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PubMed2000

Disorder of salivary secretion in inbred polydipsic mouse.

To find mechanisms of an extreme polydipsia in an inbred strain of mice, STR/N, this study was undertaken using Institute of Cancer Research (ICR) mice as a control. During food deprivation, daily water intake of both strains decreased. The decrement in the STR/N mice was larger than that in the ICR mice. During dehydration, daily food intake of the STR/N mice was smaller than that of the ICR mice. These data indicate that prandial drinking was more severely affected for the STR/N mice. Under anesthesia, the stimulated salivary secretion by pilocarpine of the STR/N mice was significantly smaller than that of the ICR mice. The submandibular gland of the STR/N mice was lighter and harder than that of the ICR mice. After desalivation from the major three salivary glands, the ICR mice drank as much as the STR/N mice. Young STR/N mice with undeveloped polydipsia did not show different salivary secretion stimulated by pilocarpine from the young ICR mice. These findings indicate a dysfunction with age in the salivary glands of the STR/N mice, and they suggest that the decreased saliva induces thirst and triggers extraordinary drinking in the polydipsic mice.

Age Factors↗

PubMed1981

Attenuation of the lithium-induced diabetes-insipidus-like syndrome by amiloride in rats.

The effect of amiloride on lithium-induced polydipsia and polyuria and on the lithium concentration in the plasma, brain, kidney, thyroid and red blood cells was investigated in rats, chronically treated with LiCl. Amiloride reduced the drinking and urine volume of rats in an acute (6 or 12 h) and a subacute (3 days) experiment. 6 h after the administration of amiloride, a reduction was observed in the lithium content of the renal medulla but not in the other organs studied. At 12 h, all the tissues showed a slight increase in lithium levels. After 3 days of combined treatment, a marked elevation in plasma and tissue lithium levels accompanied a reduction in water intake. In all the experiments, the attenuation of the lithium-induced diabetes-insipidus-like syndrome by amiloride was accompanied by a reduction of the ratio between the lithium concentration in the renal medulla and its levels in the blood and an elevation in the plasma potassium level. It is concluded that acute amiloride administration to lithium-treated patients suffering from polydipsia and polyuria might relieve these patients but prolonged amiloride supplementation would result in elevated lithium levels and might be hazardous.

Amiloride↗

PubMed1991

A rational approach to disorders of water balance in psychiatric patients.

Many mentally ill patients, particularly those with schizophrenia, have idiopathic or medication-induced disorders of water balance, which include excessive water intake, excessive water excretion, and impaired water excretion. Patients with these disorders manifest polydipsia and polyuria with or without symptomatic hyponatremia (low serum sodium concentration). Other serious sequelae include life-threatening water intoxication. The author reviews the physiology of normal water balance and the mechanism, causes, clinical presentation, and diagnosis of disorders of water balance. Interventions must first focus on identifying reversible factors. Medication-induced water imbalance can usually be reversed without compromising treatment of the underlying psychiatric disorder. A fully effective treatment for idiopathic polydipsia has not been found, although providing optimal treatment for the underlying psychiatric disorder often helps. Monitoring changes in body weight, in conjunction with measures of serum sodium, prevents water intoxication.

Drinking↗

PubMed1984

Marked hypotonic polyuria resulting from nephrogenic diabetes insipidus with partial sensitivity to vasopressin.

We studied two women with severe hypotonic polyuria whose symptoms dated from infancy. We eliminated the possibility of central diabetes insipidus (DI) and primary polydipsia, and established the presence of nephrogenic DI on the basis of: 1) the interrelationships between plasma osmolality, urine osmolality, and urinary AVP; and 2) impaired antidiuretic responses to AVP and 1 deamino-8-D-arginine vasopressin. Though 25-50 times as resistant to 1 deamino-8-D-arginine vasopressin nasal spray as patients with central DI, these patients could be treated effectively with large doses of the nasal spray. One patient has been so treated for more than a year with dramatic improvement in her polydipsia, polyuria, and sense of well-being.

Administration, Intranasal↗

PubMed1984

Spontaneous periodic hypothermia.

We studied a patient with spontaneous periodic hypothermia, agenesis of corpus callosum (Shapiro's syndrome), polydipsia polyuria, and hyponatremia. Endocrine evaluation of hypothalamic-pituitary unit, thyroid, adrenals and gonads was normal. Results of a water deprivation test implied primary polydipsia. Four of 10 reported cases of Shapiro's syndrome had abnormalities in water metabolism. In view of the known effects of arginine vasopressin in thermoregulation, the recurrent hypothermia of this syndrome and the abnormalities of water metabolism may have a common pathogenetic mechanism.

Adult↗

PubMed1997

A control of a golden retriever with renal dysplasia.

A six-month-old male Golden Retriever with a three-month history of polyuria and polydipsia was examined. Hematological examinations revealed nonregenerative anemia, azotemia, high serum creatinine level, hypercalcemia, hyperphosphatemia, hypercholesterolemia, hyperamylasemia, and low level of total serum protein. Urinalysis indicated mild proteinuria, and low specific gravity. Radiographic and ultrasonographic examinations revealed bilateral small sized kidneys. Histological examination by renal biopsy confirmed the diagnosis of renal dysplasia. Treatment with a dietary protein restriction, oral adsorbents, and dried aluminum hydroxide gel have been performed in this dog, and then, azotemia, high serum creatinine level, hypercalcemia, and hyperphosphatemia were improved. During 10 months after the initiation of treatments, no significant clinical change except polydipsia and polyuria has been observed.

Animals↗

PubMed1999

An elderly patient with transient diabetes insipidus associated with lymphocytic infundibulo-neurohypophysitis.

We present the eldest case ever reported of central diabetes insipidus (DI) associated with infundibulo-neurohypophysitis. A 77-year old woman, who complained of recent development of excessive thirst, polyuria and polydipsia, was referred to our hospital. The daily urine volume was markedly increased to 6 L. DDAVP administration effectively reduced urine volume and increased urine osmolality. The loading test using high-osmolar sodium chloride showed impaired excretion of vasopressin discordant with plasma osmolar changes. The anterior pituitary function was normal. Pituitary magnetic resonance imaging (MRI) showed thickening of the pituitary stalk and a lack of high-intensity signal of the neurohypophysis on T1-weighted images, suggestive of lymphocytic infundibulo-neurohypophysitis. The thickness of pituitary stalk on MRI improved 6 months later. DI was controlled with DDAVP for 40 days. This was followed by stabilization of the daily urine volume to less than 2.5 L without DDAVP. Our case is the eldest case of central DI associated with infundibulo-neurohypophysitis. The rapid remission of pituitary changes on MRI provides an insight that spontaneously partial remission of central DI may occur, resulting in transient polyuria and polydipsia.

Aged↗

PubMed2004

Novel mutant vasopressin-neurophysin II gene associated with familial neurohypophyseal diabetes insipidus.

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.

Adult↗

PubMed1997

Animal models with potential applications for screening compounds for the treatment of obsessive-compulsive disorder.

The availability of an animal model for obsessive-compulsive disorder (OCD) is necessary for the development of novel pharmacological treatments. To be useful, the model must be predictive of clinical performance, possess characteristic criteria and distinguish anti-OCD from antidepressant compounds. Due to the lack of OCD models useful for drug discovery, all compounds currently used for OCD were developed first as antidepressants. In this article, we discuss the relative merits of: stereotypic behaviours (canine acral lick, feather picking, amphetamine- and 5-HT-induced stereotypy); adjunctive and displacement behaviours (schedule-induced polydipsia, wheel running, resident-intruder grooming); anxiolytic tests (separation and shock-induced ultrasonic vocalisation and marble burying); and depression tests (inescapable shock-induced escape and immobility in forced swim) as potential OCD models. We conclude that adjunctive and displacement behaviours, and in particular schedule-induced polydipsia, may prove to be the best models for compulsive behaviour in animals that can be used for the discovery of novel anti-OCD agents.

Journal Article↗

PubMedDate not supplied

Water transport in the kidney and nephrogenic diabetes insipidus.

Nephrogenic diabetes insipidus is caused by an inability of the kidney to concentrate urine despite adequate concentration of vasopressin in blood and is characterized by polyuria, polydipsia, and hyposthenuria in the presence of plasma hyperosmolality. Nephrogenic diabetes insipidus is the result of defects in water homeostasis in the kidney. Nephrogenic diabetes insipidus occurs when the kidneys cannot or do not respond to vasopressin. There are 2 categories of nephrogenic diabetes insipidus. Congenital nephrogenic diabetes insipidus is a rare, inherited, irreversible cause of polyuria and polydipsia in humans that is even rarer in animals. Acquired nephrogenic diabetes insipidus is more common and is often secondary to illness or medication that interferes with the action of vasopressin in the renal tubules. Unlike congenital nephrogenic diabetes insipidus, acquired or secondary nephrogenic diabetes insipidus is often reversible with correction of the associated or causative problem.

Animals↗

PubMed1981

[One month studies on the subacute toxicity of captopril in rats].

Subacute toxicity of captopril by daily oral administration at dose levels of 10 mg/kg, 30 mg/kg, 100 mg/kg, 300 mg/kg, 900 mg/kg and 2700 mg/kg for one month was studied in Sprague-Dawley rats. In the 2700 mg/kg group, 13 of 18 males and 17 of 18 females died with marked emaciation and abdominal distension. In the 900 mg/kg group, 1 of 18 males and 3 of 18 females died also during the administration period. In dead animals, a marked dilatation of gastrointestinal tract was noted showing multiple hemorrhagic erosions and/or ulcers in the glandular stomach. The remainder of these groups exhibited polydipsia and polyuria during the dosage period. In the 300 mg/kg and 100 mg/kg groups, all animals survived throughout the entire experimental period showing polydipsia and polyuria. In the 30 mg/kg and 10 mg/kg groups, all animals survived also throughout the entire dosage period without showing any toxic sign. Regarding plasma analysis, the BUN and creatinine concentration was significantly elevated in the group of 100 mg/kg or more. In the hematological examination, there was a decrease of erythrocyte counts, hemoglobin contents and hematocrit values in the group of 300 mg/kg or more. Pathological examinations revealed a marked thickening of the wall in afferent arterioles and interlobular arteries of the kidney in association with hypertrophy and hyperplasia of juxtaglomerular cells in 100 mg/kg, 300 mg/kg, 900 mg/kg and 2700 mg/kg groups. In these groups, multiple hemorrhagic erosions with or without ulcer were also noted in the glandular stomach. In the spleen, a slight increase of extramedullary hematopoiesis and hemosiderosis was noted in the 100 mg/kg, 300 mg/kg, 900 mg/kg and 2700 mg/kg groups, in which an increase of erythropoietic elements was also noted in the bone marrow. From these results, the maximum nontoxic dose was estimated as about 30 mg/kg/day by oral administration of captopril in the rats.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2002

Diabetes insipidus in children: pathophysiology, diagnosis and management.

In diabetes insipidus, the amount of water ingested and the quantity and concentration of urine produced needs to be carefully regulated if fluid volume and osmolality are to be maintained within the normal range. One of the principal mechanisms controlling urine output is vasopressin which is released from the posterior pituitary gland and enhances water reabsorption from the renal collecting duct. In diabetes insipidus, the excessive production of dilute urine, and the causes of this clinical picture can be divided into three main groups: the first is primary polydipsia where the amount of fluid ingested is inappropriately large; the second group is cranial diabetes insipidus where the production of vasopressin is abnormally low; and, the third group is nephrogenic diabetes insipidus where the kidney response to vasopressin is impaired. The history and examination may suggest an underlying explanation for diabetes insipidus but a range of baseline and more extensive investigations may be required before a diagnosis can be reached. These investigations are not without risk, and the results need to be interpreted carefully because children do not always segregate neatly into a particular diagnostic category on the basis of one test alone. Children with cranial diabetes insipidus typically respond to arginine vasopressin or its manufactured analogue, desmopressin, with an increase in urine osmolality and an associated reduction in urine output. Such children usually require neuroimaging to look for evidence of evolving CNS pathology, such as an intracranial tumour. Vasopressin "replacement" with desmopressin is the treatment of choice in patients with cranial diabetes insipidus although extreme caution is required when treating babies or small children because of the danger of fluid overload. Abnormal production of other pituitary hormones in children with CNS disease can also influence fluid balance. Nephrogenic diabetes insipidus can be due to abnormal electrolyte concentrations, therefore these should be measured as part of the initial assessment. In a small number of children the defect is a primary abnormality of the vasopressin receptor or one of the water channel proteins (aquaporins) involved in water transport. The treatment of these patients is difficult and typically involves therapy with a diuretic such as chlorothiazide, as well as indomethacin. These agents enhance urine osmolality by their effect on circulating volume and renal solute and water handling. The fluid intake of most young children with primary polydipsia can be safely reduced to a more appropriate level.

Adolescent↗

PubMed2004

Orange juice-induced hyperkalemia in schizophrenia.

Some fruit juices have very high potassium content. However, only several cases of juice-induced hyperkalemia have been reported that involved non-psychiatric, diabetic outpatients with renal compromise. We present a highly unusual case of a 66-year-old non-diabetic, schizophrenic woman with psychogenic polydipsia and normal renal function who developed hyperkalemia secondary to excessive orange juice consumption while an inpatient. In addition to demonstrating this previously undescribed medical comorbidity of schizophrenia, this case highlights the need for careful attention when communicating with both nursing and patients when managing psychogenic polydipsia.

Aged↗

PubMed2003

Cryptococcal pyelonephritis in a dog.

A 5-year-old castrated male Golden Retriever was evaluated for polyuria, polydipsia, and progressive regurgitation thought to be a result of bacterial pyelonephritis and megaesophagus. Bacteriologic culture of urine failed to yield clinically relevant growth, and results of a urine sediment examination were normal. With time, intention tremors and progressive neurologic dysfunction were also observed. At necropsy, a diagnosis of cryptococcal disease was confirmed histologically and immunohistochemically. Findings in the dog of this report were indicative of nephrogenic diabetes insipidus with polyuria and polydipsia caused by cryptococcal pyelonephritis. Neurologic manifestations of systemic cryptococcus infection included megaesophagus, esophageal hypomotility, and regurgitation attributed to localization of cryptococcal organisms in the brain stem in the region of the dorsal motor nucleus of the vagus nerve. To the authors' knowledge, this is the first report of polyuria secondary to cryptococcal pyelonephritis.

Animals↗

PubMed1988

Antibodies to vasopressin in patients with diabetes insipidus. Implications for diagnosis and therapy.

STUDY OBJECTIVE: To determine whether antibodies to vasopressin play a role in the development of diabetes insipidus or interfere with diagnosis and treatment. DESIGN: Random plasma or serum samples for determining of antibodies to vasopressin were collected from patients and controls. SETTING: Referral university hospital with most patients studied in the clinical research center. PATIENTS: Twenty-nine healthy controls and 113 patients with polyuria (15 with primary polydipsia; 86 with neurogenic diabetes insipidus [60 studied before, 28 during, and 10 after antidiuretic hormone treatment]; and 12 with nephrogenic diabetes insipidus). INTERVENTIONS: Antibodies were detected by incubating samples with radiolabeled 125I-arginine vasopressin. The effect of antibodies on diagnosis was studied by examining the relation of plasma vasopressin to osmolality measured during dehydration or infusion of hypertonic saline and the relation of urine osmolality to plasma vasopressin measured during dehydration. MEASUREMENTS AND MAIN RESULTS: Antibodies to vasopressin were not detected in patients with primary polydipsia, nephrogenic diabetes insipidus, or neurogenic diabetes insipidus studied before therapy with antidiuretic hormone. Antibodies were detected in 6 of 28 patients studied during such treatments. All 6 patients reported decreased antidiuretic response to previously effective therapy with arginine or lysine vasopressin but had normal response to desmopressin or chlorpropamide. CONCLUSION: Diabetes insipidus does not result from spontaneously occurring antibodies to vasopressin. The antibodies occasionally develop during treatment with antidiuretic hormone and, when they do, almost always result in secondary resistance to its antidiuretic effect. Antibodies usually do not impair the response to other forms of therapy; they only rarely interfere with the diagnosis of diabetes insipidus, by falsely suggesting the presence of the partial nephrogenic form.

Adolescent↗

PubMed1978

Water disturbances in patients treated with oral lithium carbonate.

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.

Adult↗

PubMed1997

Effects of chronic ramipril treatment in streptozotocin-induced diabetic rats.

The present investigation was undertaken to study the effects of chronic oral ramipril (1 mg/kg) treatment in streptozotocin (STZ) induced diabetic rats. Single tail vein injection of STZ (45 mg/kg, i.v.) produced a diabetic state exhibiting all the cardinal symptoms such as loss of body weight, polydipsia, polyuria, glucosuria, polyphagia, hypoinsulinaemia and hyperglycaemia. The diabetic state was also found to be associated with bradycardia, hypothyroidism, cardiac depression and cardiomyopathy. Ramipril treatment prevented STZ-induced hypertension, bradycardia, hypothyroidism, hyperchosesterolaemia and partially the cardiomayopathy. Ramipril treatment could not, however prevent STZ-induced loss of body weight, polyuria, polydipsia, polyphagia, hyperglycaemia, hypoinsulinaemia, hypertriglyceridaemia and cardiac depression. Our data suggests that ramipril has a few beneficial effects in the STZ-treated diabetic rats.

Animals↗

PubMedDate not supplied

[Water intoxication and hyponatremia: report of two cases].

Two psychiatric patients suffering from psychogenic polydipsia, hyponatremia and water intoxication were evaluated at emergency room. Both of them showed organic psychiatric disease which improve with medical treatment. We illustrated the physiological and clinical features of polydipsia, hyponatremia and water intoxication as well as treatment modalities.

Adult↗