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PubMedDate not supplied

Polyuria and polydipsia and disturbed vasopressin release in 2 dogs with secondary polycythemia.

In dogs, secondary polycythemia (SP) may be associated with polyuria and polydipsia (PU/PD). The pathogenesis of this PU/PD has not yet been explained. We hypothesized that hyperviscosity and increased blood volume in SP might affect vasopressin (VP) release, resulting in PU/PD. This hypothesis was tested in 2 dogs with SP caused by renal neoplasia and PU/PD. Osmoregulation of VP release was studied by a modified water deprivation test and by investigating the VP response to hypertonic saline infusion. Water deprivation test results were consistent with an inability to produce concentrated urine despite increasing plasma osmolality. During hypertonic saline infusion, the osmotic threshold of VP release was markedly increased in both dogs, resulting in a delayed VP response to increasing plasma osmolality. The sensitivity of VP release was low normal in both dogs. We conclude that blood hyperviscosity and increased blood volume led to impaired VP release and polyuria.

Animals↗
PubMed1984

Increased sodium appetite and polydipsia induced by partial aortic occlusion in the rat.

Partly occluding the abdominal aorta between the renal arteries caused the rat to drink steadily increasing amounts of 2.7% NaCl when this solution and water were available. The increase in NaCl intake preceded the increase in water intake that also occurred after aortic occlusion, and intakes of both fluids were reaching maximal values 1-2 weeks after operation. The amounts of fluid drunk during the day increased greatly. This change in the pattern of drinking, together with the rise in fluid intake and the drop in food intake meant that drinking was less associated with feeding than it is in the normal rat. The rats went into fluid and electrolyte deficit within 24 h of partial aortic occlusion and remained in deficit for about a week (the duration of the balance experiment) despite increasing intakes of NaCl and water. Renal function was unimpaired during the first 2 weeks, and the abnormal signs were mainly and rapidly reversed by removal of the ischaemic kidney or administration of the angiotensin converting enzyme inhibitor, captopril. Therefore polydipsia and increased sodium appetite in the first 2 weeks after aortic occlusion were likely to have been caused by fluid deficit, with increased renin secretion from the ischaemic kidney contributing to both behaviours. Arterial blood pressure rose immediately after aortic occlusion, before the onset of increased drinking. Up to 3 weeks after operation the incidence and severity of the hypertension did not appear to depend on the spontaneous changes in intake of water or hypertonic NaCl.

Animals↗
PubMed1976

Drug-induced hyponatraemia in psychogenic polydipsia.

Two patients with psychogenic polydipsia developed hyponatraemia, one in association with administration of hydrochlorothiazide and the other with that of tolbutamide. It is suggested that the increased fluid intake in such patients may make them more susceptible to the development of hyponatraemia from thiazide or sulphonylurea compounds.

Humans↗
PubMed1987

Post-traumatic diabetes insipidus combined with primary polydipsia.

We describe a case of diabetes insipidus after head injury in which thirst persisted despite treatment with DDAVP and normal plasma osmolality. Symptoms were only completely relieved when plasma osmolality was below 270 mosmol/kg. We believe that this might have been due to hypothalamic injury causing resetting of the thirst osmostat. To our knowledge, this type of primary polydipsia has not been described before in association with diabetes insipidus following head injury.

Adult↗
PubMed2003

Effect of primary polydipsia on aquaporin and sodium transporter abundance.

Chronic primary polydipsia (POLY) in humans is associated with impaired urinary concentrating ability. However, the molecular mechanisms responsible for this finding have not been elucidated. The purpose of this study was to examine the effect of chronic primary POLY on water metabolism and renal aquaporin (AQP) water channels and sodium and urea transporter abundance in rats. Primary POLY was induced in male Sprague-Dawley rats by daily administration of 15 g powdered rat chow mixed in 100 ml water for 10 days. Control rats (CTL) received 15 g powdered rat chow per day and ad libitum drinking water. Rats were studied following this period before further intervention and with a 36-h period of water deprivation to examine maximal urinary concentrating ability. At baseline, POLY rats demonstrated significantly greater water intake (100 +/- 1 vs. 22 +/- 2 ml/day, P < 0.0001) and urinary output (80 +/- 1 vs. 11 +/- 1 ml/day, P < 0.0001) and decreased urinary osmolality (159 +/- 13 vs. 1,365 +/- 188 mosmol/kgH2O, P < 0.001) compared with CTL rats. These findings were accompanied by decreased inner medulla AQP-2 protein abundance in POLY rats compared with CTL rats before water deprivation (76 +/- 2 vs. 100 +/- 7% CTL mean, P < 0.007). With water deprivation, maximal urinary osmolality was impaired in POLY vs. CTL rats (2,404 +/- 148 vs. 3,286 +/- 175 mosmol/kgH2O, P < 0.0005). This defect occurred despite higher plasma vasopressin concentrations and similar medullary osmolalities in POLY rats. In response to 36-h water deprivation, inner medulla AQP-2 protein abundance was decreased in POLY rats compared with CTL rats (65 +/- 5 vs. 100 +/- 5% CTL mean, P < 0.0006). No significant differences were noted in renal protein abundance of either AQP-3 or AQP-4 or sodium and urea transporters. We conclude that the impaired urinary concentrating ability associated with primary POLY in rats is due to impaired osmotic equilibration in the collecting duct that is mediated primarily by decreased AQP-2 protein abundance.

Animals↗
PubMed1976

Renal histologic and ultrastructural findings in psychogenic polydipsia and diabetes insipidus.

The renal biopsies of 15 patients affected by polydipsia syndromes were examined under light and electron microscopes. The authors contend that the observed renal lesions (dilatation of the glomerular loops, tubular hypertrophy and vacuolization, and basal membrane swelling) are the morphologic result of tubular hyperfunction in the service of ion reabsorption. This, in turn, is secondary to the increased GFR.

Animals↗
PubMed1983

Urinary tract abnormalities due to chronic psychogenic polydipsia.

Of 10 patients who excreted urine with low specific gravity and had chronic psychogenic polydipsia, five had urinary tract abnormalities, ranging from large bladders with large postvoid residuals to severe hydronephrosis, renal back pressure atrophy, and renal failure.

Adult↗
PubMed1993

Polydipsia and tardive dyskinesia in chronic psychiatric patients--related disorders?

Dopamine supersensitivity, presumably playing a role in tardive dyskinesia, has been implicated in the unexplained polydipsia occurring in chronic psychiatric patients. To investigate this hypothesis, the authors compared laboratory measurements indicating the fluid status of 65 patients before and after the development of tardive dyskinesia. No evidence was found that patients who develop tardive dyskinesia concurrently develop abnormalities in fluid regulation.

Adolescent↗
PubMed1998

Rhabdomyolysis after correction of hyponatremia due to psychogenic polydipsia possibly complicated by clozapine.

OBJECTIVE: To report a case of rhabdomyolysis related to rapid correction of hyponatremia attributable to compulsive drinking of water, possible complicated by clozapine use. CASE SUMMARY: A 42-year-old white man treated with clozapine for schizophrenia was admitted for a generalized seizure. Marked hyponatremia due to psychogenic polydipsia was present. He developed a marked elevation of creatine kinase concentrations after correction of hyponatremia with hyperosmolar sodium solution, without clinical signs of rhabdomyolysis. DISCUSSION: Rhabdomyolysis associated with hyponatremia due to water intoxication has been reported in 17 patients to date. A possible explanation may lie within the framework of the calcium-sodium exchange across the skeletal muscle cell membrane. By increasing muscle cell permeability, clozapine treatment may possibly enhance the destruction of muscle cells. CONCLUSIONS: Hyponatremia due to water intoxication and concurrent use of clozapine should be considered in the differential diagnosis of rhabdomyolysis, especially in the severely psychiatrically disabled population.

Adult↗
PubMed1966

Schedule-induced polydipsia as a function of fixed interval length.

Rats were trained to bar-press for Noyes pellets on an FI schedule which was increased serially through several values from 2 sec to as high as 300 sec. Concurrently, water was freely available. As FI length was increased, the degree of polydipsia increased linearly to a maximum value.

Animals↗
PubMed1974

Effects of response-dependent and independent electric shock on schedule-induced polydipsia.

In Experiment I, lever pressing by rats was maintained by the delivery of food pellets under a 45-sec fixed-interval schedule. Fixed-time 180-sec and fixed-interval 180-sec schedules of shock delivery were systematically superimposed on the baseline food schedule to study effects on schedule-induced water intake. Response-dependent shock had little, if any, effect on water intake, whereas shocks independent of lever pressing attenuated fluid intake. In Experiment 2, rats received food pellets under a fixed-time 60-sec schedule. Electric shock delivered concurrently under a variable-time 180-sec schedule, but never while the animal was licking or within 5 sec after licking terminated, led to similar attenuation of water intake. These findings suggest that schedule-induced polydipsia is sensitive to differences in the functional properties of response-independent and dependent electric shock.

Journal Article↗
PubMed1991

Compulsive polydipsia following meningioma resection: an epileptic phenomenon? Case report.

The authors report the case of an individual who developed compulsive polydipsia following resection of a left sphenoidal ridge meningioma. The episodic, stereotyped nature of his symptoms, response to treatment, and electroencephalographic and magnetic resonance imaging findings are all highly consistent with temporal lobe-onset epilepsy. The pathophysiology of this underrecognized phenomenon is discussed.

Adult↗
PubMed2004

Acquisition of schedule-induced polydipsia by rats in proximity to upcoming food delivery.

Food-deprived rats that receive intermittent delivery of small amounts of food develop excessive drinking--specifically, schedule-induced polydipsia (SIP). A main characteristic of SIP is its occurrence at the beginning of interfood intervals. The purpose of this study was to demonstrate that SIP can be developed toward the end of interfood intervals, in closer proximity to upcoming than to preceding food delivery. In Experiment 1, two groups were exposed to a fixed-time (FT) 30-sec food schedule with water available during the first or the last 15 sec of each interfood interval. Two additional groups, which had access to water throughout, were exposed to FT 30-sec or FT 15-sec schedules of food presentation. The FT 30-sec group with free access to water developed the highest level of intake; similar and intermediate levels were induced in all the remaining groups. In Experiment 2, three groups of rats were exposed to an FT 90-sec food schedule with water available during the first, the second, or the last 30 sec of each interfood interval. One additional group with access to water throughout was exposed to the FT 90-sec schedule of food presentation. The group with free access to water developed a higher level of consumption than did the other groups, but by the end of training none of the four groups showed statistical differences in polydipsic drinking. Results show that adjunctive drinking can be developed in proximity to upcoming food delivery even with long interfood intervals.

Animals↗
PubMed1995

Rhabdomyolysis after correction of hyponatremia due to psychogenic polydipsia.

Severe neurologic complications resulting from correction of hyponatremia are common, but reports of nonneurologic sequelae are scarce. This article describes a patient in whom rhabdomyolysis developed during correction of severe hyponatremia attributable to psychogenic polydipsia. Relevant material about volume regulation in the cell is presented, and a potential mechanism of cell damage is proposed. This case report emphasizes the importance of monitoring for nonneurologic complications during correction of hyponatremia.

Adult↗
PubMed2000

Unusual combination: polydipsia with hypernatremia in a schizophrenic patient.

OBJECTIVE: The authors describe a patient with an unusual combination of polydipsia and isolated hypernatremia without any other changes of electrolytes. The patient had two attacks of hypernatremia which were successfully treated with clozapine. Some speculations about possible mechanisms of this unusual combination are discussed.

Drinking↗
PubMedDate not supplied

[Primary polydipsia and eating disorders: three case reports].

We present three patients with eating disorders and primary polydipsia with different severity and clinical relevance. This association is underestimated in common clinical practice, either due to hidden symptoms or lie over the real hydric intake, or due to lack of nosology location as a differentiated entity in nowadays nosologies, or by ignorance of the clinical features it can generate. These and other similar cases published in the literature indicate the real need to make a medical history focussed on hydric intake as part of the whole medical and psychiatric story and be alert if previous positive hyponatremia is recorder. Finally we propose five recommendations for the management and praecox diagnosis in order to avoid severe clinical consequences.

Adolescent↗