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At least 541 records · Page 30Linked to original sources
PubMed2006

Circadian variation of angiotensin II and aldosterone in nocturnal enuresis: relationship to arterial blood pressure and urine output.

PURPOSE: We investigated the circadian rhythm of solute excretion and regulating hormones as well as blood pressure in patients with monosymptomatic nocturnal enuresis. MATERIALS AND METHODS: We included 15 patients with a mean age +/- SE of 13.4 +/- 0.9 years who had monosymptomatic nocturnal enuresis with at least 3 wet nights weekly and a control group of 10 healthy children with a similar age and sex distribution. During inpatient circadian studies urine was collected during 6 periods and blood was drawn at 7 time points during 24 hours. Heart rate and blood pressure was recorded with an ambulatory blood pressure monitor every 30 to 60 minutes. RESULTS: The total patient group excreted a significantly larger nocturnal urine volume than controls (p <0.01). Five patients had marked nocturnal polyuria (nocturnal urine volume greater than the mean in the control group +2 SD), whereas urine output in the remaining patients without polyuria were similar to controls. Nocturnal polyuria was caused mainly by increased nocturnal solute excretion, especially Na. Serum aldosterone and plasma angiotensin II showed a marked circadian rhythm in normal children with a nocturnal increase concomitant with a significant decrease in mean arterial blood pressure during sleep. In contrast, the group of patients with nocturnal polyuria showed a lack of circadian rhythm in all excretion variables as well as an attenuated rhythm in plasma angiotensin II and mean arterial blood pressure. Interestingly this group had normal circadian rhythms of the circadian rhythm markers plasma cortisol and heart rate. CONCLUSIONS: The study suggests that an abnormally large nocturnal excretion of Na caused by selectively attenuated circadian rhythms of Na regulating hormones might be an important pathogenic factor in monosymptomatic nocturnal enuresis.

Adolescent↗
PubMed1998

Effects of experimental salt depletion on urinary prostanoid excretions in normal women.

The effects of moderate salt depletion on urinary excretions of prostanoids (PG)E2, 6-keto-PGF1alpha (6KPGF) and thromboxane (TX)B2 have been investigated in healthy women (SD group, n = 14). Salt depletion was obtained by combining a low sodium chloride dietary intake (< 60 mmol per day) with natriuretic and potassium sparing treatment. At the end of the treatment, the cumulative sodium deficit was 438 +/- 42 mmol (mean +/- SEM). Plasma renin activity (PRA) and urinary aldosterone excretion were determined in basal conditions. Renal functional exploration was performed during hypotonic polyuria (by oral water load) and subsequent moderate antidiuresis (by low dose infusion of an antidiuretic hormone analogue). In both phases, renal function was estimated by the clearance (cl.) method and the urinary concentrations of PGE2, 6KPGF and TXB2 by RIA method. The control group was composed of 20 healthy women in normal sodium and potassium balance (N group). Salt depletion was effective in increasing the basal values of plasma renin activity (PRA) and urinary aldosterone excretion. Moreover, it was effective in inducing the following during polyuria: (a) a depression of the diuretic response to water load in presence of a reduction in plasma osmolality; (b) a reduction in creatinine cl. in the absence of significant changes in mean arterial pressure; (c) an increase in the fractional reabsorption of sodium and chloride, in particular at the level of the diluting segments. Both in polyuria and in antidiuresis, the excretions of 6KPGF and TXB2 were higher in the SD vs. N group, while the excretion of PGE2 was not significantly different. In SD and N pooled groups, significant positive correlations were shown between basal PRA and urinary excretions during polyuria of 6KGPF and TXB2, (but not of PGE2) as well as between the excretions of the two metabolites. In conclusion, functionally effective salt depletion induces in healthy women a stimulation of renal synthesis of both prostacyclin and thromboxane. The excretory data do not give evidence of a similar effect on PGE2 synthesis.

6-Ketoprostaglandin F1 alpha↗
PubMed2003

Functional bladder capacity and urodynamics in males with nocturia.

Previous studies in males with lower urinary tract symptoms (LUTS) have shown that nocturia in some patients is associated with nocturnal polyuria whereas other patients have preserved circadian urine output rhythm. This outpatient study based on 7-dayss frequency/volume (FV) charts showed that patients with nocturnal polyuria and age-matched controls without nocturia had a diurnal variation in functional bladder capacity (FBC) with higher night-time values. In contrast, patients without nocturnal polyuria no diurnal variation was observed in FBC with lower day and night-time values than both controls and nocturnal polyuric patients. Nocturia volumes correlated significantly to daytime FBC in both patient groups. Voided volumes obtained from daytime pressure/flow urodynamic investigations correlated significantly with night-time FBC obtained from the FV chart. In patients with LUTS nocturia was caused by nocturnal polyuria in 10 of 23 patients and by diminished night-time functional bladder capacity in the remaining 13 patients. In conclusion, nocturia in males with LUTS referred for BPH evaluation is caused by a mismatch between nocturnal urine production and night-time FBC analogous with the pathophysiology of nocturnal enuresis. The evaluation of circadian urine production and FBC seems mandatory in the assessment of patients with nocturia and LUTS.

Adult↗
PubMed2004

[Etiology of nocturia and clinical efficacy of naftopidil on nocturia in patients with benign prostatic hyperplasia--analysis of frequency volume charts].

The etiology of nocturia in 70 patients with benign prostatic hyperplasia (BPH) who had nocturia of two or more times were examined based on frequency volume charts (FVC). Nocturia was classified into four groups: nocturnal polyuria, low capacity, combined nocturia, and no evidence of abnormality. Nearly half of the cases had nocturnal polyuria only. A little under 70% of patients had associated nocturnal polyuria (nocturnal polyuria+combined nocturia). Naftopidil was administered for three months to the patients with BPH who had nocturia with a urinary frequency of two or more times. Clinical efficacy was evaluated in 32 patients based on FVC and naftopidil was shown to improve nocturia. The improvement in nocturia was determined by the increment in voided volume.

Adrenergic alpha-Antagonists↗
PubMed1998

Nocturia in adults: etiology and classification.

Nocturia is one of the most bothersome of all urologic symptoms, yet even a rudimentary classification does not exist. We herein propose a classification system of nocturia based on a retrospective study. The records of 200 consecutive patients with nocturia were reviewed. Evaluation included history, micturition diary (including day, night, and 24-hr voided volume), postvoid residual urine (PVR), and videourodynamic study (VUDS). Functional bladder capacity (FBC) was determined to be the largest voided volume in a 24-hr period. The etiology of nocturia was thus classified into one of three groups: nocturnal polyuria ([NP] in which voided urine volume during the hours of sleep exceeds 35% of the 24-hr output), nocturnal detrusor overactivity ([NDO] defined as nocturia attributable to diminished bladder capacity during the hours of sleep), and mixed (NP+NDO); polyuria (24-hr urine output >2,500 cc) was classified separately. There were 129 women and 65 men ranging in age from 17 to 94 years (x=59). Overall 13 (7%) had NP, 111 (57%) NDO, and 70 (36%) had a mixed etiology of their nocturia (both NP and NDO). Forty-five (23%) also had polyuria. These data confirm that the etiology of nocturia is multifactorial and in many instances unrelated to the underlying urologic condition. Nocturnal overproduction of urine is a significant component of nocturia in 43% of patients, most of whom will also have NDO. We believe that treatment should be directed at both conditions.

Adolescent↗
PubMed2006

Central diabetes insipidus in a patient with malaria tropica.

Up to 21% of severe cases of malaria tropica are associated with polyuria and are life-threatening. We describe a 39-yr-old man with malaria tropica who developed disseminated intravascular coagulation, polyuria, and a pituitary lesion. Empiric treatment with vasopressin improved the polyuria. This is the first case of malaria tropica in which central diabetes insipidus has been documented.

Adrenal Insufficiency↗
PubMed2006

Dipsogenic diabetes insipidus: report of a novel treatment strategy and literature review.

Dipsogenic diabetes insipidus is a syndrome of disordered thirst, in patients without psychiatric disease, which may be confused with partial central diabetes insipidus. Distinguishing these entities involves monitored water testing. Therapy with antidiuretic hormone in patients with dipsogenic diabetes insipidus is thought to be contraindicated for fear of inducing water intoxication. We report a case of a 26-year-old woman without psychiatric illness referred for longstanding polyuria and polydipsia. Otherwise healthy, she complained of near-constant thirst and frequent urination, causing severe disruption of her personal and professional life. She had been consistently eunatremic and polyuric, with low urine osmolality. Results of extensive water testing revealed intact urinary concentrating and diluting capacity, physiologic though blunted antidiuretic hormone (ADH) release, and an abnormally low thirst threshold, consistent with the diagnosis of dipsogenic diabetes insipidus. To control her polyuria we initiated treatment with intermittent, low-dose, intranasal desmopressin and strict water restriction during drug dosing. In follow-up she reported excellent control of polyuria and significant functional improvement. The reviewed literature demonstrates a limited number of reports about dipsogenic diabetes insipidus, and no prior report of a similar treatment strategy. Dipsogenic diabetes insipidus is an uncommonly (and not universally) recognized disorder, requiring monitored testing in order to distinguish it from incomplete forms of central diabetes insipidus. Though therapy with desmopressin cannot be recommended based on the results of a single case, the outcome presented here is intriguing and suggests that larger studies in such patients is warranted to assess the broader application of such an intervention.

Adult↗
PubMed1987

Prevalence, pathogenesis, and treatment of renal dysfunction associated with chronic lithium therapy.

From the analysis of several studies published from 1979 to 1986 comprising 1,172 patients, we estimated that glomerular filtration rate (GFR) was normal in 85% of unselected patients on chronic lithium therapy. The remaining 15% of patients displayed only mild reduction in GFR, clustering at approximately 60 mL/min. Thus, the data available to date do not support earlier concerns that long-term lithium therapy could eventuate into renal insufficiency. The most prevalent renal effect of lithium is impairment of concentrating ability, which we estimated to be present in at least 54% of 1,105 unselected patients on chronic lithium therapy. This defect translated into overt polyuria in only 19% of unselected cases. A renal lesion confined to the collecting tubule has been described in humans who have taken lithium for short periods of time. This lesion may represent the collecting tubule's response to the intracellular accumulation of lithium, which interferes with cAMP formation and results in an early and probably reversible inhibition of antidiuretic hormone (ADH)-mediated water transport. However, long-term lithium therapy may induce a progressive and partly irreversible defect in concentrating ability. The potential risk for dehydration associated with lithium-induced polyuria, as well as the discomfort inherent to this side effect, deserves evaluation and consideration for therapeutic intervention. Amiloride has additional advantages over conventional treatment of nephrogenic diabetes insipidus using thiazide diuretics. The action of amiloride on ADH-mediated water transport seems specific in as much as it is capable of preventing the uptake of lithium in high resistance epithelia and thereby prevents the inhibitory effect of intracellular lithium on water transport. Unlike thiazides, amiloride has a weak natriuretic effect and is less likely to increase plasma lithium levels by causing volume contraction. In addition, amiloride, by conserving potassium, obviates the need for potassium supplementation that is usually required to prevent hypokalemia when thiazides are used to treat lithium-induced polyuria. Since amiloride may prevent chronic intracellular lithium accumulation in the collecting tubule, future studies should elucidate whether amiloride also has a role in preventing lithium-induced chronic tubulo-interstitial damage.

Acidosis, Renal Tubular↗
PubMed1999

Diurnal variation of antidiuretic hormone and urinary output in spinal cord injury.

INTRODUCTION: Healthy individuals have a nocturnal decrease in urine output due to increased plasma antidiuretic hormone levels at night. This does not occur in spinal cord injury and most patients experience nocturnal polyuria, which triggers dysreflexic crises secondary to urinary bladder overdistension, and interferes with patients' sleep due to the need for extra catheterization. OBJECTIVE: To evaluate the diurnal variation in ADH level, urinary output, and plasma and urine osmolality in SCI patients with regard to their level of injury and in comparison with age- and sex-matched healthy individuals. MATERIALS AND METHODS: Sixteen ASIA-A spinal cord-injured patients, eight with paraplegia, eight with tetraplegia, and eight healthy individuals, were evaluated for urinary output, urine and serum osmolality, and antidiuretic hormone levels during day and night hours. RESULTS: Absence of diurnal variation in urinary output and antidiuretic hormone secretion was detected in both paraplegic and tetraplegic patients, while antidiuretic hormone levels rose significantly at night in the control group. CONCLUSION: Antidiuretic hormone levels should be monitored both day and night in spinal cord injury patients, with severe nocturnal polyuria. Treatment with desaminocystein-D-arginine vasopressin can be attempted when conservative measures fail to control nocturnal polyuria, especially in patients who are on an intermittent catheterization program.

Adult↗
PubMed1991

Aggravation of subclinical diabetes insipidus during pregnancy.

BACKGROUND: Transient polyuria and polydipsia during pregnancy are rare, and their cause is not entirely clear. Possible explanations include the exacerbation of preexisting abnormalities in the secretion or action of vasopressin and abnormally large increases in plasma vasopressinase activity. METHODS: We studied two women in whom overt polyuria and polydipsia developed during the third trimester of pregnancy and disappeared after delivery. The secretion and action of vasopressin were studied both when the women had polyuria and polydipsia and later, when their water intake and urine volume were normal. RESULTS: One patient had partial nephrogenic diabetes insipidus. She had little increase in urine osmolality in response to water deprivation, hypertonic-saline infusion, and vasopressin injection and no response to desmopressin acetate (1-deamino-8-D-arginine vasopressin) during the immediate postpartum period. Her basal and stimulated plasma vasopressin concentrations were high (16.5 to 203.4 pmol per liter) before and during hypertonic-saline infusion 30 months post partum. The other patient had partial neurogenic diabetes insipidus. She had subnormal basal plasma vasopressin concentrations, a subnormal increase in the plasma vasopressin level and a subnormal decrease in urine flow in response to the administration of vasopressin, and a normal response to desmopressin. After pregnancy, when her urine volume was normal, she had no increase in plasma vasopressin in response to hypertonic-saline infusion, but she had a normal rise in the plasma vasopressin level and a normal renal response to vasopressin administration. CONCLUSIONS: Pregnancy may unmask subclinical forms of both nephrogenic and neurogenic diabetes insipidus. This exacerbation may result from both increased vasopressinase activity and diminished renal responsiveness to vasopressin.

Adult↗
PubMed2003

Swallowing, urine flow, and amniotic fluid volume responses to prolonged hypoxia in the ovine fetus.

OBJECTIVE: Four days of hypoxia produce an extensive fetal polyuria with little change in amniotic fluid volume in the ovine fetus. We hypothesized that fetal swallowing and intramembranous absorption would increase with prolonged hypoxia to offset the polyuria. STUDY DESIGN: After a 24-hour normoxic period, nine ovine fetuses were subjected to 4 days of hypoxia induced by lowering maternal inspired oxygen content. Seven fetuses were monitored for 5 days as normoxic time controls. Measurements included fetal swallowed volume by a computerized system with Transonic flow probes, urine production by gravity drainage, and amniotic fluid volume by an indicator dilution technique. Data were averaged over 12-hour intervals, and a three-factor repeated-measures analysis of variance was used for statistical testing. RESULTS: During days 2 to 5, arterial oxygen tension was 20.7+/-1.1 (SE) mm Hg in the normoxic and 13.9+/-0.8 mm Hg in the hypoxic fetuses (P<.0001). Urine flow was unchanged over time in the normoxic fetuses and increased gradually from 693+/-88 to 2189+/-679 mL per day during hypoxia (P<.0001). The prehypoxia swallowed volume was similar in the two groups, averaging 447+/-95 mL per day. Although transiently decreased in eight of nine hypoxic fetuses, the 12-hour average swallowed volumes were not significantly different at any time in the hypoxic versus normoxic fetuses (P=.62). Amniotic fluid volume increased in the hypoxic fetuses relative to that in the normoxic fetuses (520+/-338 mL vs -226+/-136 mL, P<.01), although the increase was small (P<.01) relative to the excess volume of urine (4269+/-1306 mL). Estimated intramembranous absorption increased from 209+/-95 mL per day during normoxia to average 1032+/-396 mL per day during hypoxia. CONCLUSIONS: The current study supports the concept that prolonged hypoxia produces a progressive fetal polyuria with relatively small changes in amniotic fluid volume. Concomitantly, hypoxia does not induce prolonged changes in fetal swallowing; rather, intramembranous absorption greatly increases, thereby preventing severe polyhydramnios.

Absorption↗
PubMed2005

Nocturia in relation to sleep, health, and medical treatment in the elderly.

Nocturia is a common condition in the elderly that profoundly influences general health and quality of life. It appears to predict a higher risk of death. One consequence of nocturia is sleep deterioration, with increased daytime sleepiness and loss of energy and activity. Accidents, e.g. falls, are increased both at night and during the day in elderly persons with nocturia. Nocturia is caused by nocturnal polyuria, reduced voided volumes, or a combination of the two. Nocturnal polyuria can be caused by numerous diseases, e.g. diabetes insipidus, diabetes mellitus, congestive heart failure, and sleep apnoea. A disorder of the vasopressin system, with very low or undetectable vasopressin levels at night, is manifested as an increased nocturnal urine output, which in the most extreme cases reaches 85% of the 24-h diuresis: the prevalence of low or undetectable vasopressin levels at night has been estimated to be 3-4% in those aged >or= 65 years. Treatment of nocturia may include avoiding excessive fluid intake and use of diuretic medication in the afternoon rather than the morning, oral desmopressin at bedtime in cases of nocturnal polyuria, and antimuscarinic agents in the case of overactive bladder or impaired storage capacity of the bladder.

Age Factors↗
PubMed2006

The value of urine specific gravity in detecting diabetes insipidus in a patient with uncontrolled diabetes mellitus: urine specific gravity in differential diagnosis.

When a patient with diabetes mellitus presents with worsening polyuria and polydipsia, what is a sensible, cost-effective approach? We report the unique coincidence of type 2 diabetes mellitus and diabetes insipidus. A 46-year-old woman with poorly controlled type 2 diabetes complained of polyuria with a daily output of 5 L. Although urinalysis demonstrated significant glucosuria, diabetes insipidus was suspected owing to a low urine specific gravity (1.008). The low specific gravity persisted during a water deprivation test. Ultimately, diabetes insipidus was confirmed when urine specific gravity and urine osmolality normalized following desmopressin administration. This case emphasizes the importance of accurately interpreting the urine specific gravity in patients with polyuria and diabetes mellitus to detect diabetes insipidus.

Diabetes Insipidus↗
PubMed1993

Effect of lithium dosing schedule on urinary output.

Lithium has been reported to induce polyuria in up to 35% of patients receiving it. It has been suggested that polyuria may be reduced by using single rather than multiple daily dosing. However, this information is based on non-randomized studies, which used higher serum lithium levels than are currently used. In fact, the incidence of polyuria may be lower at currently used lithium levels, and the benefits of a single daily dose regimen on urine volume at these levels have not been assessed. We conducted a prospective randomized study to test the hypothesis that switching patients from multiple daily dose lithium to single daily dose lithium would significantly lower urine volume. Twenty-four patients previously stabilized on multiple daily dosing were randomly allocated to either single or multiple daily dose lithium. Twenty-four-hour urine volume, serum creatinine, creatinine clearance and serum lithium were measured at study entry and completion. Switching to single daily dose lithium did not significantly reduce the 24-h urine volume.

Adolescent↗
PubMed1988

Lithium-induced morphological changes in the rat kidney at different levels of urine flow.

Lithium treated rats become polyuric and at the same time develop pronounced dilatations of distal tubular segments and characteristics enzyme histochemical changes. In the present study we have compared lithium-polyuric Wistar rats with lithium treated rats in which the polyuria was prevented either by administration of a vasopressin analogue or by water restriction. The kidneys were studied using enzyme histochemistry and light microscope morphometry. The characteristic lithium induced changes were present in all groups irrespective of the presence or absence of polyuria. It is concluded therefore, that the morphological and enzyme histochemical changes are induced by the lithium ion per se and not by the accompanying polyuria.

Animals↗
PubMed2000

Renal dysplasia in boxers and Finnish harriers.

Puppies from two litters of dogs were found to have severe polyuria and polydipsia. Four of the dogs were investigated by means of clinical examination, haematological and biochemical analysis, and urinalysis. A modified water deprivation response test was also performed in two of the dogs. Renal changes on postmortem examination in three of the dogs were found to be consistent with renal dysplasia. A possible explanation for the finding of hyposthenuria and the extreme polyuria and polydipsia in association with renal dysplasia may be lack of response to antidiuretic hormone owing to anomalous maturation of the renal tubules. Six other puppies from the two litters of dogs did not show any clinical signs of polyuria and polydipsia, although postmortem examination in one of them also revealed renal dysplasia. The clinical features of renal dysplasia may therefore vary greatly between individuals.

Animals↗
PubMed2007

COX-2 activity transiently contributes to increased water and NaCl excretion in the polyuric phase after release of ureteral obstruction.

Release of bilateral ureteral obstruction (BUO) is associated with reduced expression of renal aquaporins (AQPs), polyuria, and impairment of urine-concentrating capacity. Recently, we demonstrated that 24 h of BUO is associated with increased cyclooxygenase (COX)-2 expression in the inner medulla (IM) and that selective COX-2 inhibition prevents downregulation of AQP2. In the present study, we tested the hypothesis that COX-2 activity increases in the postobstructive phase and that this increase in COX-2 activity contributes to polyuria and impaired urine-concentrating capacity. We examined the effect of the selective COX-2 inhibitor parecoxib (5 mg.kg(-1).day(-1) via osmotic minipumps) on renal functions and protein abundance of AQP2, AQP3, Na-K-2Cl cotransporter type 2 (NKCC2), and Na-K-ATPase 3 days after release of BUO. At 3 days after release of BUO, rats exhibited polyuria, dehydration and urine and IM tissue osmolality were decreased. There were inverse changes of COX-1 and COX-2 in the IM: COX-2 mRNA, protein, and activity increased, while COX-1 mRNA and protein decreased. Parecoxib reduced urine output 1 day after release of BUO, but sodium excretion and glomerular filtration rate were unchanged. Parecoxib normalized urinary PGE(2) and PGI(2) excretion and attenuated downregulation of AQP2 and AQP3, while phosphorylated AQP2 and NKCC2 remained suppressed. Parecoxib did not improve urine-concentrating capacity in response to 24 h of water deprivation. We conclude that decreased NKCC2 and collapse of the IM osmotic gradient, together with suppressed phosphorylated AQP2, are likely causes for the impaired urine-concentrating capacity and that COX-2 activity is not likely to mediate these changes in the chronic postobstructive phase after ureteral obstruction.

Animals↗
PubMed2006

Mouse model of inducible nephrogenic diabetes insipidus produced by floxed aquaporin-2 gene deletion.

Transgenic mouse models of defective urinary concentrating ability produced by deletion of various membrane transport or receptor proteins, including aquaporin-2 (AQP2), are associated with neonatal mortality from polyuria. Here, we report an inducible mouse model of AQP2 gene deletion with severe polyuria in adult mice. LoxP sequences were inserted into introns 1 and 2 in the mouse AQP2 gene by homologous recombination in embryonic stem cells. Mating of germ-line AQP2-loxP mice with tamoxifen-inducible Cre-expressing mice produced offspring with inducible homozygous Cre-AQP2-loxP, which had a normal phenotype. Tamoxifen injections over 10 days resulted in AQP2 gene excision, with undetectable full-length AQP2 transcript in kidney and a >95% reduction in immunoreactive AQP2 protein. Urine osmolality decreased from approximately 2,000 to <500 mosmol/kgH(2)O after 4-5 days, with urine output increasing from 2 to 25 ml/day. Urine osmolality did not increase after water deprivation. Interestingly, AQP3 protein expression in the collecting duct was increased by about fivefold after AQP2 gene excision. Mild renal damage was seen after 6 wk of polyuria, with collecting duct dilatation, yet normal creatinine clearance and serum chemistries. These results establish the first adult model of nephrogenic diabetes insipidus (NDI) caused by AQP2 deficiency, with daily urine output comparable to body weight, although remarkable preservation of renal function compared with non-inducible NDI models.

Animals↗