were unusually sensitive to water deprivation. This polyuria was not observed when progesterone alone was injected into Chinese hamsters or when MPA was given to other related hamster species (Armenian, Syrian, Turkish or Djzungarian). The MPA-injected Chinese hamster represents a unique model of vasopressin sensitive diabetes insipidus induced by a steroid in a species-specific fashion.

Topics: Animals; Arginine Vasopressin; Cricetinae; Cricetulus; Diabetes Insipidus; Disease Models, Animal; Female; Kidney Concentrating Ability; Male; Medroxyprogesterone; Medroxyprogesterone Acetate; Polyuria; Sex Factors; Species Specificity; Vasopressins; Water Deprivation

Topics: Animals; Bufonidae; Hypercalcemia; Kidney Tubules; Kidney Tubules, Collecting; Polyuria; Rabbits; Rats; Vasopressins

Topics: Acute Kidney Injury; Blood; Humans; Kidney Failure, Chronic; Metabolic Clearance Rate; Polyuria; Renin-Angiotensin System; Ultrafiltration; Uremia; Vasopressins

Topics: Animals; Cephaloridine; Diabetes Insipidus; Male; Polyuria; Rats; Rats, Inbred Strains; Vasopressins

Polyuria subsequent to pituitary surgery was studied in 64 cases. Most cases of postoperative polyuria were due to diabetes insipidus. These cases showed a triphasic pattern in daily urinary volume. Observation of hourly urinary volume in polyuria revealed four diurnal patterns of urinary excretion: rhythmic, continuous, transient, and unspecific. Clinical observation of diurnal patterns has an advantage, in terms of simplicity of procedure, in immediately determining the nature of the polyuria, prognosticating diabetes insipidus, and eliminating inappropriate procedures in treatment. Indomethacin suppository is considered to be a favorable agent in reducing polyuria without disturbing the diurnal pattern in diabetes insipidus.

Topics: Adenoma; Adolescent; Adult; Aged; Circadian Rhythm; Diabetes Insipidus; Female; Humans; Indomethacin; Male; Middle Aged; Pituitary Diseases; Pituitary Neoplasms; Polyuria; Postoperative Complications; Sodium; Vasopressins

Topics: Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Polyuria; Syndrome; Thirst; Vasopressins

Topics: Adolescent; Adult; Diabetes Insipidus; Diagnosis, Differential; Female; Humans; Male; Polyuria; Pregnancy; Vasopressins

Topics: Adolescent; Adult; Diabetes Insipidus; Diagnosis, Differential; Female; Humans; Hypertonic Solutions; Male; Osmolar Concentration; Polyuria; Sodium Chloride; Vasopressins; Water Deprivation

Topics: Autoimmune Diseases; Benzothiadiazines; Chlorpropamide; Clofibrate; Diabetes Insipidus; Diuretics; Drinking; Humans; Osmolar Concentration; Polyuria; Sodium Chloride Symporter Inhibitors; Vasopressins

Electrolytic lesion of the medio-ventral septal (MVS) area produces, 3 days after the surgery, a remarkable increase of daily diuresis and water intake in the rat. This polyuria and polydipsia is associated with decreased levels of circulating radioimmunoassayable vasopressin. In addition, if these lesioned animals were water-deprived (48 h), the usual vasopressin release observed in sham-lesioned and normal controls was markedly blunted. These results suggest that the MVS area exerts a modulatory control on vasopressin secretion both in basal and thirst-evoked conditions.

Topics: Animals; Denervation; Diabetes Insipidus; Drinking; Male; Polyuria; Rats; Rats, Sprague-Dawley; Septum of Brain; Thirst; Vasopressins; Water Deprivation

The present studies were carried out to delineate the mechanism of the polyuric state and renal concentration defect seen after gentamicin. Gentamicin was given at a dosage of 100 mg/kg/day subcutaneously for either 4 or 5 days to Sprague-Dawley rats and resulted in a reversible, polyuric form of acute renal failure. This nonoliguric acute renal failure was accompanied by significant polydipsia and a renal concentrating defect 11 days after gentamicin. To assess the role of polydipsia in the polyuria and renal concentrating abnormality, water intake was restricted in gentamicin-treated animals to match intake of control animals. Elimination of the polydipsia failed to eliminate the polyuria and to improve the renal concentrating abnormality. Postdehydration plasma vasopressin levels were higher in gentamicin-treated than control animals, suggesting that the renal concentrating defect was nephrogenic in origin. Daily urinary prostaglandin E2 excretion was comparable in gentamicin-treated and control animals. However, indomethacin failed to improve urinary concentrating ability, suggesting that the renal concentrating defect was prostaglandin E2 independent. Finally, depressed postdehydration inner medullary tonicity was found in gentamicin-treated animals In summary, gentamicin administration in the rat was associated with a reversible polyuric form of acute renal failure and a renal concentrating defect. This concentration defect was nephrogenic in origin, independent of polydipsia and prostaglandin E2, and was associated with a decrease in inner medullary tonicity.

Topics: Acute Kidney Injury; Animals; Dinoprostone; Gentamicins; Kidney Concentrating Ability; Kidney Medulla; Male; Polyuria; Prostaglandins E; Rats; Rats, Inbred Strains; Vasopressins; Water Deprivation

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

Topics: Adult; Brain Death; Diabetes Insipidus; Female; Humans; Osmolar Concentration; Polyuria; Sodium; Sodium Chloride; Time Factors; Urea; Vasopressins

A patient with lifelong severe polyuria and polydipsia had normal serum antidiuretic hormone (ADH) levels and responded to water deprivation with a prompt increase in urine osmolality and maintenance of normal plasma osmolality (less than 290 mOsm/kg), despite extreme thirst. When treated with desmopressin acetate and allowed free access to water, she was able to reduce plasma osmolality below 270 mOsm/kg, and her compelling thirst disappeared. The disorder is interpreted to be the result of excessive fluid intake in response to a thirst stimulus that was not inhibited by normal plasma osmolality. This study indicates that osmoreceptor control of ADH secretion is normal. Continued administration of vasopressin has relieved the symptoms and has not resulted in water intoxication.

Topics: Adult; Deamino Arginine Vasopressin; Female; Humans; Osmolar Concentration; Polyuria; Pregnancy; Syndrome; Thirst; Vasopressins

Topics: Animals; Diabetes Insipidus; Diabetic Nephropathies; Diagnosis, Differential; Drinking; Female; Horse Diseases; Horses; Polyuria; Vasopressins

The effects of potassium depletion on urine concentration ability, renal PGE2 excretion, and ADH release were studied in 28 female dogs made K depleted by oral K-exalate and a K-free diet. After K depletion was established (serum K 2.9 +/- 0.1 mEq/L), urine volume increased from control measurements, 596.4 +/- 34.0 to 1201.5 +/- 96.9 ml/24 hr (p less than 0.001); urine PGE2 excretion increased, 985.4 +/- 91.1 to 2122.0 +/- 328.5 ng/24 hr, (p less than 0.001); and Umax decreased, 2006 +/- 74.0 to 1186 +/- 71.9 mOsm/kg H2) (p less than 0.001). Indomethacin (5 mg/kg/day, s.c.) administered on 3 consecutive days after K depletion had been established, resulted in no significant improvement in Umax, 1186.8 +/- 71.9 to 1341.8 +/- 105.6 mOsm/kg H2O. Release of ADH from the neurohypophysis was evaluated by measuring plasma ADH during graded increases in serum tonicity with intravenous hypertonic saline before and after K depletion. Although ADH increased with increasing serum tonicity during both control and K depletion periods, there was a blunting of ADH release during K depletion. The regression coefficient of plasma ADH and serum tonicity was significantly lower during K depletion, 0.24, than in the control period, 0.65, (p less than 0.01). After 3 days of indomethacin (5 mg/kg/day, s.c.) ADH release from the neurohypophysis in response to graded increases in serum tonicity was partially normalized in the K-depleted animals without changes in serum K (regression coefficient, 0.53). K depletion in dogs therefore leads to an increase in the urine volume and an increase in renal PGE synthesis associated with a decrease in Umax. The increase in PGE2 synthesis is not responsible for the defect in Umax, since it is not corrected with indomethacin. The release of ADH in response to raising serum tonicity is blunted during K depletion, which is partially corrected by indomethacin. These data suggest an inhibiting role for PGE2 in the release of ADH from the neurohypophysis during K depletion.

Topics: Animals; Dinoprostone; Diuresis; Dogs; Female; Hypokalemia; Indomethacin; Kidney; Kidney Concentrating Ability; Pituitary Gland, Posterior; Polyuria; Prostaglandins E; Saline Solution, Hypertonic; Sodium Chloride; Vasopressins

A polyuric state is often observed after cis-dichlorodiammine platinum (cisplatin). To study the mechanism of this polyuria we gave 5-6 mg/kg cisplatin to conscious rats and observed polydipsia and a polyuric form of mild acute renal failure. A defect in renal concentrating ability was observed 1 and 8 days after cisplatin. Animals demonstrated diminished postdehydration plasma vasopressin at 1 but not at 8 days after cisplatin, and exogenous vasopressin corrected the renal concentration defect at 1 but not at 8 days after cisplatin. To assess the role of polydipsia in the concentration defect, water intake in cisplatin-treated animals was matched to pair-fed controls. Prevention of polydipsia improved the polyuria but not the concentration defect seen 8 days after cisplatin. To assess intrarenal factors in the renal concentration defect, postdehydration interstitial solute was measured and was significantly lower in cisplatin-treated than in control animals. To determine whether the diminished interstitial solute was due to vascular mechanisms, inner medullary plasma flow was measured and was identical in cisplatin-treated and control rats. Treatment with cisplatin also resulted in decreased excretion of a water load. We conclude that either impaired synthesis or release of vasopressin is the cause of the impaired renal concentration seen 1 day after cisplatin. Eight days after cisplatin, the renal concentration defect is due in part to decreased interstitial tonicity.

Topics: Animals; Arginine Vasopressin; Body Water; Cisplatin; Dinoprostone; Drinking; Inulin; Kidney Medulla; Male; p-Aminohippuric Acid; Polyuria; Prostaglandins E; Rats; Rats, Inbred Strains; Vasopressins

Topics: Animals; Body Water; Diabetes Insipidus; Diagnosis, Differential; Dog Diseases; Dogs; Drinking; Kidney; Kidney Concentrating Ability; Kidney Diseases; Polyuria; Thirst; Vasopressins

Topics: Diagnosis, Differential; Humans; Osmolar Concentration; Polyuria; Vasopressins

Topics: Arginine Vasopressin; Body Water; Chlorpropamide; Deamino Arginine Vasopressin; Diabetes Complications; Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Polyuria; Time Factors; Vasopressins

The present experiments examined the role of prostaglandin biosynthesis in the increase in urine flow rate seen in rats with hypercalcemia induced by the administration of 1,25-dihydroxycholecalciferol. In a first group, rats receiving the vitamin D metabolite developed hypercalcemia, polyuria, and increased urine prostaglandin E excretion. Indomethacin resulted in a fall in urine prostaglandin E excretion. A second group was fluid restricted to ascertain whether increased thirst could be an etiologic mechanism of the polyuria. This resulted in a trivial fall in urine flow rate despite a fall in body weight and a rise in both urine and plasma osmolality. In a final group, prostaglandin inhibition restored the vasopressin sensitivity of the hypercalcemic kidney. Accordingly, the polyuria seen in hypercalcemic rats after the administration of 1,25-dihydroxycholecalciferol is associated with an increase in urine prostaglandin E excretion and can be reversed by inhibition of prostaglandin synthesis. In addition, this polyuria can occur independent of the thirst mechanism. Finally, there is evidence that the vasopressin resistance of the hypercalcemic kidney could be reversed by prostaglandin inhibition.

Topics: Animals; Calcitriol; Female; Hypercalcemia; Indomethacin; Kidney; Polyuria; Prostaglandins; Prostaglandins E; Rats; Rats, Inbred Strains; Urine; Vasopressins

The diagnoses provided by a standard indirect test of vasopressin function were compared with those obtained by radioimmunoassay of plasma vasopressin in 24 patients with nonglucosuric polyuria. All seven cases of severe neurogenic diabetes insipidus diagnosed by the indirect tests were confirmed by the vasopressin assay. However, two of six patients with partial neurogenic diabetes insipidus by indirect criteria had normal vasopressin secretion by the direct assay; one was found to have primary polydipsia, and the other nephrogenic diabetes insipidus. Moreover, three of 10 patients diagnosed as having primary polydipsia by the indirect test had clear evidence of partial vasopressin deficiency by the direct assay. The inability of the indirect test to distinguish accurately between partial neurogenic diabetes insipidus and primary polydipsia may be explained by increased sensitivity to low concentrations of vasopressin in the former disorder and a reduction of maximal concentrating ability in both. We conclude that the incorporation of a vasopressin assay improves accuracy in the differential diagnosis of polyuria.

Topics: Adolescent; Adult; Arginine Vasopressin; Child; Deamino Arginine Vasopressin; Diabetes Insipidus; Diagnosis, Differential; False Negative Reactions; Female; Humans; Male; Middle Aged; Osmolar Concentration; Polyuria; Radioimmunoassay; Saline Solution, Hypertonic; Vasopressins; Water Deprivation

Topics: Deamino Arginine Vasopressin; Diabetes Insipidus; Diagnosis, Differential; Female; Humans; Osmolar Concentration; Polyuria; Radioimmunoassay; Saline Solution, Hypertonic; Vasopressins; Water Deprivation

The distribution of the endorphins, beta-endorphin and enkephalin (Met5-enkephalin and Leu5-enkephalin), was determined in the pars distalis, intermedia, and nervosa of the rat pituitary using both immunocytochemical and radioimmunological methods. Immunoreactive (ir) beta-endorphin was found in pars distalis and pars intermedia. On gel filtration of the pars distalis extracts, beta-endorphin immunoreactivity was eluted in three peaks corresponding to pro-opiocortin (5%), beta-lipotropin (75%), and beta-endorphin (20%). beta-Endorphin was the only component in the pars intermedia. Enkephalin was found in high amount in the pars nervosa. A new enkephalinergic hypothalamic-pars nervosa pathway was observed. Dehydration experiments on normal rats and analysis of the genetically polyuric Brattleboro rat suggest that this enkephalinergic pathway may modulate neurohypophyseal neurosecretion.

Topics: Animals; Endorphins; Enkephalins; Hypothalamo-Hypophyseal System; Hypothalamus; Melanocyte-Stimulating Hormones; Neural Pathways; Neurotransmitter Agents; Pituitary Gland; Pituitary Gland, Posterior; Pituitary Hormones, Posterior; Polyuria; Rats; Vasopressins

A 20-year-old patient was evaluated because of polydipsia and polyuria; by means of the dehydration test a partial defect in the secretion of antidiuretic hormone (ADH) was demonstrated, since the urinary osmolality after the administration of exogenous vasopressin was superior by 25 percent to the maximum spontaneous urinary osmolality reached after a period of fluid restriction. Nevertheless, there was also a component of psychogenic polydipsia because the daily basal fluid intake was superior to 15 liters, and in view of the fact that the urinary osmolality could reach 600 mOsm/kg, the endocrine defect cannot totally be responsible for the enormous volume of fluid intake. This is the first case in the world literature in which the association between potomania and deficiency in the secretion of ADH is reported. Since ADH is one of the factors which regulate the behaviour of various animal species it is possible that its deficiency may be directly responsible for the psychic disorder which led to the potomania. It is also possible that an anatomical hypothalamic lesion, too small to be demonstrated, might have a simultaneous effect on the centers regulating thirst and the neurons producing vasopressin.

Topics: Adult; Clofibrate; Female; Humans; Inappropriate ADH Syndrome; Osmolar Concentration; Polyuria; Thirst; Vasopressins; Water-Electrolyte Balance

Eight burn patients with smoke inhalation were studied. High levels of plasma vasopressin and plasma cortisol in the presence of polyuria were observed. Stress and pain seem to be the main factors in the vasopressin oversecretion; the polyuria probably resulted from fluid administration and osmotic diuresis.

Topics: Burns; Humans; Hydrocortisone; Polyuria; Shock, Traumatic; Vasopressins

Permanent diabetes insipidus following head trauma is uncommon, but potentially fatal. The neurologic, roentgenographic, and endocrinologic findings in ten patients with this condition are reported. Eight of the patients were males under the age of 35 years. Unconsciousness (nine) and skull fracture (seven) were frequent findings. Cranial nerve damage (four) and anterior pituitary hormone deficiency requiring replacement (one) were less frequent. An automobile accident caused the trauma in six patients. Standard water deprivation tests revealed that five of the patients had total deficiency of antidiuretic hormone (ADH), and the other five had partial deficiency. The diagnosis of diabetes insipidus was markedly simplified by using a new screening test based on comparing urine and plasma osmolality in candidates with those of normal subjects.

Topics: Adult; Craniocerebral Trauma; Diabetes Insipidus; Female; Humans; Male; Osmolar Concentration; Polyuria; Vasopressins

Micropuncture and clearance studies were performed on normal untreated and polyuric lithium chloride treated rats (10-12 days). A persistent hypernatremic state quickly developed in the polyuric lithium treated rats during hydropenia resulting from an increased urinary loss of water over sodium chloride, as the fractional excretion of sodium remained at control levels. Superficial proximal tubule and loop of Henle fluid reabsorption was depressed by 8 and 17%, respectively, in lithium-treated rats during this period. By contrast, water reabsorption in the distal tubule and collecting system was significantly increased in the lithium animals, being 27% of the filtered load compared with 20% in normal rats. These results suggest that the urinary-concentrating defect induced by lithium treatment is due primarily to a depression of proximal tubule and possibly loop of Henle function, and that water reabsorption within the distal nephron may in fact be augmented: thus it is unlikely that the action of antidiuretic hormone is significantly impaired. Marked phosphaturia and hypocalciuria were also noted in the lithium-treated rats.

Topics: Animals; Calcium; Kidney Concentrating Ability; Kidney Function Tests; Kidney Tubules; Lithium; Male; Phosphates; Polyuria; Rats; Vasopressins

Topics: Adult; Drug Resistance; Hormones; Humans; Kidney; Male; Osmolar Concentration; Polyuria; Vasopressins

Topics: Animals; Humans; Kidney; Lithium; Polyuria; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Child; Child, Preschool; Dehydration; Diagnosis, Differential; Humans; Infant; Infant, Newborn; Metabolic Diseases; Polyuria; Urine; Vasopressins

Topics: Humans; Polyuria; Vasopressins; Water Deprivation

Forty-eight patients treated with oral lithium carbonate and 20 control subjects were studied to define the causes of lithium-induced water disturbances. Measurement of plasma immunoreactive arginine vasopressin, plasma osmolality, and urine osmolality after a period of dehydration separated nephrogenic diabetes insipidus, cranial diabetes insipidus, and primary polydipsia, the three postulated mechanisms of lithium-induced polyuria. Seventeen patients had a urinary concentrating defect despite serum lithium concentrations in the therapeutic range. Ten of these patients had nephrogenic diabetes insipidus, one had results suggestive of cranial diabetes insipidus, but none had evidence of primary polydipsia. Symptoms of thirst and polyuria were poor indicators of the degree of hypo-osmolar urine. No patient had electrolyte abnormalities, and none had sufficiently severe polyuria to stop lithium treatment.

Topics: Adult; Aged; Female; Humans; Lithium; Male; Mental Disorders; Middle Aged; Osmolar Concentration; Polyuria; Thirst; Vasopressins

Topics: Adult; Aged; Bipolar Disorder; Deamino Arginine Vasopressin; Female; Humans; Lithium; Middle Aged; Polyuria; Thirst; Vasopressins

The antidiuretic and urinary cyclic AMP response to supramaximal vasopressin infusion was studied in normal rats and in rats with lithium-polyuria. The animals were anaesthetized and then infused with a solution designed to produce excessive water diuresis and to lower basal cyclic AMP excretion. In 6 control animals not infused with vasopressin (1) urinary cyclic AMP excretion decreased during the infusion period. Vasopressin infusion (300 muU/min.) consistantly induced antidiuresis in all of 13 control rats (II); but the urinary cyclic AMP response varied individually from a significant increase in 6 animals to either no change or to a decrease in the remaining animals. The antidiuretic response to vasopressin was inhibited by 85% in 10 animals with marked polyuria induced by lithium administration (III). None of the animals in this group showed a significant increase of cyclic AMP excretion in response to vasopressin. The average rate of cyclic AMP excretion, which was equal in the two groups before vasopressin, was signifimantly lower in group III than in group II during vasopressin infusion. It is suggested that the increase in cyclic AMP excretion during vasopressin antidiuresis, although not consistant, most likely reflects hormone-induced changes of intracellular cyclic AMP levels in the renal medulla. Thus, the data suggest that the nephrogenic diabetes insipidus syndrome produced by lithium is associated with a defect in the renal formation of cyclic AMP in response to vasopressin.

Topics: Animals; Cyclic AMP; Diabetes Insipidus; Diuresis; Infusions, Parenteral; Lithium; Male; Polyuria; Rats; Rats, Inbred Strains; Vasopressins

Marked polydipsia and polyuria developed subsequent to trauma in a 1 1/2-year-old male Abyssinian cat. Diabetes insipidus was suspected, inasmuch as intramuscualr vasopressin administration resulted in amelioration of polydipsia and polyuria. However, hypertonic (3%) saline solution given intravneously resulted in anuria, an indication of antidiuretic hormone activity. Polyuria and polydipsia were abolished by oral chlorpropamide therapy, which was indirect evidence for partial deficiency of antidiuretic hormone.

Topics: Animals; Cat Diseases; Cats; Chlorpropamide; Diabetes Insipidus; Dogs; Male; Pituitary Gland; Polyuria; Thirst; Vasopressins

Topics: Aged; Female; Humans; Infant; Middle Aged; Polyuria; Postoperative Complications; Vasopressins

Acute renal artery stenosis in hydropenic dogs caused a contralateral increase in urine volume and free water clearance without change in glomerular filtration, renal blood flow, or osmolar clearance. The increase in urine volume was not dependent on the development of hypertension since it occurred in animals pretreated with trimethaphan but was dependent upon angiotensin since it was presented with angiotensin blockade with Saralasin. The effect was not caused by angiotensin inhibiting antidiuretic hormone release since the polyuria occurred in hypophysectomized animals receiving a constant infusion of 10 muU/kg per min of aqueous Pitressin. Since the rise in urine volume was associated with an increase in renal vein prostaglandin E concentration and was prevented by pretreatment with indomethacin (5 mg/kg) the results suggest that the rise in plasma angiotensin after renal artery stenosis causes an increase in contralateral prostaglandin E synthesis with resultant antagonism to antidiuretic hormone at the collecting tubule.

Topics: Animals; Blood Pressure; Dogs; Glomerular Filtration Rate; Indomethacin; Polyuria; Prostaglandins E; Renal Artery Obstruction; Renin; Saralasin; Sodium; Trimethaphan; Vasopressins

Dietary protein and NaCl are the precursors of about 60% of the urinary osmoles (urea and NaCl). This investigation tested the hypothesis that in patients with dieabetes insipidus, intake of dietary protein and salt will directly influence the degree of polyuria. Four subjects with pituitary and one with nephrogenic diabetes insipidus were studied. All medications were discontinued. To provide diets ranging between "low-solute" and "high-solute," protein was varied in increments from 40 to 130 g/day and NaCl was varied simultaneously from 0.5 to 10 g/day. In all patients, each increment in protein and salt caused a prompt increase in 24-hr urinary osmoles in the form of urea, Na+, and Cl-. The 24-hr urine volume likewise increased progressively. Average increase in urine osmoles and volume from low- to high-solute diet was +224% and +127%, respectively. In four of the five patients, Reduction of protein/salt intake from habitual dietary at home to the recommedded daily allowance caused a 50 to 100% reduction in the magnitude of polyuria.

Topics: Adolescent; Child; Diabetes Insipidus; Dietary Proteins; Drinking; Drug Resistance; Female; Humans; Male; Osmolar Concentration; Polyuria; Sodium Chloride; Urine; Vasopressins

A 38-year-old physician developed polyuria and hypodipsia four days after the onset of an upper respiratory tract infection. Subsequent investigation showed a concentration defect with dehydration that partially corrected with vasopressin injection (Pitressin) administration compatible with partial central diabetes insipidus (DI). Skull roentgenograms, EEG, and lumbar puncture were normal. The polyuria and hypodipsia slowly resolved without treatment. Normal urinary concentration ability was achieved by the 48th day, but a residual elevation in serum osmolarity persisted for one year. Review of the literature failed to show previous documentation of transient DI with elevated serum osmolarity from an acute, febrile illness. The mechanism is speculative, but may be related to a subclinical encephalitis. The true frequency of this syndrome and its relationship to the frequent observation of transient polydipsia and polyuria in "benign" febrile illness remains to be determined.

Topics: Acute Disease; Adult; Blood; Diabetes Insipidus; Humans; Hypothalamus; Kidney Concentrating Ability; Male; Osmolar Concentration; Polyuria; Respiratory Tract Infections; Thirst; Vasopressins

Interaction between lithium+ and water balance was studied in nine patients suffering manic-depressive trouble. Nephrogenic diabetes insipidus with polyuria and polydipsia was induced by Li+ in one case only. No trouble was apparent in eight cases. However, the applied method of investigation by lacking, and next, excess of water, vasopressin and ADH tests, measurements of urinary osmolarity and clearances, showed up a trouble of concentration in four cases, improved by ADH. The Li+ frequently (50%) induces a trouble of urinary concentration, without polyuria; it is brought to light only by biological investigations. Its origin is double, nephrogenic, which is the most important, and central by a pituitary component. In the other hand, the change in water metabolism, studied by the same tests, showed us a decrease of the clearance Li+ after lacking of water (deshydratation), and an increase after water surcharge. That result is not concordant, chiefly in regards to the water surcharge, with former experiments. It appears that our method (division by horary periods for measurement of clearance, study of circadian cycle of urinary Li+) permits some observations more precise than global gathering and measurement of clearances. That method also allows to make evident a circadian cycle of renal clearance of Li+, according to, for some part, with the renal movement of water. That remark would also have some consequence on lithium-therapy practice.

Topics: Bipolar Disorder; Diabetes Insipidus; Humans; Lithium; Osmolar Concentration; Polyuria; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Diuresis; Eating; Lithium; Male; Osmolar Concentration; Polyuria; Rats; Vasopressins

Topics: Child; Diabetes Insipidus; Diagnosis, Differential; Humans; Pituitary Gland, Posterior; Polyuria; Thirst; Vasopressins

Male rats with a portacaval anastomosis, placed in metabolic cages excreted twice as much urine as unoperated control rats. After subcutaneous injection of one unit of pitressin tannate in oil, the rats on average exhibited a 27% reduction in fluid intake and a 37% reduction in urine volume. Nevertheless the rats still excreted 60% more urine than control rats. Fluid restriction resulted in a reduction in urine volume and an increase in urine osmolality in both groups of rats. Shunted rats, however, continued to excrete 49 ml.kg.(-1)24h-1, while drinking only 43 ml.kg.(-1)24h-1. Owing to the negative water balance plasma osmolality rose by 22 mosm/kg H2O. Two weeks after portacaval anastomosis arterial prostaglandin-E concentrations were 412 ng/1, compared to 158 ng/1 in control rats. The results are consistent with the idea, that the shunt induced diuresis may be due to the renal effects of prostaglandin-E.

Topics: Animals; Diuresis; Male; Polyuria; Portacaval Shunt, Surgical; Prostaglandins E; Rats; Vasopressins; Water Deprivation

1. A patient with polyuria in whom diabetes insipidus had been diagnosed was treated with Pitressin. Resistance to this therapy developed after 18 months and a circulating antibody to vasopressin was then demonstrated. Withdrawal of therapy led to a fall in titre of the antibody and an increase in maximal urinary concentration. 2. The antibody to vasopressin was associated with the IgA fraction of the serum immunoglobulins and its characteristics are described.

Topics: Adult; Animals; Antibodies; Humans; Male; Polyuria; Rats; Urine; Vasopressins

The authors have studied in the dog--normal or diabetic insipidus after hypothalamic lesion--submitted to oral ingestion of ethanol the effects of a few antidiuretic drug: chlorpropamid, atromid-S, carbamazepin and carisoprodol. The carisoprodol only can reduce the diuresis and the drinking provoked by ethanol.

Topics: Animals; Carbamazepine; Carisoprodol; Chlorpropamide; Clofibrate; Diabetes Insipidus; Dogs; Drinking; Ethanol; Kidney; Male; Polyuria; Vasopressins

Topics: Animals; Diuresis; Female; Hydrogen-Ion Concentration; Injections, Intravenous; Kidney; Osmolar Concentration; Polyuria; Potassium; Sheep; Sheep Diseases; Sodium; Urine; Vasopressins; Vitamin A Deficiency

A single case of gastric plasmacytoma showing unusual clinical and pathological features is described. The patient had gluten sensitive enteropathy, and showed increased circulating IgA levels prior to gastrectomy. Progression of the disease was associated with both K and L light chain proteinuria, hypoalbuminaemia, and vasopressin resistant polyuria. Pathological investigation revealed the coexistence of IgA secreting soft tissue plasmacytoma, with IgG secreting myeloma. The significance of these findings is discussed.

Topics: Autopsy; Blood Transfusion; Celiac Disease; Gastrectomy; Glutens; Humans; Immunoglobulin Fragments; Immunoglobulins; Kanamycin; Lymph Nodes; Male; Middle Aged; Multiple Myeloma; Osmolar Concentration; Plasmacytoma; Polyuria; Proteinuria; Serum Albumin; Sodium; Stomach; Stomach Neoplasms; Vasopressins

Studies were carried out in the rat to detemine if hypothalamic lesions which caused polydipsia and polyuria had their effect mediated through an alteration of the ability of the neurohypophyseal system to release ADH. Rats with medial preoptic lesions hadincreased water intake while on ad libitum access to water and slightly impaired ability to conserve water following dehydration, but with no impairment of urine-concentrating ability. These were associated with an increase in plasma osmolality both during ad libitum fluid intake and after dehydration. Urinary ADH excretion was at leastas great as in shamoperated controls during ad libitum water intake, but failed to increase during dehydration in spite of a marked increase in plasma osmolality. Pituitary ADH content did not differ from control animals either during ad libitum water intake of after dehydration. Animals with lesions in the lateral preoptic and septal areas did not differ from control animals during ad libitum fluid intake and after dehydration even though lateral preoptic lesions produced polydipsia. In all animals, lesions were remote from the supraoptic nuclei, which showed no histological evidence of damage. It is concluded thatareas of the central nervous system away from the supraoptic nuclei are involved in the regulation of both water intake and ADH release.

Topics: Animals; Blood; Drinking; Hypothalamo-Hypophyseal System; Hypothalamus; Kidney Concentrating Ability; Male; Osmolar Concentration; Pituitary Gland; Polyuria; Preoptic Area; Radioimmunoassay; Rats; Vasopressins; Water-Electrolyte Balance

Topics: Diagnosis, Differential; Humans; Kidney Concentrating Ability; Kidney Diseases; Kidney Tubules; Osmolar Concentration; Polyuria; Vasopressins

Topics: Animals; Blood Pressure; Extracellular Space; Hypophysectomy; Natriuresis; Polyuria; Rats; Sodium; Vasopressins

Topics: Aldosterone; Animals; Lithium; Male; Polyuria; Prolactin; Rats; Vasopressins

Topics: Acne Vulgaris; Adult; Demeclocycline; Diabetes Insipidus; Female; Gonorrhea; Humans; Male; Polyuria; Vasopressins

The mechanism of lithium-induced diabetes insipidus was investigated in 96 patients and in a rat model. Polydipsia was reported by 40% and polyuria (more than 3 liter/day) by 12% of patients receiving lithium. Maximum concentrating ability after dehydration and vasopressin was markedly impaired in 10 polyuric patients and was reduced in 7 of 10 nonpolyuric patients studied before and during lithium therapy. Severe polyuria (more than 6 liter/day) was unresponsive to trials of vasopressin and chlorpropamide, but improved on chlorothiazide. Rats receiving lithium (3-4 meq/kg/day) developed massive polyuria that was resistant to vasopressin, in comparison to rats with comparable polyuria induced by drinking glucose. Analysis of renal tissue in rats with lithium polyuria showed progressive increase in the concentration of lithium from cortex to papilla with a 2.9-fold corticopapillary gradient for lithium. The normal corticopapillary gradient for sodium was not reduced by lithium treatment. The polyuria was not interrupted by brief intravenous doses of vasopressin (5-10 mU/kg) or dibutyryl cyclic AMP (10-15 mg/kg) capable of reversing water diuresis in normal and hypothalamic diabetes insipidus rats (Brattleboro strain). The present studies suggest that nephrogenic diabetes insipidus is a common finding after lithium treatment and results in part from interference with the mediation of vasopressin at a step distal to the formation of 3',5' cyclic AMP.

Topics: Animals; Bucladesine; Chlorothiazide; Chlorpropamide; Diabetes Mellitus; Diuresis; Glomerular Filtration Rate; Humans; Inulin; Kidney; Kidney Concentrating Ability; Lithium; Polyuria; Potassium; Rats; Sodium; Tritium; Vasopressins

Topics: Aldosterone; Angiotensin II; Animals; Diabetes Insipidus; Diuresis; Extracellular Space; Glomerular Filtration Rate; Glucose; Humans; Kidney; Polyuria; Potassium; Sodium; Sodium Chloride; Thiosulfates; Vasopressins; Water; Water-Electrolyte Balance

Topics: Administration, Oral; Animals; Biological Assay; Carbamazepine; Diabetes Insipidus; Diuresis; Drinking; Female; Humans; Osmolar Concentration; Polyuria; Rats; Urination; Vasopressins

Topics: Animals; Body Weight; Diabetes Insipidus; Diet; Drinking; Lithium; Male; Osmolar Concentration; Photometry; Polyuria; Rats; Sodium; Time Factors; Urination; Vasopressins

Topics: Child, Preschool; Diabetes Insipidus; Humans; Kidney Tubules; Male; Mikulicz' Disease; Polyuria; Syndrome; Vasopressins

Topics: Animals; Antibodies; Antibody Formation; Humans; Immunoglobulin A; Male; Polyuria; Rats; Vasopressins

Topics: Adult; Demeclocycline; Diabetes Insipidus; Drug Resistance; Humans; Male; Polyuria; Thirst; Vasopressins

Topics: Adrenalectomy; Adrenocorticotropic Hormone; Animals; Creatinine; Diuresis; Dogs; Glomerular Filtration Rate; Kidney; Lysine; Natriuresis; Oxytocin; Photometry; Pituitary Hormones, Posterior; Polyuria; Potassium; Time Factors; Urinary Catheterization; Vasopressins

Topics: 17-Hydroxycorticosteroids; 17-Ketosteroids; Adrenal Glands; Animals; Cerebral Cortex; Cortisone; Creatinine; Diabetes Insipidus; Diencephalon; Diuresis; Dogs; Female; Humans; Hypothalamus; Male; Middle Aged; Pituitary Gland, Posterior; Polyuria; Prednisone; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Blood Proteins; Diabetes Insipidus; Diagnosis, Differential; Dog Diseases; Dogs; Hydrochlorothiazide; Kidney Diseases; Leukocyte Count; Male; Osmolar Concentration; Phenolphthaleins; Polyuria; Specific Gravity; Thirst; Urine; Vasopressins

Topics: Bipolar Disorder; Chlorothiazide; Diabetes Insipidus; Evaluation Studies as Topic; Evoked Potentials; Female; Hospitalization; Humans; Kidney Concentrating Ability; Lithium; Middle Aged; Polyuria; Sodium; Somatosensory Cortex; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Bipolar Disorder; Diabetes Insipidus; Diuresis; Humans; Hypothalamo-Hypophyseal System; Kidney Concentrating Ability; Lithium; Male; Osmosis; Polyuria; Vasopressins; Water Deprivation

Topics: Anesthesia, General; Animals; Anuria; Blood; Blood Pressure; Diuresis; Electric Stimulation; Epinephrine; Ethanol; Female; Kinetics; Male; Osmolar Concentration; Physical Stimulation; Polyuria; Potassium; Rabbits; Sodium; Stomach; Urethane; Urine; Vagotomy; Vagus Nerve; Vasopressins

Topics: Adenosine Triphosphate; Adenylyl Cyclases; Animals; Carbon Isotopes; Cyclic AMP; Diuresis; Fluorides; Kidney; Lithium; Male; Polyuria; Rats; Vasopressins

The physiological basis for the polyuria and polydipsia occurring in some manic-depressive patients treated with lithium salts was studied in vivo and in vitro. Three lithium-treated polyuric patients, in whom other causes of a concentrating defect were excluded, had abnormal urinary concentrating abilities after a standard water depreviation test. Two of these patients failed to respond to exogenous vasopressin (ADH) and one had a subnormal response. The abilities of these patients to excrete solute-free water (C(H2O)) was comparable to normal subjects during steady-state water diuresis, suggesting no gross abnormalities in sodium transport. However, each of these patients demonstrated abnormally low capacities to reabsorb solute-free water (T(C) (H2O)) under hydropenic conditions after administration of hypertonic saline and vasopressin. These in vivo findings demonstrate at least a nephrogenic basis for the diabetes insipidus syndrome manifested by these three patients. The defect in water transport was further characterized in toad urinary bladders in vitro. Short-circuit current (I) and water flow (W) were studied under basal, ADH-stimulated, and cyclic adenosine 3',5'-monophosphate (c-AMP)-stimulated conditions. Increasing mucosal [Li(+)] progressively inhibited basal I, and both I and W induced by ADH. Significant inhibition of basal and ADH-induced I was observed at mucosal [Li(+)] < 1.1 mEq/liter, and of ADH-induced W at mucosal [Li(+)] = 11 mEq/liter. On the other hand, at these lithium concentrations, neither c-AMP-stimulated W nor I was inhibited. Increasing serosal [Li(+)] produced significant inhibition of basal I only at [Li(+)] at least 50-fold greater than at the mucosal (urinary) surface. These in vitro studies confirm that mucosal lithium inhibits the action of ADH, but not c-AMP. Hence, lithium appears to be a significant inhibitor of ADH-stimulated water flow, probably acts from the urinary surface, and appears to exert its effect at a site biochemically proximal to c-AMP action.

Topics: Adult; Animals; Anura; Biological Transport, Active; Bipolar Disorder; Cyclic AMP; Diabetes Insipidus; Drinking Behavior; Humans; In Vitro Techniques; Kidney; Kidney Concentrating Ability; Lithium; Male; Membrane Potentials; Middle Aged; Osmolar Concentration; Polyuria; Sodium; Urinary Bladder; Vasopressins; Water-Electrolyte Balance

Topics: Carcinoma, Small Cell; Diabetes Insipidus; Hormones, Ectopic; Humans; Hyponatremia; Lung Neoplasms; Osmolar Concentration; Plasma Volume; Polyuria; Radioimmunoassay; Syndrome; Vasopressins

Topics: Aerosols; Body Weight; Child; Child, Preschool; Chlorothiazide; Diabetes Insipidus; Diuresis; Drinking Behavior; Drug Resistance; Follow-Up Studies; Humans; Male; Oils; Osmolar Concentration; Polyuria; Psychophysiologic Disorders; Thirst; Urination Disorders; Vasopressins; Water Deprivation; Water-Electrolyte Balance

Topics: Diabetes Insipidus; Drinking; Humans; Kidney Function Tests; Polyuria; Thirst; Vasopressins

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: Aldosterone; Animals; Dextrans; Diuresis; Dogs; Infections; Polyuria; Vasopressins

Topics: Adenylyl Cyclases; Animals; Kidney; Lithium; Male; Polyuria; Rats; Vasopressins

Topics: Animals; Biological Assay; Chickens; Cloaca; Diabetes Insipidus; Drinking Behavior; Female; Heterozygote; Homozygote; Hypothalamus; Male; Mutation; Osmotic Pressure; Pituitary Gland, Posterior; Polyuria; Poultry Diseases; Sodium; Thirst; Urine; Vasopressins; Water Deprivation; Water-Electrolyte Balance

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: Adult; Bipolar Disorder; Carbonates; Humans; Kidney Concentrating Ability; Lithium; Male; Middle Aged; Osmolar Concentration; Polyuria; Thirst; Time Factors; Vasopressins; Water Deprivation

Topics: Adult; Diabetes Insipidus; Drinking Behavior; Female; Humans; Male; Middle Aged; Osmolar Concentration; Polyuria; Vasopressins; Water Deprivation

Topics: Animals; Antibody Specificity; Diabetes Insipidus; Immunity, Active; Iodine Isotopes; Polyuria; Rabbits; Thirst; Vasopressins

Triamcinolone acetonide was administered in excessive dosage to dogs to study the renal mechanism responsible for polyuria which is a clinically undesirable side effect of long term glucocorticoid therapy.Polyuria occurred coincident with a significant increase in urinary solute output. Although continuous administration of triamcinolone acetonide at 0.1 or 0.2 mg/lb/day caused a small but significant increase in creatinine output, the primary mechanism for the polyuria was increased solute excretion. Associated with the polyuria was pronounced hyperphagia and polydipsia. The cause of the hyperphagia was not established. The increase in electrolyte excretion caused by this synthetic steroid was probably compensated for by the hyperphagia. Because all the dogs showed muscle weakness and loss of body condition, it is likely that alteration in protein and amino acid metabolism was responsible for the hyperphagia.

Topics: Animals; Blood Glucose; Creatinine; Diuresis; Dog Diseases; Dogs; Feeding and Eating Disorders; Humans; Kidney; Kidney Function Tests; Muscular Diseases; Polyuria; Potassium; Sodium; Thirst; Time Factors; Triamcinolone Acetonide; Vasopressins

Topics: Aldosterone; Angiotensin II; Cardiac Output; Cardiac Volume; Cardiovascular System; Heart Atria; Humans; Hypothalamo-Hypophyseal System; Juxtaglomerular Apparatus; Kidney; Polyuria; Pressoreceptors; Renin; Tachycardia, Paroxysmal; Vasopressins

Topics: Animals; Arginine; Chlorides; Ducks; Hypophysectomy; Kidney; Male; Oxytocin; Polyuria; Potassium; Sodium; Thirst; Time Factors; Urine; Vasopressins; Vasotocin

Topics: Aldosterone; Anemia; Anuria; Child; Child, Preschool; Diuresis; Diuretics; Glomerulonephritis; Humans; Infant; Kidney; Kidney Concentrating Ability; Kidney Diseases; Osmolar Concentration; Osmotic Pressure; Polyuria; Pyelonephritis; Thalassemia; Vasopressins; Water; Water-Electrolyte Balance

Topics: Adolescent; Child; Child, Preschool; Creatinine; Diabetes Insipidus; Diuresis; Humans; Infant; Infant, Newborn; Kidney Concentrating Ability; Lymphatic Diseases; Male; Osmolar Concentration; Polyuria; Specific Gravity; Urine; Vasopressins; Water Deprivation

Topics: Adolescent; Adult; Chlorpropamide; Diabetes Insipidus; Diazoxide; Drinking Behavior; Female; Humans; Hypoglycemia; Kidney Tubules; Long-Term Care; Male; Middle Aged; Nephritis, Interstitial; Polyuria; Psychophysiologic Disorders; Vasopressins

Topics: Adult; Aged; Breast Neoplasms; Diabetes Insipidus; Female; Humans; Leukemia, Erythroblastic, Acute; Leukemia, Myeloid; Male; Middle Aged; Neoplasm Metastasis; Pancreatic Neoplasms; Pituitary Neoplasms; Polyuria; Vasopressins

A radioimmunoassay for arginine vasopressin has been developed that is sensitive to the hormone at 1 pg/ml. When plasma was filtered on G-25 Sephadex, immunoreactivity was detected in three regions. Endogenous arginine vasopressin was the third and smallest of the peaks and was recovered just after the salt. By combining gel filtration with immunoassay, we have made precise measurements of arginine vasopressin in a few milliliters of plasma.

Topics: Adult; Arginine; Chromatography; Chromatography, Gel; Diabetes Insipidus; Female; Humans; Immune Sera; Immunoassay; Male; Polyuria; Vasopressins

Topics: Adult; Cardiac Surgical Procedures; Female; Heart Septal Defects; Humans; Hypotension; Hypothalamus; Mitral Valve Stenosis; Polyuria; Postoperative Complications; Vasopressins

Topics: Breast Neoplasms; Carcinoma; Deficiency Diseases; Diabetes Insipidus; Female; Humans; Injections, Subcutaneous; Male; Neoplasm Metastasis; Osmolar Concentration; Pituitary Function Tests; Pituitary Gland, Posterior; Pituitary Neoplasms; Polyuria; Vasopressins; Water Deprivation

Topics: Diuretics; Extracellular Space; Heart Diseases; Hepatitis; Homeostasis; Humans; Hypothalamo-Hypophyseal System; Pericarditis, Constrictive; Pituitary Diseases; Polyuria; Vasopressins

Topics: Adrenal Glands; Adult; Angiotensin II; Animals; Child; Diabetes Insipidus; Diet, Sodium-Restricted; Diuresis; Diuretics; Dogs; Female; Humans; Hypopituitarism; Natriuresis; Polyuria; Pregnancy; Renin; Vasopressins

Topics: Cephalothin; Chloramphenicol; Humans; Hypokalemia; Male; Meningoencephalitis; Middle Aged; Oxacillin; Penicillin G; Penicillin Resistance; Polyuria; Potassium; Sepsis; Staphylococcal Infections; Vancomycin; Vasopressins

Topics: Edema; Humans; Liver Cirrhosis; Male; Polyuria; Vasopressins

Topics: Anticonvulsants; Diabetes Insipidus; Dibenzazepines; Diuretics; Humans; Hypophysectomy; Polyuria; Thirst; Vasopressins

Topics: Diabetes Insipidus; Diagnosis, Differential; Humans; Male; Middle Aged; Polyuria; Thirst; Vasopressins

Topics: Animals; Diuresis; Dog Diseases; Dogs; Glomerular Filtration Rate; Kidney; Kidney Tubules; Polyuria; Rats; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Anesthesia; Animals; Cardiac Catheterization; Cardiomegaly; Diabetes Insipidus; Diuresis; Dogs; Heart Atria; Hypothalamo-Hypophyseal System; Methods; Polyuria; Pressoreceptors; Pressure; Respiration; Vagotomy; Vasopressins

Polydipsia and polyuria are pronounced in chickens of a selected strain and this diabetes insipidus is inherited. The kidneys of such birds are capable of an antidiuretic response when lysine vasopressin or arginine vasotocin is injected. Osmotic pressure and sodium concentration of the plasmas of normal and mutant chickens are identical. Chicks predicted to have diabetes insipidus on the basis of parental pedigree are polydipsic.

Topics: Animals; Arginine; Body Weight; Chickens; Diabetes Insipidus; Female; Kidney Tubules; Lysine; Male; Molecular Biology; Mutation; Osmotic Pressure; Polyuria; Poultry Diseases; Sodium; Thirst; Turkeys; Vasopressins; Vasotocin; Water-Electrolyte Balance

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

1. With the aim of producing diabetes insipidus in sheep, electrolytic lesions were placed in the ventral medial hypothalamus immediately posterior to the optic chiasm.2. After formation of lesions, the pattern of urine excretion showed a triphasic response consisting of (i) an immediate diuresis reaching a maximum within 4 days, (ii) an interphase of about 12 days wherein rates of urine flow were normal, and (iii) a final phase of permanent polyuria. With the four sheep used in this work, the time between placement of the lesions and onset of permanent hyposthenuria was 19-22 days.3. In the final polyuric phase, the sheep were unable to concentrate their urine in response to dehydration or to feeding.4. Infusions of arginine vasopressin restored the ability of these animals to excrete urine that was hypertonic to plasma.5. The evidence showed that the hypothalamic lesions were effective in producing permanent diabetes insipidus. It was concluded that anti-diuretic hormone (ADH) has essentially the same function in sheep as it has in other mammalian species; that is, the hormone facilitates the elaboration of hypertonic urine. There was no evidence to suggest that ADH had a special effect on potassium excretion in the sheep.

Topics: Animals; Arginine; Dehydration; Diabetes Insipidus; Diet; Diuresis; Female; Hypothalamus; Kidney; Kidney Concentrating Ability; Osmosis; Osmotic Pressure; Polyuria; Potassium; Sheep; Time Factors; Urination; Vasopressins

Topics: Adult; Chlorpropamide; Diabetes Insipidus; Female; Humans; Injections, Intramuscular; Male; Middle Aged; Myocardial Infarction; Polyuria; Vasopressins

Topics: Diabetes Insipidus; Diabetes Mellitus; Diuresis; Female; Glomerular Filtration Rate; Humans; Hyperthyroidism; Kidney Diseases; Kidney Tubules; Male; Neurotic Disorders; Polyuria; Thirst; Vasopressins

Topics: Adult; Diabetes Insipidus; Diagnosis, Differential; Diuresis; Female; Humans; Hypertonic Solutions; Hypopituitarism; Male; Middle Aged; Nicotine; Osmosis; Polyuria; Sodium Chloride; Thirst; Vasopressins

Topics: Adolescent; Child; Child, Preschool; Cystinosis; Diabetes Insipidus; Diuresis; Glomerulonephritis; Humans; Hydronephrosis; Infant; Infant, Newborn; Kidney Diseases; Kidney Diseases, Cystic; Polyuria; Pyelonephritis; Uremia; Vasopressins

Topics: Animals; Estrogens; Hunger; Kidney; Male; Natriuresis; Polyuria; Potassium; Rabbits; Thirst; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Child, Preschool; Circadian Rhythm; Diabetes Insipidus; Humans; Hydrochlorothiazide; Male; Pituitary Function Tests; Polyuria; Urination; Vasopressins

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: Diabetes Insipidus; Histiocytosis, Langerhans-Cell; Humans; Hypothalamo-Hypophyseal System; Male; Middle Aged; Pituitary Gland; Polyuria; Thirst; Vasopressins

Topics: Behavior Therapy; Diabetes Insipidus; Diuretics; Glycosuria, Renal; Humans; Hypoglycemic Agents; Polyuria; Psychotherapy; Vasopressins

Topics: Adult; Animals; Child; Diabetes Insipidus; Diabetes Mellitus, Type 1; Diabetic Nephropathies; Humans; Infant; Male; Middle Aged; Polyuria; Rats; Vasopressins

Topics: Alcoholic Intoxication; Blood Glucose; Diabetic Coma; Ethanol; Humans; Mathematics; Osmolar Concentration; Polyuria; Thirst; Urea; Vasopressins

Topics: Acromegaly; Adult; Aged; Breast Neoplasms; Cushing Syndrome; Diabetes Insipidus; Diabetic Retinopathy; Female; Humans; Male; Middle Aged; Pituitary Gland; Polyuria; Prostatic Neoplasms; Ultrasonic Therapy; Vasopressins

Topics: Adult; Aminopyrine; Diabetes Insipidus; Female; Humans; Hydrochlorothiazide; Polyuria; Pregnancy; Pregnancy Complications; Vasopressins

Topics: Adrenal Cortex Hormones; Adrenal Glands; Adrenocorticotropic Hormone; Animals; Anuria; Diabetes Insipidus; Hypophysectomy; Hypothalamo-Hypophyseal System; Hypothalamus; Pituitary Gland; Pituitary-Adrenal System; Polyuria; Rats; Stress, Physiological; Tissue Extracts; Vasopressins

Topics: Blood Pressure; Cardiac Output; Creatine; Humans; Kidney Function Tests; Middle Aged; Polyuria; Tachycardia, Paroxysmal; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Adult; Aminohippuric Acids; Blood Chemical Analysis; Creatine; Dehydration; Diuresis; Female; Humans; Hypertonic Solutions; In Vitro Techniques; Infusions, Parenteral; Male; Paraplegia; Polyuria; Quadriplegia; Vasopressins

Topics: Angiotensin II; Diabetes Insipidus; Diet, Sodium-Restricted; Glomerular Filtration Rate; Humans; Hypertension, Malignant; In Vitro Techniques; Kidney Diseases; Male; Middle Aged; Natriuresis; Periodicity; Polyuria; Renin; Vasopressins

Topics: Adult; Brain Neoplasms; Chlorothiazide; Diabetes Insipidus; Diagnosis, Differential; Humans; Hypertonic Solutions; Infusions, Parenteral; Male; Nicotine; Obsessive-Compulsive Disorder; Polyuria; Psychosomatic Medicine; Sodium Chloride; Thirst; Vasopressins

Topics: Animals; Anura; Cell Membrane Permeability; Dextropropoxyphene; Diabetes Insipidus; Humans; In Vitro Techniques; Kidney Tubules; Polyuria; Urinary Bladder; Vasopressins; Water

Topics: Chlorothiazide; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diagnosis; Diagnosis, Differential; Diuretics; Humans; Hydrochlorothiazide; Physiology; Polyuria; Syndrome; Thirst; Vasopressins

Topics: Alcoholic Intoxication; Calcium Metabolism Disorders; Child; Diabetes Insipidus; Diagnosis; Diuresis; Genetics, Medical; Histiocytosis, Langerhans-Cell; Humans; Kidney Diseases; Measles; Polyuria; Prednisone; Psychosomatic Medicine; Sarcoidosis; Syndrome; Thirst; Toxicology; Urine; Vasopressins; Whooping Cough

Topics: Arginine Vasopressin; Mannitol; Osmolar Concentration; Osmosis; Pharmacology; Polyuria; Rats; Research; Sodium; Thyroid Gland; Thyroidectomy; Urine; Vasopressins

Topics: Blood Chemical Analysis; Carbon Dioxide; Chlorides; Diabetes Insipidus; Diabetes Mellitus; Glucose Tolerance Test; Glycosuria; Hematuria; Humans; Hydronephrosis; Hyperglycemia; Nitrogen; Polyuria; Potassium; Pseudomonas Infections; Sodium; Urea; Urinary Tract Infections; Urine; Urography; Vasopressins

Topics: Autopsy; Bone Marrow Examination; Busulfan; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Humans; Leukemia; Leukemia, Myeloid; Mercaptopurine; Polyuria; Prednisone; Vasopressins

Topics: Arginine Vasopressin; Diet; Diet Therapy; Glucose; Humans; Kidney; Polyuria; Thirst; Urine; Vasopressins

Topics: Child; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Dilatation; Enuresis; Humans; Hydronephrosis; Polyuria; Surgical Procedures, Operative; Urinary Bladder Neck Obstruction; Urography; Vasopressins

Topics: Chlorides; Desoxycorticosterone; Drug Therapy; Glycosuria; Humans; Hydrocortisone; Kidney Function Tests; Male; Natriuresis; Polyuria; Prostatic Neoplasms; Urethral Stricture; Urine; Vasopressins

Topics: Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Humans; Polyuria; Syndrome; Thirst; Vasopressins

Observations are presented on two patients with chronic compulsive polydipsia who showed a relative defect in renal concentrating capacity. After excluding all possible metabolic and renal causes of hyposthenuria and after obtaining normal kidney biopsies, both patients were studied in metabolic balance on a constant diet under the following conditions: (a) dehydration (loss of 3-5% body weight), (b) water loading and response to hypertonic saline, and (c) water loading and response to intravenous vasopressin (Pitressin). Throughout these studies the following parameters were observed: plasma and urine osmolality, glomerular filtration rate (inulin), renal plasma flow (P.A.H.), osmolar clearance and clearance of free water. In both patients the concentration defect was not related to variations in glomerular filtration rate or osmotic load. There was no correlation between the degree of hypoosmolality and the renal concentrating defect. Contrary to reports from other laboratories, restriction of water intake and chronic administration of intramuscular vasopressin did not correct the concentration defect.

Topics: Arginine Vasopressin; Body Weight; Compulsive Behavior; Drinking; Glomerular Filtration Rate; Humans; Inulin; Kidney; Kidney Diseases; Osmolar Concentration; Osmosis; Polydipsia; Polyuria; Saline Solution, Hypertonic; Thirst; Vasopressins

Topics: Acidosis; Acidosis, Renal Tubular; Amino Acids; Humans; Kidney Diseases; Polyuria; Vasopressins

Topics: Addison Disease; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diuresis; Diuretics; Humans; Hyperglycemia; Kidney Tubules; Osmosis; Physiology; Polyuria; Syndrome; Vasopressins

Topics: Amyl Nitrite; Deamino Arginine Vasopressin; Diabetes Insipidus; Female; Humans; Polyuria; Pregnancy; Pregnancy Complications; Vasopressins

Topics: Arginine Vasopressin; Breast Neoplasms; Calcium; Calcium, Dietary; Female; Homeostasis; Humans; Hypophysectomy; Interphase; Polyuria; Vasopressins

Topics: Arginine Vasopressin; Hypothyroidism; Kidney; Polyuria; Vasopressins; Water

Topics: Animals; Cobalt; Cobalt Radioisotopes; Gamma Rays; Polydipsia; Polyuria; Rats; Thirst; Urination Disorders; Vasopressins

Topics: Arginine Vasopressin; Humans; Polyuria; Urination Disorders; Vasopressins

Topics: Animals; Arginine Vasopressin; Edema; Female; Humans; Menstruation; Ovulation; Papio; Papio hamadryas; Papio ursinus; Polyuria; Urination Disorders; Vasopressins