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PubMed2004

Nocturia, nocturnal polyuria, and sleep quality in the elderly.

Nocturia is a common symptom in the elderly, which profoundly influences general health and quality of life. One consequence of nocturia is sleep deterioration, with increased daytime sleepiness and loss of energy and activity. Accidents, e.g., fall injuries, are increased both at night and in the daytime in elderly persons with nocturia. Nocturia is caused by nocturnal polyuria, a reduced bladder capacity, or a combination of the two. Nocturnal polyuria can be caused by numerous diseases, such as diabetes insipidus, diabetes mellitus, congestive heart failure, and sleep apnoea. In the nocturnal polyuria syndrome (NPS), the 24-h diuresis is normal or only slightly increased, while there is a shift in diuresis from daytime to night. NPS is caused by a disturbance of the vasopressin system, with a lack of nocturnal increase in plasma vasopressin or, in some cases, no detectable levels of the hormone at any time of the 24-h period. The calculated prevalence of NPS is about 3% in an elderly population, with no gender difference. In NPS, there are serious sleep disturbances, partly due to the need to get up for micturition, but there is also increased difficulty in falling asleep after nocturnal awakenings and increased sleepiness in the morning. The treatment of NPS may include avoidance of excessive fluid intake, use of diuretics medication in the afternoon rather than the morning, and desmopressin orally at bedtime.

Aged↗
PubMedDate not supplied

Nocturia, nocturnal polyuria and secondary nocturnal voiding.

Getting up once to the toilet at night is normal. Getting up more than once may be abnormal. Potential causes include: nocturia, which is bladder related; nocturnal polyuria, which is cardiac in origin; and being awake for a variety of reasons that are not linked to the bladder. Bladder problems, therefore, are not always the reason for frequency in micturition at night and treatment will only be effective if the correct cause and/or causes are identified. The most useful investigation to help with diagnosis is a frequency volume chart linked to an assessment identifying causes of secondary nocturnal voiding and nocturnal polyuria. Getting up to the toilet at night will not always be successfully treated by anticholinergics. Charting is the key to diagnosis, appropriate interventions and successful outcomes. This article will focus on working definitions, prevalence, causes, investigations and treatment options for nocturia, nocturnal polyuria and secondary nocturnal voiding.

Diagnosis, Differential↗
PubMed2001

[Polyuria, pollakiuria, and nocturia in children: diagnostic and therapeutic approach].

Polyuria is defined as the passage of large volumes of diluted urine secondary to an abnormality of urine concentration. This disorder can result either from deficient secretion of vasopressin (cranial diabetes insipidus), or from renal resistance to vasopressin (nephrogenic diabetes insipidus), primary polydipsia, osmotic diuresis, electrolytic disorders or drugs. Suspicion of impaired renal concentration ability can be confirmed by a fluid deprivation test. The administration of exogenous vasopressin allows to clarify the pathogenetic mechanism. Once the mechanism responsible for polyuria has been clarified it is mandatory to search for underlying causes. Treatment of polyuria should be causal, if its origin is known, and/or symptomatic in order to prevent severe dehydration. Symptomatic treatment of cranial diabetes insipidus consists of administering exogenous vasopressin. Salt restriction associated to a combined administration of hydrochlorothiazide/amiloride or hydrochlorothiazide/indomethacin can reduce urine output by 20 to 50% in case of nephrogenic diabetes insipidus. Pollakiuria is defined as a daytime urinary frequency. It can be isolated or may be a manifestation of lower urinary tract infections, bladder instability, nephrolithiasis or concentrated acidic urines. Detailed history and physical examination represent major clues to diagnostic. Therapy of pollakiuria can be causal or symptomatic using anticholinergic drugs or reeducation in case of bladder instability. Nocturia is characterized by voluntary nocturnal micturitions secondary to conditions inducing impaired renal concentration ability, or to heart failure.

Child↗
PubMed2001

[Postobstructive polyuria in unilateral hydronephrosis. A case with 58 l/day].

Increased urinary outputs are common after release of bilateral ureteral or subvesical obstruction. However, polyuria is rare following unilateral obstruction. We report a case of excessive postobstructive diuresis of more than 58,000 ml per day (204 l in 10 days) after release of a left ureteral obstruction in a 56-year-old female, being the highest amounts reported in the literature. Polyuria was derived from the obstructed as well as from the normal contralateral kidney. The involved pathomechanism is complex and not completely understood. Treatment includes careful monitoring of the patient and replacement of fluid and electrolytes. In our case complete recovery of kidney function was observed after several days.

Female↗
PubMed2006

Persistent post-transplant polyuria managed by bilateral native-kidney laparoscopic nephrectomy.

Polyuria is not considered an absolute indication for pre-transplant nephrectomy; however, it may complicate post-transplantation fluid management. Bilateral native-kidney laparoscopic nephrectomy was performed at our centre in two patients (four kidneys) 1 month after they had received a living related-donor renal transplant. The indication for nephrectomy was severe post-transplant polyuria secondary to the patient's underlying disease: juvenile nephronophthisis. Both patients had a persistent post-transplant daily urine output of 7-8 l/day and continued to have a variable serum creatinine level, dependent on intravenous hydration, more then 3 weeks after transplantation. Bilateral laparoscopic native-kidney nephrectomy in children has previously been reported. However, to the best of our knowledge, laparoscopic nephrectomy has not been described after kidney transplantation and certainly not in the immediate post-transplantation period. The procedure was well tolerated and did not affect renal graft function. In fact, following the procedure, serum creatinine levels stabilized, while daily fluid requirements decreased to 2.5-3.5 l/day in both patients. We concluded that bilateral native-kidney nephrectomy can be safely performed in paediatric renal transplant recipients in the immediate post-transplantation period. This new approach may allow preemptive transplantation and avoid the need for a transition period on dialysis in patients for whom pre-transplant nephrectomy is not absolutely indicated.

Child↗
PubMed2003

The effect of intranasal desmopressin on nocturnal waking in urination in multiple system atrophy patients with nocturnal polyuria.

Nocturnal waking in urination (nocturia) is a common feature in patients with multiple system atrophy (MSA). Degeneration of arginine vasopressin (AVP) neurons in the suprachiasmatic nucleus in this disorder may lead to nocturnal polyuria, which has been treated with intramuscular desmopressin. We also prescribed 5 microg of intranasal desmopressin once a night in 3 MSA patients, who had nocturnal polyuria with abnormal circadian rhythm of the plasma AVP. During the treatment, all patients showed an improvement in their nocturia without serious adverse effects.

Administration, Intranasal↗
PubMed1991

Atrial regulation of intravascular volume: observations on the tachycardia-polyuria syndrome.

The atria, strategically located at the junction of the venous and arterial circulation, contain a network of neural and humoral structures by which they sense and regulate intravascular volume. Atrial receptors, most commonly consisting of complex unencapsulated nerve endings discharging into myelinated vagal fibers, are located in the intrapericardial portions of the caval and pulmonary veins and the adjacent atrial walls. Receptor activation by atrial distension results in increased afferent vagal fiber discharge, which in turn leads to tachycardia (Bainbridge's reflex) and decreased renal sympathetic nerve activity, renal vasomotor tone, and antidiuretic hormone activity. In addition, atrial distension also releases ANF, a peptide with potent diuretic, natriuretic, and vasorelaxant actions. The combined effect of these neurohumoral changes is the production of a large hypotonic diuresis. In the clinical setting the volume-regulating role of the atria is demonstrated by the tachycardia-polyuria syndrome. Laboratory and clinical evidence points to the activation of atrial neurohumoral mechanisms in response to atrial distension as the mediators of the polyuria that often accompanies paroxysmal tachycardias. The involvement of these mechanisms in other forms of cardiac congestion and the capability to easily measure in the blood an index of atrial distension, namely ANF, provide the opportunity to elucidate the pathophysiology and hence to open new therapeutic avenues in many cardiac disorders.

Animals↗
PubMed1991

Different mechanisms of polyuria and natriuresis associated with paroxysmal supraventricular tachycardia.

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.

Adult↗
PubMedDate not supplied

A patient with monosomy 7 and polyuria.

Diabetes insipidus (DI) is a rare complication of leukaemia. An association between monosomy 7 and DI in leukaemias has been proposed. We present a case of Ph1-positive CML who developed polyuria at the time of lymphoid blast transformation associated with loss of chromosome 7. Biochemical results were not diagnostic of DI and a therapeutic trial of DDAVP was unsuccessful. Post-mortem showed a peripituitary and renal leukaemic infiltrate and although DI is a possibility, the cause of his polyuria remains unresolved.

Blast Crisis↗
PubMed1980

The role of urinary prostaglandin E and cyclic AMP in the polyuria of hypokalemia in rats.

The effect of potassium depletion on urinary prostaglandin E and cyclic AMP excretion was studied in female Sprague-Dawley and in Brattleboro rats. The animals were fed a potassium-free diet for 20 days which resulted in an average decrease in serum potassium of 25% in both strains. In the Sprague-Dawley rats, potassium depletion increased urine volume from 5.5 +/- 0.9 ml/day to 25.9 +/- 3.5 ml/day (p less than 0.001), decreased urinary osmolality from 1483 +/- 87 mosmol/kg H2O to 372 +/- 12 mosmol/kg H2O (p less than 0.001) and suppressed urinary cyclic AMP excretion from 56.95 +/- 3.81 nmoles/day to 0.83 +/- 0.40 nmoles/day (p less than 0.001). Potassium depletion in the Brattleboro rats did not affect these parameters. Excretion of prostaglandin E-like immunoreactivity in urine did not change in either strain with potassium depletion. The findings support the hypothesis that prostaglandins do not play a significant role in the polyuria caused by potassium deficiency in rats. Hypokalemia may cause polyuria by suppression of vasopressin-sensitive cyclic AMP generation, leading to a decrease in water permeability.

Animals↗
PubMed2005

Effectiveness of oral desmopressin therapy in posterior urethral valve patients with polyuria and detection of factors affecting the therapy.

OBJECTIVES: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Antidiuretic Agents↗
PubMed1978

Polydipsia, polyuria, and hypertension associated with renin-secreting Wilms tumor.

A 16-month-old black male infant had unusual thirst, polyuria, hyponatremia, and hypertension. His polyuria was unresponsive to vasopressin therapy, and his high blood pressure was not effectively controlled by antihypertensive drugs. Radiographic examinations revealed an occult Wilms tumor in the right kidney. After removal of the tumor, the signs and symptoms were relieved. The tumor had a renin activity about 280 times that of the adjacent renal cortex, and many intracytoplasmic secretory granules were found on electron microscopy. The pathogenesis of these clinical manifestations appears to be mediated through the physiologic pathways of renin-angiotensin II and renin-aldosterone.

Humans↗
PubMed2002

Urinary concentrating defect in rats given Shiga toxin: elevation in urinary AQP2 level associated with polyuria.

Shiga toxin (Stx) plays a central role in the etiology of hemolytic uremic syndrome (HUS) associated with Stx-producing Escherichia coli infection. The deposition of Stx2 in the renal collecting duct epithelial cells of rats administered Stx2 intravenously has been demonstrated by immunohistochemistry, and these rats were shown to develop substantial morphological changes in the kidney tubules, associated with polyuria. Severe polyuria was observed as an early event with no other obvious sequelae after Stx administration, in parallel with elevated urinary level of aquaporin 2 (AQP2) water channel protein that was determined by a sandwich EIA assay. Immunoblotting revealed that Stx treatment markedly induced an elevation in urinary AQP2 level and reduction in AQP2 protein in the renal plasma membranes. Elevated urinary AQP2 level was a more sensitive marker to assess Stx-induced renal tubular damage than urinary beta2-microglobulin or N-acetyl-beta-D-glucosaminidase in rats. Stx2 caused more severe renal tubular impairment than Stx1. Change in urinary AQP2 level by Stx1 and Stx2 at non-lethal doses of 40 ng/kg and 10 ng/kg, respectively, was reversed at 7 days in association with recovery of urinary concentrating ability, suggesting that there is a causative link.

Acetylglucosaminidase↗
PubMed2005

[Intravenous ketoprofen for severe lithium-induced polyuria].

INTRODUCTION: Although lithium has a narrow therapeutic range, it is widely used in psychiatry because of its antipsychotic and antidepressant properties. During long-term treatment, the onset of nephrogenic diabetes insipidus is common, but few cases of severe hypotonic polyuria, which would be an aggravating factor, have been reported. Appropriate treatment in such cases is an open question. CASE: We report a case of acute lithium poisoning in a 42-year-old man, due to chronic lithium treatment (plasma lithium=2.6 mmol/L). This patient, admitted to our intensive care unit, presented neurological disorders complicated by the early emergence of severe nephrogenic diabetes insipidus. After perfusion of hypotonic solution and intravenous treatment with ketoprofen (100 mg x 3/24 h), the polyuria improved rapidly. COMMENTS: The beneficial action of nonsteroidal antiinflammatory drugs lies in their capacity to inhibit prostaglandin synthesis. Lithium causes excess production of prostaglandins, which decrease the ability of kidneys to reabsorb free water. Some publications report indomethacin to be effective in this case. Because it is available only in oral or rectal forms, however, its effect may be delayed. Our case suggests that intravenous ketoprofen, with its rapid onset of action, is effective in the treatment of severe lithium-induced nephrogenic diabetes insipidus. Rehydration must be strictly monitored because of the risk of renal failure connected with nonsteroidal antiinflammatory drugs.

Adult↗
PubMed2006

[Polyuria].

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.

Humans↗
PubMed1999

A case of nocturnal polyuria in olivopontocerebellar atrophy.

We report a case of olivopontocerebellar atrophy without sleep apnea syndrome who presented nocturnal polyuria. It is considered that a disturbance in the circadian rhythm for arginine vasopressin secretion due to degeneration of suprachiasmatic nuclei and marked increase in the secretion of atrial natriuretic peptide due to abnormal diurnal variation in blood pressure may be involved in the mechanism of nocturnal polyuria.

Arginine Vasopressin↗
PubMed1999

Nocturia and polyuria in men referred with lower urinary tract symptoms, assessed using a 7-day frequency-volume chart.

OBJECTIVES: To investigate if a 7-day frequency-volume (FV) chart could identify nocturia on a polyuric basis in patients with lower urinary tract symptoms (LUTS) suggestive of benign prostatic hyperplasia (BPH). PATIENTS AND METHODS: The study included 23 patients (mean age 62.8 years, range 42-78) with LUTS who were referred for the evaluation of potential BPH and 11 men (control subjects, mean age 63.3 years, range 58-69); all completed a 7-day FV chart investigation as outpatients. RESULTS: Nocturia was associated with nocturnal polyuria in 10 of 23 patients with LUTS; these 10 patients had a diminished diurnal variation of urine production, whereas 13 patients had a diurnal variation in urine production comparable with that in controls with no nocturia. The degree of nocturia correlated positively with nocturnal urine production but showed no relationship with sleep duration. The nocturnal polyuria in these patients was associated with a higher 24-h urine production and seemed at least partly to be caused by a higher fluid intake during daytime. CONCLUSION: Nocturia on a polyuric basis can be detected by using a FV chart. In these patients, a 3-day FV chart would be sufficient to detect nocturia on a polyuric basis and seems therefore to be a valuable tool in evaluating patients with LUTS referred for potential BPH.

Adult↗
PubMed2000

Expression of renal aquaporins 1, 2, and 3 in a rat model of cisplatin-induced polyuria.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Animals↗