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PubMed1976

Polyuria associated with an antibody to vasopressin.

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.

Adult↗
PubMed1998

A novel therapy for nocturnal polyuria: a double-blind randomized trial of frusemide against placebo.

OBJECTIVE: To report a randomized, double-blind, placebo-controlled trial of an afternoon dose of the diuretic frusemide, used to establish an early evening diuresis and so diminish nocturnal voiding frequency and voided volume in elderly men presenting with lower urinary tract symptoms (LUTS). PATIENTS AND METHODS: After a 2-week placebo run-in period, 49 men aged > 50 years were randomized to receive 40 mg of frusemide or placebo, taken 6 h before their usual bedtime. Day and night-time frequency and voided volume during the run-in and treatment periods were compared between the placebo and frusemide groups. RESULTS: In the 43 men completing the study, there was a significant reduction in night-time frequency (-0.5 and 0) and percentage night-time voided volume (-18% and 0%) in those taking frusemide compared with placebo. Of patients on active treatment, seven of 19 had a reduction in night-time frequency of > or = 1, compared with only one of 20 on placebo, and 14 of 21 felt that frusemide had helped their nocturia, compared with only five of 22 on placebo. CONCLUSION: Men with LUTS whose most prominent symptom is nocturia should complete a frequency-volume chart. In those with nocturnal polyuria, 40 mg of frusemide resulted in a significant reduction in night-time frequency and percentage voided volume.

Aged↗
PubMed1998

Desmopressin for the treatment of nocturnal polyuria in the elderly: a dose titration study.

OBJECTIVE: To evaluate the decrease in nocturnal polyuria and the tolerability of three different doses of oral desmopressin in elderly subjects. SUBJECTS AND METHODS: Subjects were included in the study if they; (i) were healthy and free from medication with possible influence on their diuresis or voiding pattern: (ii) had an increased nocturnal frequency (> or = 2 nocturnal voids, as reported in the pre-screening period); and (iii) had a nocturnal urinary output of > or = 0.9 mL/min. Seventeen men and six women (mean age 68.1, SD 4.7 years) met these criteria and were treated with 0.1, 0.2 and 0.4 mg oral desmopressin given at bedtime, each dose taken for one week on three consecutive weeks. RESULTS: The mean (SD) nocturnal diuresis before treatment was 1.6 (0.7) mL/min, which decreased significantly to 1.1 (0.4) mL/min when 0.1 mg desmopressin was given. A dose of 0.2 mg desmopressin resulted in a further small decrease in the nocturnal diuresis to 0.9 (0.4) mL/min, whereas the 0.4 mg dose produced no additional effect. The reduction in nocturnal diuresis occurred almost exclusively in the group with a nocturnal urinary output of > or =1.3 mL/min. After treatment, diuresis returned to pretreatment levels. There was no change in body weight or in ankle circumference during desmopressin treatment and no serious adverse effects were observed. CONCLUSION: Desmopressin reduces nocturnal diuresis in polyuric elderly subjects and this reduction, occurring with doses of 0.1 mg given at bedtime, does not increase in a dose-dependent way.

Administration, Oral↗
PubMed1999

Oral desmopressin for nocturnal polyuria in elderly subjects: a double-blind, placebo-controlled randomized exploratory study.

OBJECTIVE: To evaluate the decrease in nocturnal diuresis, nocturnal polyuria and the safety of oral desmopressin in elderly subjects with nocturia. SUBJECTS AND METHODS: After being identified using a population-based questionnaire, subjects were included in the study if they; (i) were healthy and free from medication with possible influence on the diuresis or voiding pattern; (ii) had an increased nocturnal frequency (>/=2 nocturnal voids/night, as reported before screening); (iii) had a nocturnal urinary output of >/=0.9 mL/min; (iv) completed and responded to an initial dose-titration study. Twelve men and five women (mean age 67.7 years, sd 4.6 years) met these criteria and were treated with oral desmopressin or placebo at bedtime for 2 weeks on each medication in a randomized, double-blind, crossover design. RESULTS: Subjects treated with desmopressin had a significantly reduced nocturnal diuresis of 0.59 mL/min compared with those on placebo (95% confidence interval, CI, 0.33-0.85). The 24-h diuresis was unaffected by desmopressin treatment. Patients treated with desmopressin had fewer micturitions at night than had those on placebo (1.1 and 1.7, respectively; P<0.001; mean difference=0.59; 95% CI, 0.32-0.85). The reduction in nocturnal diuresis was dependent on the baseline level of night-time diuresis (r=0.886; r2=0.785; P<0.0001) and the nocturnal part of the baseline 24 h-diuresis (r=0.708; r2=0.502; P<0.001). After desmopressin treatment was withdrawn, diuresis returned to the levels before treatment. The time from falling asleep to first awakening was improved by 1.4 h in patients treated with desmopressin. There was no change in body weight or ankle circumference during desmopressin treatment. Overall, the treatment was well tolerated and no serious adverse events were observed. CONCLUSION: Desmopressin was effective in reducing nocturnal diuresis and nocturnal voids in polyuric elderly subjects, with no significant adverse events or inconvenience to the patient. The length of uninterrupted sleep was also improved.

Administration, Oral↗
PubMed1978

Effect of carbamazepine in polyuria associated with lithium therapy.

Ten patients, suffering from affective disorders, were treated with carbamazepine for polyuria and polydipsia associated with long-term lithium therapy. Oral carbamazepine (300--600 mg daily for six weeks) was observed to have no beneficial effect in alleviating these symptoms when compared with placebo tablets in a double blind crossover study. Plasma and urinary osmolality were observed to be within normal range in these patients and there was no antidiuretic response following subcutaneous Pitressin injection. There was 50% drop-out due to severe side-effects like ataxia, dizziness, restlessness and confusional states. It appears that lithium exacerbates carbamazepine induced CNS side-effects or vice versa, the mechanism of which is not very clear. It may be due to their mutual effect on sodium metabolism or on nervous conduction velocity. Hence, simultaneous administration of these two drugs should preferably be avoided.

Adult↗
PubMed2001

Hyponatremia and polyuria in children with central diabetes insipidus: challenges in diagnosis and management.

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.

Adolescent↗
PubMed2000

Night-time polyuria and urine hypo-osmolality in enuretics identified by nocturnal sequential urine sampling--do they represent a subset of relative ADH-deficient subjects?

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.

Child↗
PubMed1989

Persistent polyuria in two dogs following adrenocorticolysis for pituitary-dependent hyperadrenocorticism.

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.

Adrenal Cortex Hormones↗
PubMed1996

Evidence for circulating vasopressin-like peptides in a case of polyuria.

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.

Female↗
PubMed1982

Massive perioperative polyuria.

A 25-year-old man with a spinal cord transection secondary to a gunshot wound underwent surgical repair of a perforated prepyloric ulcer on the eighth hospital day. He received 68 liters and excreted 43 liters of intravenous fluid during the perioperative period. Causes of this massive polyuria during and after the second operation are unknown, although iatrogenically induced glycosuria and natriuresis may have contributed to its severity. The problems and their management are discussed.

Adult↗
PubMed1996

Ketorolac appears to decrease polyuria during intracranial surgery.

Two cases are described of patients, undergoing surgery for intracranial pathology, who developed polyuria intraoperatively. The urine output decreased to within normal range shortly after the administration of ketorolac, a nonsteroidal antiinflammatory drug. The possible mechanisms producing the increased urinary output and the influence of prostaglandins on renal function are discussed.

Adult↗
PubMed2004

Selective decrease in urinary aquaporin 2 and increase in prostaglandin E2 excretion is associated with postobstructive polyuria in human congenital hydronephrosis.

This study was undertaken to determine the role of aquaporin 2 (AQP2) in the impaired urinary concentrating capacity observed in patients who underwent pyeloplasty because of congenital unilateral hydronephrosis as a result of pyeloureteral junction disease. Twelve children (mean age, 8 +/- 2 mo) were examined in the study. From day 1 to day 5 after surgery, the urine was collected separately from pyelostomy draining only from the postobstructed kidney and from the bladder catheter draining mostly from the contralateral kidney used as internal control. After pyeloplasty, the postobstructed kidney was characterized by a reduced urinary excretion of AQP2 (approximately 54%) associated with polyuria that persisted from day 1 to day 5 (433 +/- 58 versus 310 +/- 74 ml/24 h at day 1; 326 +/- 44 versus 227 +/- 26 ml/24 h at day 5). In parallel, urine osmolality from the postobstructed kidney was significantly reduced compared with the contralateral kidney (111 +/- 12 versus 206 +/- 49 at day 1; 136 +/- 24 versus 235 +/- 65 mOsm/kg at day 5). Creatinine clearance from the postobstructed kidney was not significantly different compared with the contralateral kidney throughout the 4 d after surgery. However, on day 5, creatinine clearance from the postobstructed kidney became significantly lower. Prostaglandin E2 in the urine from postobstructed kidneys was found to be twofold higher than in the contralateral samples (26.0 +/- 6.7 versus 13.5 +/- 2.5 at day 5). It is concluded that (1) the selective downregulation of AQP2 in postobstructed kidney may account for the higher excretion of hypotonic urine, and (2) the local increase in prostaglandin E2 synthesis in postobstructed kidney may be involved in AQP2 downregulation and in maintaining a GFR similar to that of the contralateral kidney.

Adolescent↗
PubMed2003

Arginine vasopressin and nocturnal polyuria in older adults with frequent nighttime voiding.

PURPOSE: 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. MATERIALS AND METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.

Aged↗
PubMed2004

Cyclooxygenase-2 inhibitor preserves medullary aquaporin-2 expression and prevents polyuria after ureteral obstruction.

PURPOSE: Renal obstruction causes impairment of urinary concentrating ability, partly by decreasing aquaporin-2 (AQP-2) water channel level in the collecting ducts. We reported previously that ureteral obstruction induced cyclooxygenase-2 (COX-2) in the medullary collecting duct cells by increased mechanical stretch. In this study we investigated whether AQP-2 decrease after obstruction was regulated by COX-2. MATERIALS AND METHODS: Sprague-Dawley rats were subjected to bilateral ureteral obstruction for 24 to 48 hours. During obstruction rats were given NS398, a COX-2 specific inhibitor, by oral gavage (2 mg/kg per day). COX-2 and AQP-2 levels were assessed in the inner medulla using Western blot. Urine output was measured after releasing obstruction to assess the degree of polyuria. RESULTS: With obstruction COX-2 protein levels increased and AQP-2 levels decreased in the inner medulla. Corresponding to the loss of AQP-2, urine output increased 4.2-fold after obstruction. The obstructed rats receiving NS398 exhibited significant preservation of AQP-2 level (72% of control), as well as significant normalization of urine output. The sham operated rats receiving NS398 exhibited an increased amount of AQP-2 protein level. CONCLUSIONS: These findings suggest that COX-2 mediated prostaglandin has an important role in the down-regulation of AQP-2 water channel level in the medullary collecting duct cells after ureteral obstruction.

Animals↗
PubMed1995

Development of polyuria in Tsukuba hypertensive mice carrying human renin and angiotensinogen genes.

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.

Aldosterone↗
PubMed1995

Persistent polyuria after posterior urethral valves.

OBJECTIVE: To assess urinary concentrating ability, urine production and glomerular filtration rates in a cohort of boys with previously treated posterior urethral valves. PATIENTS AND METHODS: Urinary concentrating capacity was assessed in 51 boys aged 5.4-9.9 years with previously treated posterior urethral valves. They all completed urinary frequency/volume charts, permitting calculation of 24 h urine volumes. The osmolality of an overnight urine collection was measured and, if < 800 mOsm/kg (n = 40), an intramuscular injection of desamino-cys-1-8-D-arginine vasopressin was given to determine the maximum concentrating ability. The glomerular filtration rate (GFR) was estimated from the plasma clearance of 51Cr-ethylenediamine tetra-acetic acid following a single intravenous injection. RESULTS: The mean 24 h urine volume was 1025 +/- 448 (SD) mL. The mean overnight urine flow rate was 28.4 +/- 17.9 mL/h. Urinary concentrating capacity was impaired (< 800 mOsm/kg) in 30 (59%) of the boys and < 300 mOsm/kg in eight (16%). The mean GFR was 81 +/- 38 mL/min/1.73 m2SA. Significant correlations were noted between the GFR, the maximum urine concentration and the 24 h urine volume. CONCLUSION: Persistent polyuria after valve ablation occurs in boys with posterior urethral valves. This has implications both in terms of urinary continence and on-going renal impairment.

Catheter Ablation↗
PubMed1990

Effects of experimental potassium depletion on renal function and urinary prostanoid excretion in normal women during hypotonic polyuria.

During hypotonic polyuria renal function studies by the clearance (cl.) method, and urinary PGE2, 6-keto-PGF1 alpha and TxB2 determinations were performed on 14 healthy women in normal potassium balance (N) and 14 healthy women in sustained potassium depletion (KD) induced by low dietary potassium intake (less than or equal to 10 mmol day-1) and natriuretic treatment. By using different depletive patterns, two groups with estimated cumulative potassium deficits of 160 +/- 43 mmol (KD1, n = 8) and 198 +/- 22 mmol (KD2, n = 6), respectively, were obtained. (1) In both the KD1 and KD2 groups as compared to normal potassium balance (N), plasma potassium concentration and urinary potassium excretion were significantly lower; plasma renin activity was significantly higher. (2) Only in KD2 did significant changes appear in renal function and urinary prostanoid excretions. Besides a decrease in creatinine cl. and the urinary flow rate, an increase in fractional chloride excretion and a reduction in distal fractional chloride reabsorption were manifest. The plasma chloride concentration was reduced too. Urinary prostanoid excretions were significantly (6-keto-PGF1 alpha, TxB2) or tendentially (PGE2) lower. (3) Indomethacin treatment resulted in changes in mean arterial pressure (increase) and creatinine cl. (decrease) which were not significantly different in normal potassium balance and KD groups. Only in KD2 did the drug significantly reduce the fractional salt and water excretions and the fractional sodium and chloride deliveries to the diluting segments. However, indomethacin was unable to correct the inhibition of distal fractional chloride reabsorption. Therefore, the potassium depletion attained in the KD2 group was efficacious in depressing renal prostanoid synthesis. This fact, in the presence of high levels of angiotensin II, induced a reduction of the glomerular filtration rate thus contributing to renal ability to retain chloride and potassium.

Adult↗
PubMed1988

Differential diagnosis of polyuria.

Diabetes insipidus (DI) is a syndrome characterized by chronic polyuria and polydipsia. It can result from any of three basic defects: (a) inadequate urinary concentration caused by a deficiency in the secretion or action of the antidiuretic hormone vasopressin (neurogenic or nephrogenic DI), or excessive intake of water caused by a defect in (b) thirst or (c) psychological function (dipsogenic or psychogenic DI). These four types of DI can be differentiated clinically only if they present in a complete and classical form. However, more sophisticated diagnostic approaches involving assays of plasma vasopressin or closely monitored trials of antidiuretic therapy usually are necessary when the patient has mild or incomplete defects in thirst or vasopressin function. Accurate diagnostic differentiation among the four basic types of DI is essential not only for safe and effective management but also for a proper understanding of the basic physiology and pathophysiology of water homeostasis.

Arginine Vasopressin↗