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PubMed2004

Down-regulation of Na+ transporters and AQP2 is responsible for acyclovir-induced polyuria and hypophosphatemia.

BACKGROUND: Acyclovir (ACY) is a useful therapeutic agent for the systemic treatment of herpes virus infection. An increase in urinary phosphate excretion and polyuria has been described. The objective of this study was to analyze the exact mechanism of the urinary-concentrating dysfunction and the increase in phosphaturia associated with ACY. METHODS: We first analyzed 7 (adult and pediatric) non-AIDS cases of encephalitis receiving 15 mg/kg bw/d of intravenous ACY. Fractional phosphate and sodium excretion, urinary potassium volume, and plasma phosphate concentrations were analyzed. Additional studies in rats treated with intraperitoneal ACY (100 mg/kg bw) were also conducted. Animals were maintained in metabolic cages and 24-hour urine samples were collected to measure volume, osmolality, and sodium/potassium/phosphate excretion. Treated rats were also evaluated after 24 hours and 48 hours of water deprivation. Northern hybridization and semiquantitative immunoblotting were performed to evaluate (in both control and treated animals) expression of the cotransporters Na-Pi type IIa (Na-Pi-IIa) and Na-K-2Cl (NKCC2). Semiquantitative immunoblotting was carried out in the kidneys of ACY rats and control rats in order to analyze aquaporin 2 (AQP2) protein expression. RESULTS: Patients started on ACY developed polyuria and hyperphosphatemia after 48 hours. In rats, ACY-induced hyperphosphaturia and hypophosphatemia were accompanied by increased excretion of sodium, potassium, and magnesium, increased urine output, lower urinary osmolality, and a partial urinary concentrating defect. Concurrent downregulation of Na-Pi-IIa and NKCC2 expression was observed. There was also a decrease in medullar expression of the AQP2 collecting duct water channel. CONCLUSION: Downregulation of Na-Pi-IIa appears to play a crucial role in the downregulation of ACY-induced hyperphosphaturia. The accompanying polyuria and urinary-concentrating defect can in part be explained by the downregulation of NKCC2 and AQP2.

Acyclovir↗
PubMed2000

Nocturnal polyuria in older people: pathophysiology and clinical implications.

OBJECTIVES: To review the physiological changes of aging which affect the systems involved in urine formation and to consider how these changes interact with changes in bladder function, thereby leading to the onset of nocturnal polyuria with associated urinary frequency, nocturia, and incontinence. Based on this information, data are presented on the effectiveness of pharmacological interventions which reduce the rate of urine formation and, thus, can be of benefit in reducing symptoms, especially during the nighttime. METHODS: Peer-reviewed journal articles were identified by MEDLINE Search and by review of the literature. CONCLUSIONS: As a consequence of age-associated diminished renal concentrating capacity, diminished sodium conserving ability, loss of the circadian rhythm of antidiuretic hormone secretion, decreased secretion of renin-angiotensin-aldosterone, and increased secretion of atrial natriuretic hormone, there is an age-related alteration in the circadian rhythm of water excretion leading to increased nighttime urine production in older people. The interaction of nocturnal polyuria with age-related diminution in functional bladder volume and detrusor instability results in the symptoms of urinary frequency, nocturia and, in some persons, incontinence. The additional impact of Alzheimer's disease on these physiological and aging changes, as well as on a diminished perception of bladder fullness, leads to an even greater risk of urinary incontinence in these patients. Treatment of nocturnal polyuria with the antidiuretic hormone analog, DDAVP (desmopressin), can result in decreased nocturnal urine production with improvement in symptoms of frequency, nocturia, and incontinence.

Age Factors↗
PubMed1984

Mechanism of polyuria and natriuresis in atrioventricular nodal tachycardia.

A woman with tachycardia associated with polyuria was investigated. Electrophysiological analysis showed that the tachycardia was an atrioventricular nodal re-entrant tachycardia. Programmed stimulation was then used to provoke and sustain the tachycardia for 40 minutes. Polyuria, with an appreciable increase in free water clearance, was observed. This was associated with reduction in plasma and urinary arginine vasopressin concentrations. Appreciable natriuresis also developed. These results support the hypothesis that the polyuria with increased free water clearance and the natriuresis occurring during sustained tachycardia in man are due to inhibition of secretion of vasopressin and the release of natriuretic factor.

Arginine Vasopressin↗
PubMed1993

Mechanism of polyuria after cisplatin therapy.

Cisplatin is an antineoplastic agent. Several nephrotoxic effects are associated with its use including chronic and acute renal failure, renal magnesium wasting, and polyuria. We have investigated polyuria in groups of rats treated with cisplatin at doses of 2.5 and 5 mg/kg body weight given once weekly for 3 weeks to determine possible mechanisms of this impairment. After cisplatin administration, glomerular filtration rate was reduced and significant increases in sodium and water loss were also seen. These changes were associated with decreases in urinary cAMP. Inner medullary collecting duct (IMCD) cells were removed from these animals and were stimulated with graded doses of vasopressin. Cells from cisplatin-treated rats showed an impaired response in cAMP generation to vasopressin stimulation as compared to cells from normal animals. To determine more precisely the site of impairment, the adenylate cyclase complex of the IMCD cells was further studied with forskolin and NaF. Forskolin was used to probe the catalytic unit activating adenylate cyclase, and NaF the guanine nucleotide regulatory protein (G protein). In response to forskolin, cells from cisplatin-treated rats and normal rats responded similarly in generating cAMP. However, following NaF, the cAMP response was blunted in the cells from the cisplatin rats. These results suggested that the catalytic unit was not injured by cisplatin (forskolin study) but the G protein was (NaF). In conclusion, the present study suggests that the polyuria seen following cisplatin administration is associated with an end-organ resistance to vasopressin manifested by reduced cAMP generation, secondary in part or whole to a defect at the level of the G protein.

Animals↗
PubMed1996

A case of renovascular hypertension with marked polyuria after percutaneous transluminal renal angioplasty.

A 43-year-old female patient with hypertension was diagnosed as having one-kidney renovascular hypertension with dysfunction of the contralateral kidney, and percutaneous transluminal renal angioplasty was carried out. Marked polyuria was observed during the 2- to 72-hour postoperative period. During the 12- to 18-hour period of polyuria, the urine volume was 8.9 liters/6 h, which was 62% of the glomerular filtration, and was accompanied by high fractional excretion of sodium and of potassium and a high urine beta 2-microglobulin level. The mechanism of polyuria in this case is discussed.

Adult↗
PubMed1977

On the mechanism of polyuria in potassium depletion. The role of polydipsia.

The association of potassium (K) depletion with polyuria and a concentrating defect is established, but the extent to which these defects could be secondary to an effect of low K on water intake has not been systematically investigated. To determine whether hypokalemia has a primary effect to increase thirst and whether any resultant polyuria and polydipsia contribute to the concentrating defect, we studied three groups of rats kept in metabolic cages for 15 days. The groups were set up as follows: group 1, normal diets and ad lib. fluids (n = 12); group 2, K-deficient diet on ad lib. fluids (n = 12); and group 3, K-deficient diet and fluid intake matched to group 1 (n = 14). Daily urine flow and urinary osmolality of groups 1 and 3 were not significantly different throughout the study. In contrast, as of day 6, group 2 rats consistently had a higher fluid intake (P < 0.0025), higher urine flow (P < 0.001), and lower urinary osmolality (P < 0.001) than the other two groups. These alterations in fluid intake and urine flow preceded a defect in maximal concentrating ability. On day 7, maximal urinary osmolality was 2,599+/-138 msmol/kg in rats on K-deficient intake and 2,567+/-142 msmol/kg in controls. To determine whether this primary polydipsia is itself responsible for the development of the concentrating defect, the three groups of rats were dehydrated on day 15. Despite different levels of fluid intake, maximal urinary osmolality was impaired equally in groups 2 and 3 (1,703 and 1,511 msmol/kg, respectively), as compared to rats in group 1 (2,414 msmol/kg), P < 0.001. We therefore conclude that K depletion stimulates thirst, and the resultant increase in water intake is largely responsible for the observed polyuria. After 15 days of a K-deficient diet, the impaired maximal urinary concentration in hypokalemia, however, was not related to increased water intake, since fluid restriction did not abolish the renal concentrating defect.

Animals↗
PubMed1991

Polyuria in childhood.

Polyuria may result from either a water or a solute diuresis. Although the history and physical examination may provide clues to the cause of the polyuria, the definitive diagnosis requires laboratory tests which focus on the osmolality of the urine and serum in combination with the urine volume and the rate of excretion of osmoles. An isoosmolar or hyperosmolar urine is found in children with a solute diuresis or in normal children, whereas a hypoosmolar urine is found in children with a water diuresis. In the latter case, a low serum osmolality suggests primary polydipsia whereas a high serum osmolality suggests antidiuretic hormone (ADH) deficiency or insensitivity. A water deprivation test is necessary when the initial evaluation fails to establish the cause of polyuria. A vasopressin test enables the differentiation between neurogenic and nephrogenic diabetes insipidus (DI).

Child↗
PubMedDate not supplied

Vasopressin response to osmotic stimulation in 18 young dogs with polyuria and polydipsia.

Common disorders of water homeostasis leading to polyuria include a variety of endocrine, metabolic, and renal disturbances. After exclusion of most of these conditions, the diagnostic dilemma of differentiating between central diabetes insipidus, primary polydipsia, and nephrogenic diabetes insipidus may remain. Here, we report on 18 young dogs with polyuria that had been present in most cases since the dogs were puppies. The conditions were categorized according to the plasma vasopressin (VP) response to hypertonicity. The VP response to osmotic stimulation was tested by IV infusion of 20% NaCl for 2 hours. The VP response in all dogs was abnormal. Three categories could be distinguished: an exaggerated response (n = 3), a subnormal response (n = 4), and a nonlinear response with high plasma VP concentrations unrelated to increases in plasma osmolality (n = 11). The VP response to hypertonicity did not consistently distinguish among different clinical entities. In the 9 dogs with variations in urine osmolality compatible with primary polydipsia, exaggerated, subnormal, and nonlinear responses were observed. Examination of the present data questions the generally accepted notion that VP measurements during hypertonic saline infusion are the "gold standard" for the diagnostic interpretation of causes of polydipsia and polyuria. Studies of the peripheral reflection in plasma of the pulsatile VP release in healthy and polyuric individuals, with and without osmotic provocation, should be performed.

Animals↗
PubMed2005

Nocturnal polyuria with abnormal circadian rhythm of plasma arginine vasopressin in post-stroke patients.

OBJECTIVE: Nocturia is a common reason for interrupted sleep in post-stroke patients. These patients often have neurogenic bladder overactivity. However, little is known about the possible contribution of nocturnal polyuria in the patients. METHODS: We measured the number of nocturia, the circadian plasma arginine vasopressin (AVP) level and urinary excretion in 4 patients with stroke. RESULTS: All patients had nocturnal urinary frequency (three times in one and twice in 3). All patients were revealed to have nocturnal polyuria, and the ratio of nocturnal urinary output to 24 hour volume ranged from 36% to 63%. Measurement of daily plasma AVP variation showed that all patients lost normal nocturnal rise of the plasma AVP concentration. Two patients were successfully treated with 5 mug of intranasal desmopressin once a night, a potent analogue of AVP, without hypertension particularly in the night, signs of congestive cardiac failure or any electrolyte abnormality such as hyponatremia. CONCLUSION: Our post-stroke patients had nocturnal polyuria with abnormal circadian rhythm of plasma AVP secretion. Desmopressin reduced nocturnal waking in urination. It also ameliorated nocturnal dehydration that might trigger a stroke recurrence in the patients.

Administration, Intranasal↗
PubMed1980

DDAVP (1-desamino-8-D-arginine-vasopressin) treatment of lithium-induced polyuria in the rat.

The antidiuretic responses of arginine vasopressin (AVP) and 1-desamino-8-D-arginine vasopressin (DDAVP) were studied in rats with marked lithium-polyuria (about 100 ml/100 g/24 h) induced by administration of lithium to the diet for 3-4 months. The hormones were infused i.v. and s.c. at a constant rate for 7 days using implantable osmotic minipumps. Body weight, food consumption and urine volume and osmolality were recorded daily. Whereas supramaximal doses of AVP only had little effect on spontaneous urine flow and osmolality, DDAVP (0.1 microgram/h i.v. or 1 microgram/H s.c.) restored urine volume and osmolality to near-normal values. Although the mechanism of the antidiuresis evoked by DDAVP was not investigated the ability of this compound to reverse AVP-resistant polyuria may be due to its specificity and high intrinsic activity in stimulating the vasopressin receptor. The reversibility of lithium-induced impairment of renal concentrating ability caused by excessive hormonal stimulation is not immediately compatible with the recent hypothesis that lithium-polyuria may reflect irreversible structural kidney damage.

Animals↗
PubMed2003

[Usefulness of nocturnal urethral indwelling catheter for treating bladder dysfunction with nocturnal polyuria: case report of 3 women].

Clean intermittent catheterization is a well-known procedure of urinary drainage for patients who are unable to empty the bladder sufficiently. However, some patients with bladder dysfunction and nocturnal polyuria fail to obtain the benefits of intermittent catheterization and have annoying symptoms of nocturnal incontinence and low-compliance bladder, which threaten both their quality of life and renal function. We report the usefulness of nocturnal urethral indwelling catheterization using a specially designed catheter to treat patients (three women) with lower urinary tract dysfunction and nocturnal polyuria. Case 1: A 45-year-old woman with mental retardation suffered from difficulty of micturition and residual urine. A nocturnal urethral indwelling catheter freed her from difficulty with micturition and residual urine. Case 2: A 28-year-old woman with spina bifida and neuropathic bladder dysfunction suffered from urinary incontinence and recurrent pyelonephritis. The recurrent pyelonephritis was prevented and bladder compliance was improved with use of the nocturnal urethral indwelling catheter. Case 3: A 66-year-old woman with cervical myelopathy and multiple episodes of cerebral infarction suffered from nocturnal urinary incontinence. She underwent clean intermittent catheterization by her husband. Use of the nocturnal urethral indwelling catheter solved the problem of her nocturnal incontinence and relieved her husband of her nocturnal care. Nocturnal urethral indwelling catheterization is useful for treatment of nocturnal incontinence and recovery of bladder compliance in patients with lower urinary tract dysfunction and nocturnal polyuria.

Adult↗
PubMed2004

[The role of vasopressin in dogs with polyuria].

Polyuria and polydipsia (PUPD) occur frequently in dogs and may be caused by a variety of endocrine, metabolic, and renal disturbances. The studies described in this PhD Thesis, which was defended in January 2004 in Utrecht, investigated the role of the antidiuretic hormone vasopressin (VP) in the pathogenesis of different forms of canine polyuria. Experiments in healthy dogs demonstrated that the ranges of urine specific gravity and urine osmolality are much larger than previously thought. A water deprivation test is not required in all polyuric dogs, because serial measurements of urine osmolality may already lead to the diagnosis of primary polydipsia, in some cases. In dogs with primary polydipsia a wide variation in VP responses to hypertonic stimulation can be found, including a hyperresponse, a hyporesponse, and a non-linear response. The significance of the VP response to hypertonic saline infusion as the 'gold standard' for a diagnosis of canine polyuria is discussed. In the dog, VP is secreted in a pulsatile fashion with a wide variation in the number of VP pulses, VP pulse duration, and VP pulse amplitude and height. The occurrence of spontaneous VP pulses may severely hamper the interpretation of the curve describing the relationship between plasma osmolality and plasma VP concentration during osmotic stimulation. A radioimmunoassay to measure the VP-dependent water channel aquaporin-2 (AQP2) in urine was developed in dogs. In healthy dogs, urinary AQP2 excretion closely reflects changes in collecting duct exposure to VP. Measurement of urinary AQP2 excretion in polyuric dogs may be helpful to distinguish between central diabetes insipidus, nephrogenic diabetes insipidus, and primary polydipsia.

Animals↗
PubMed2006

[Polyuria and polydipsia due to renal diabetes insipidus during the use of lithium].

Polyuria, thirst and polydipsia due to renal diabetes insipidus (RDI) are common side effects of long-term lithium treatment. In a man aged 56 years, the polyuria could be reduced considerably by diuretics. However, as shown in the case of a 49-year-old man, such treatment carries the risk of acute lithium intoxication due to volume depletion and reduced renal lithium clearance. A reduction in the dose of lithium prior to diuretic treatment is therefore mandatory. Although polyuria and polydipsia are generally mainly a nuisance, the condition may become life-threatening when free access to fluids is impossible. This is demonstrated by the case of a 46-year-old man who was on chronic lithium treatment with probable RDI and who developed fatal severe dehydration and hypernatraemia after traumatic brain injury. Awareness of the possibility of RDI in patients on chronic lithium treatment is therefore important.

Diabetes Insipidus, Nephrogenic↗
PubMed1991

[Transient polyuria in pregnancy in diabetes insipidus and gestational diabetes].

Two pregnant women developed overt polyuria (up to 11 l/day) and polydipsia during their second and third trimesters of pregnancy. In one patient hydronephrosis was present. Both patients suffered from mild gestational diabetes mellitus. Plasma sodium was 145 and 162 mmol/l. Polyuria and urinary hypo-osmolality responded well to desmopressin acetate. After delivery, polyuria and polydipsia disappeared in one patient and significantly improved in the other. Infusion of hypertonic saline one and two weeks respectively after delivery led to plasma hyper-osmolality (294 mosmol/kg and 305 mosmol/kg) without detectable stimulation of arginine vasopressin (AVP). Anterior pituitary function was normal. No stimulation of AVP occurred following insulin-induced hypoglycemia. AVP plasma disappearance after i.v. pulse injection of 1 microgram AVP as well as AVP plasma concentration after continuous infusion of 10 ng AVP/min was studied two weeks after delivery in one patient. The results suggested markedly elevated degradation of AVP compared to control subjects, probably due to an increased vasopressin activity. Eight months after delivery, hypertonic saline infusion in one patient led to a plasma-osmolality of 312 mosmol/kg without stimulation of AVP. In the second patient, AVP was not detectable (less than 0.2 pg/ml) six months after delivery when plasma osmolality was 290 mosmol/kg. Our studies demonstrate that a subclinical compensated diabetes insipidus was preexistent in both patients. Exacerbation occurred due to an increased AVP-clearance and presumably due to the hemodynamic and hormonal alterations during pregnancy, including a mild gestational diabetes mellitus.

Adult↗
PubMed1990

Polyuria and polydipsia. Problems associated with patient evaluation.

Primary disorders of water balance (central diabetes insipidus, congenital nephrogenic diabetes insipidus, and psychogenic polydipsia) should always be considered in the differential diagnosis of polyuria and polydipsia. In general, animals with these disorders have only one laboratory abnormality, a low urine specific gravity. The more common causes of polyuria and polydipsia (eg, hypercalcemia, chronic renal insufficiency, pyelonephritis, hyperadrenocorticism), in most instances, have specific and obvious abnormalities associated with the complete blood count (CBC), serum chemistry profile, and urinalysis. However, in some cases, a low urine specific gravity may initially be the only abnormality in these more common ruleouts. The workup for polyuria and polydipsia, especially in those cases with normal or near normal blood work, can be tedious, time consuming, confusing, and not without significant patient morbidity. This chapter will focus on the problems associated with diagnostic testing used to evaluate animals with disorders of water balance.

Animals↗
PubMed1989

[Polyuria and polydipsia in acute fatty liver of pregnancy. Discussion based on a case].

We report the case of a 25-year-old nullipara in whom polyuria and polydipsia occurred 8 weeks before the first symptoms of acute fatty liver of pregnancy and disappeared a few days after delivery. This time course suggests that polyuria and polydipsia were closely related to acute fatty liver of pregnancy. Thus, this diagnosis should be envisaged in any woman with normal blood levels of glucose and calcium, and complaining of polyuria and polydipsia in the third trimester of pregnancy.

Adult↗
PubMed1984

[Relation between acute changes in diuresis and renal prostaglandins. I: Induced hypotonic polyuria].

We have evaluated the effects of indomethacin (I) and of a rich in linoleic acid phosphatidylcholine (E) on the renal function and on the PGE urinary excretion during steady hypotonic polyuria. 5 normal subjects have been studied in the absence of treatment (TA) and after treatment with I, E, E + I. The renal function has been estimated by clearance (cl.) method during hypotonic polyuria induced by oral water loading and i.v. infusion of 5% dextrose solution. The glomerular filtration rate has been estimated by cl. of endogenous creatinine; moreover have been measured the osmotic clearances (Cosm, CH2O), the sodium and potassium clearances (CNa, CK), the mean arterial pressure (PA) and the urinary prostaglandins of E series (PGE) by RIA method. In I condition is observed: a) a trend to a glomerular filtration rate decrement; b) a significant decline of the urinary flow rate, CH2O, UPGV and a significant increment of the urinary osmolarity; c) a trend to an increment of potassium and a decrement of sodium urinary excretions; d) a significant increase of PA. It is possible that the contrary effects observed during the hypotonic polyuria in E condition depend on the stimulating effects of this material on the PG intrarenal synthesis.

Adult↗
PubMed1982

Early polyuria in the rat following single-dose cis-dichlorodiammineplatinum (II): effects on plasma vasopressin concentration and posterior pituitary function.

Central effects associated with DDP-induced early polyuria are described. Male Sprague-Dawley rats injected intraperitoneally with DDP (5 mg/kg) have a threefold increase in urine volume in the first 24 hr after treatment. This is accompanied by a corresponding decrease in Uosm but no decrease in renal function as indicated by serum creatinine or GFR. Treated animals having free access to water have reduced levels of plasma AVP, 1.42 +/- 0.14 pg/ml compared to 2.63 +/- 0.47 for control, at 8 hr after injection, and treated animals deprived of water have decreased plasma AVP at 12 and 24 hr after injection. The early polyuria in DDP-treated animals can be prevented by the administration of exogenous AVP. At 8 hr after DDP injection, posterior pituitary AVP content is identical in treated and control rats. In vitro studies with isolated pituitaries show that DDP, either 0.85 and 1.7 mM, in the medium inhibits AVP release by 60% to 90% during two successive 10 min incubation periods. These results suggest that DDP inhibits AVP release from the posterior pituitary but has no effect on AVP synthesis. This inhibition of AVP release results in lowered plasma AVP levels, which reduces water reabsorption and causes polyuria.

Animals↗