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PubMed2001

Expression of salt and urea transporters in rat kidney during cisplatin-induced polyuria.

BACKGROUND: Cisplatin (CP) induced polyuria in rats is associated with a reduction in medullary hypertonicity, normally generated by the thick ascending limb (TAL) salt transporters, and the collecting duct urea transporters (UT). To investigate the molecular basis of this abnormality, we determined the protein abundance of major salt and UT isoforms in rat kidney during CP-induced polyuria. METHODS: Male Sprague-Dawley rats received either a single injection of CP (5 mg/kg, N = 6) or saline (N = 6) intraperitoneally five days before sacrifice. Urine, blood, and kidneys were collected and analyzed. RESULTS: CP-treated rats developed polyuric acute renal failure as assessed by increased blood urea nitrogen (BUN), urine volume and decreased urine osmolality. Western analysis of kidney homogenates revealed a marked reduction in band density of the bumetanide-sensitive Na-K-2Cl cotransporter in cortex (60% of control values, P < 0.05), but not in outer medulla (OM) (106% of control values). There were no differences in band densities for the renal outer medullary potassium channel (ROMK), the type III Na-H exchanger (NHE3), the alpha-subunit of Na,K-ATPase in the OM; or for UT-A1, UT-A2 or UT-A4 in outer or inner medulla. However, the band pattern of UT-A2 and UT-A4 proteins in the OM of CP-treated rats was different from the control rats, suggesting a qualitative modification of these proteins. CONCLUSIONS: Changes in the abundance of outer or inner medullary salt or urea transporters are unlikely to play a role in the CP-induced reduction in medullary hypertonicity. However, qualitative changes in UT proteins may affect their functionality and thus may have a role.

Animals↗
PubMed2006

[Postoperative polyuria after laparoscopic adrenalectomy for pheochromocytoma].

Disturbances of osmoregulation leading to polyuria are well known complications after operations in the sella region. In contrast, increased urinary output following adrenalectomy is rare. We report a case of postoperative polyuria after laparoscopic adrenalectomy for pheochromocytoma with urine output up to 15 l per day. Treatment included careful monitoring of the patient and intravenous and oral replacement of fluids and electrolytes. In our case a normalisation of the urine output was observed after few days. A further treatment with vasopressin was not undertaken as the osmolality at all times was in normal range.

3-Iodobenzylguanidine↗
PubMed1981

A comparison of plasma vasopressin measurements with a standard indirect test in the differential diagnosis of polyuria.

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.

Adolescent↗
PubMed1996

Lithium induced polyuria and renal vasopressin receptor density.

BACKGROUND: Lithium, a drug frequently used for treatment of affective disorders, is known to cause a vasopressin-resistant state, leading to polyuria and polydipsia. It has been suggested that lithium interacts with the renal V2-vasopressin receptor. Detailed studies on the influence of lithium on the AVP receptor, however, have so far been difficult due to the lack of a suitable radioligand with high specific activity and high affinity. METHODS: Using 125I-[8-(p-(OH)-phenylpropionyl)]- LVP, we studied the effects of lithium on V2-vasopressin receptors in male Sprague-Dawley rats and LLC-PK1 cells. Rats, having free access to water, were orally treated with 10 mg lithium/100 mg b.w./day or placebo for 10 days. Scatchard analysis was performed using membranes prepared from homogenized renal papillae. RESULTS: Lithium caused significant polyuria and an impaired renal concentration capacity after water deprivation. Binding studies showed no effect of lithium on binding affinity KD (0.98 +/- 0.21 nmol/l vs. 0.86 +/- 0.15 nmol/l (Li) (n.s.). Receptor density, however, significantly decreased from 130 +/- 12.3 nmol/kg protein in controls (n = 8) to 101.7 +/- 13.4 nmol/kg protein (n = 8), (P < 0.05). Plasma osmotically and AVP were not significantly altered by lithium treatment. Vasopressin receptor density on LLC-PK1-cells, a pig renal cell line, was not changed by preincubation with lithium (312 +/- 22 nmol/kg vs. 329 +/- 25 nmol/kg (Li) (n = 6, n.s.). CONCLUSIONS: The decrease of AVP-receptor density in vivo might be related to vasopressin resistance, either primary, or secondary to other factors, e.g. actual water transport.

Animals↗
PubMed1986

Polyuria among patients with psychosis.

Using the criterion of early morning urinary specific gravity (SPGR) of 1.008 or less to define the presence of polyuria, we identified 26 of 72 male (36 percent) and 14 of 31 female (45 percent) institutionalized chronically psychotic patients as polyuric during a comprehensive survey of one of the chronic care units at a State mental hospital. Factors including diagnosis, sex, age, weight, and serum sodium did not distinguish the polyuric from the nonpolyuric patients. For men, administration of lithium was associated with polyuria. Urinary creatinine concentration (UCR) correlated well with SPGR, and UCR may provide an alternate index to separate polyuric from nonpolyuric patients. The clinical implications of our findings are discussed.

Adult↗
PubMed1997

Single dose imipramine reduces nocturnal urine output in patients with nocturnal enuresis and nocturnal polyuria.

PURPOSE: We investigated the effect of imipramine on nocturnal urine output in patients with nocturnal enuresis. MATERIALS AND METHODS: There were 15 monosymptomatic enuretic patients 15 to 37 years and 8 control subjects 25 to 32 years old. We measured nocturnal urine output, urine osmolality, creatinine clearance, osmolal clearance, free water clearance, excretion of solutes, fractional excretion of sodium, fractional excretion of potassium and plasma vasopressin with and without a single oral dose of imipramine (1 mg./kg. of body weight) taken at 8 p.m. RESULTS: Baseline studies showed significantly larger and less concentrated nocturnal urine among enuretics compared with controls. We observed a marked antidiuretic effect of imipramine in 6 enuretics with severe nocturnal polyuria. The imipramine induced decrease in urine output was accompanied by reduced osmolal clearance. Approximately a third of the observed decrease in solute excretion was attributed to lower excretion of sodium and potassium. The remaining two-thirds were most likely caused by an increased tubular reabsorption of urea, which may be secondary to a sympathomimetic effect of imipramine tubules, possibly because of altered adrenal medullary function with an increase in proximal tubular sodium and water reabsorption. The resultant lower tubular flow rate facilitates tubular reabsorption of urea in the distal part of the nephron. CONCLUSIONS: Imipramine has a vasopressin independent antidiuretic effect if nocturnal polyuria is present. The antidiuretic effect of imipramine can be attributed primarily to increased alpha-adrenergic stimulation in the proximal tubules with a secondary increased urea and water reabsorption more distally in the nephron.

Adolescent↗
PubMed2005

Differential diagnosis of polyuria and polydipsia in a patient with spinal cord injury.

We report the case of a 35-yr-old tetraplegic man who experienced increased water intake, constant thirst, and a copious amount of urine excretion after his spinal cord injury and in whom an intermittent catheterization program was unmanageable. Laboratory evaluation revealed low serum and urine osmolality, which were suggestive of psychogenic polydipsia, and hypokalemia, which might lead to polyuria with a compensatory polydipsia. His water intake was reduced with antidepressant therapy and potassium supplementation and normalized on the third month of the treatment. Physicians should be aware of the differential diagnosis of polyuria and polydipsia, which interfere with neurogenic bladder management in patients with spinal cord injury.

Adult↗
PubMed2006

Improvement of polyuria, bladder sensation and bladder capacity following renal transplantation.

Here, we report a patient with renal failure and bladder dysfunction whose symptoms improved following renal transplantation. A 23-year-old woman underwent renal transplantation for renal failure as a result of dysplastic kidneys. Urodynamic evaluation prior to transplantation showed decreased bladder sensation and increased bladder capacity, probably because of congenital polyuria. One week after surgery, dry mouth disappeared, and urine volume normalized gradually. Urodynamic studies performed 3 and 10 months after transplantation showed improvement of bladder function, and the frequency/volume charts of urination also showed normalization of urine volume. Renal and bladder functions were almost normal 45 months after transplantation. Bladder dysfunction involves numerous factors, but the primary cause was probably congenital polyuria in the present case. This case suggested that blood purification and correction of urine volume by renal transplantation might lead to restoration of normal bladder function.

Adult↗
PubMed1988

Lithium, polyuria and abnormal diurnal weight gain in psychosis.

We evaluated diurnal weight gain and polyuria among 31 institutionalized chronically psychotic patients receiving lithium and 42 controls not receiving this drug. The patients were weighed weekly for three weeks at 7 a.m. and 4 p.m. We normalized the diurnal weight gain (NDWG) as a percentage by subtracting the 7 a.m. weight from the 4 p.m. weight, multiplying the difference by 100, and then dividing the result by the 7 a.m. weight. Polyuria was assessed using mean urine creatinine concentration (MUCR). NDWG was abnormal among study patients (1.9 +/- 1.2%) and controls (1.6 +/- 1.5%) independent of lithium treatment. The variation in MUCR explained about 20% of the variation in NDWG in both groups.

Adult↗
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↗
PubMed1980

Nocturnal polyuria and saluresis in renal allograft recipients.

The evolution of nocturnal polyuria and saluresis in renal allograft recipients was studied by comparing the day to night (D:N) ratios of urine volume and sodium excretion in 15 patients who had undergone transplantation less than one year previously (recent-transplant group) with those in 11 patients who had undergone transplantation at least one year previously. Eleven patients with chronic renal failure and 12 normal subjects served as controls. Patients in the recent-transplant group had significantly lower D:N ratios of urine volume and sodium excretion than the patients who had undergone transplantation at least a year before, while the ratios in this last group did not differ significantly from those in the normal subjects. Nocturnal polyuria and saluresis gradually subsided in five patients studied for three months. Chronic renal failure and uraemic autonomic neuropathy were unlikely causes of the nocturia. The patients in the recent-transplant group had significantly lower D:N ratios of urine volume than the controls with chronic renal failure, and the mean Valsalva ratio in eight of them was not significantly different from that in the normal subjects. An undue sensitivity of renal allografts to postural influences was proposed.

Creatinine↗
PubMed1986

The effect of desmopressin on nocturnal polyuria, overnight weight loss, and morning postural hypotension in patients with autonomic failure.

Day and night urine volume, morning and evening body weight, and supine and sitting blood pressure were measured in five patients with chronic autonomic failure who were not receiving treatment with drugs. All had nocturnal polyuria, overnight weight loss, and a pronounced postural fall in blood pressure, with lowest levels in the morning. Desmopressin (2-4 micrograms given intramuscularly at 8 pm) reduced nocturnal polyuria, diminished overnight weight loss, raised supine blood pressure, and reduced the postural fall, especially in the morning, when patients were often at their worst. Desmopressin may be a useful alternative to, or may supplement, other forms of treatment in some patients with autonomic failure.

Aged↗
PubMed1988

Involvement of prostaglandin E2, cAMP, and vasopressin in lithium-induced polyuria.

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.

1-Methyl-3-isobutylxanthine↗
PubMed2001

Food restriction prevents age-related polyuria by vasopressin-dependent recruitment of aquaporin-2.

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.

Aging↗
PubMed1999

Role of atrial natriuretic peptide in nocturnal polyuria in elderly males.

OBJECTIVES: To demonstrate nocturnal polyuria objectively and to assess the role of atrial natriuretic peptide (ANP) in healthy elderly males with and without nocturnal polyuria (NP). PATIENTS AND METHODS: 31 healthy elderly men known to have NP (passing more than 33% of their 24-hour urine output during an 8-hour period overnight) and 12 controls without NP were invited to take part in the study. Blood and urine samples were collected at 4-hourly intervals in order to measure urine output, serum and urine electrolytes and osmolality as well as serum cortisol, renin, aldosterone, arginine vasopressin (AVP) and ANP. RESULTS: 26 men with NP and 8 controls agreed to take part in the study. Subjects with NP were found to have a diuresis and natriuresis as well as a significant increase in ANP overnight compared to the control group. There was no difference in the other parameters between the 3 groups, with the exception of aldosterone and AVP. CONCLUSIONS: This study has shown a group of subjects with increased natriuresis and diuresis overnight, associated with an increase in ANP. It is possible that subclinical cardiac failure causes an increase in ANP therefore causing nocturnal urinary symptoms and this theory needs further exploration.

Aged↗
PubMed1986

Plasma atrial natriuretic polypeptide and polyuria during paroxysmal tachycardia in Wolff-Parkinson-White syndrome patients.

The human atrial natriuretic polypeptide (hANP) concentration in plasma was measured during paroxysmal supraventricular tachycardia provoked in 2 patients with Wolff-Parkinson-White syndrome. A 10- to 20-fold increase in plasma hANP concentration was observed during the tachycardia: from 12 to 291 pg/ml in 1 case and from 14 to 174 pg/ml in the other. Although polyuria was associated with the tachycardia, urinary sodium excretion as well as urinary osmolality were decreased. The urinary arginine vasopressin was appreciably decreased during the tachycardia. These results suggest that hANP released by paroxysmal tachycardia might not act as a natriuretic factor in this range of plasma concentration. Polyuria during paroxysmal tachycardia was attributed mainly to the inhibition of arginine vasopressin release.

Adult↗
PubMed1987

The role of prostaglandins in early polyuria induced by cisplatin in the rat.

To assess a possible role of prostaglandins in the early phase of cisplatin-induced abnormalities in renal concentrating ability, three groups of rats were studied. In a first group we measured prostaglandin production from renal medullary microsomes isolated from rats sacrificed at different time periods after cisplatin, 5 mg/kg alone (PB/CP) or cisplatin plus aspirin, 300 mg/kg p.o., 1 h before cisplatin and daily (ASA/CP). In a second group of rats, balance studies were performed in PB/CP and ASA/CP animals for 4 days after cisplatin to determine the effect of such treatment on the renal excretion of solute and water. In another group of rats inulin clearance was measured in PB/CP and ASA/CP animals 4 days after such treatment. The rats received aspirin or phosphate buffer alone (50 mg/ml sodium phosphate, pH 8) to determine the effect of such treatment on prostaglandin production and renal function. In PB/CP Uosm fell and prostaglandin synthesis increased on days 1-3. Prostaglandin synthesis returned to baseline values by day 4, but Uosm remained low. Inulin clearance was low 4 days after cisplatin. In ASA/CP rats prostaglandin synthesis did not increase and the early polyuria was ameliorated. Aspirin did not prevent the later polyuria. Inulin clearance in the ASA/CP group was markedly reduced to levels below those observed with cisplatin alone. These data demonstrate that elevated rates of prostaglandin synthesis occur early in the course of cisplatin-induced renal failure and suggest that prostaglandins may play a role in the early cisplatin-induced concentrating defect.

Animals↗
PubMed1986

Treatment of severe lithium-induced polyuria with amiloride.

One of the major side effects of lithium is nephrogenic diabetes insipidus. The established treatment for the disorder is thiazide diuretics, which are associated with hypokalemia and reduced lithium excretion, predisposing the patient to lithium toxicity. Amiloride is a new diuretic that reduces lithium-induced polyuria in animals without affecting lithium or potassium levels. The authors found that 10-20 mg/day of amiloride given to eight patients who had become hypokalemic while being treated with hydrochlorothiazide for lithium-induced nephrogenic diabetes insipidus increased renal concentrating ability and reduced polyuria. They conclude that amiloride can be useful in treating lithium-induced nephrogenic diabetes insipidus and merits future randomized clinical trials.

Adult↗