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PubMed1980

Effect of prostaglandin inhibition on demeclocycline administration in conscious rats.

Studies were performed in conscious rats to evaluate the role of renal prostaglandin biosynthesis in demeclocycline-induced polyuria. Three groups of animals were evaluated. Group 1 animals received only the diluents used for both demeclocycline and indomethacin. Group 2 received demeclocycline (20 mg/kg/day) and the indomethacin diluent. Group 3 received both demeclocycline and indomethacin (10 mg/kg/day). After eight days of demeclocycline administration, urine flow rate increased in the group 2 animals from 15.1 +/- 2.1 to 31.1 +/- 5.1 ml/day. Indomethacin failed to alter the magnitude of demeclocycline-induced polyuria despite a 60% reduction in urine prostaglandin E excretion rats. These studies demonstrate that the concentrating defect induced by demeclocycline can occur independent of alterations in praostaglandin biosynthesis and suggest that a change in renal prostaglandin biosynthesis is not an etiologic factor in demeclocycline-induced polyuria.

Animals↗
PubMed1997

Do aquaporins have a role in nocturnal enuresis?

Aquaporins are proteins that mediate transmembrane water transport in a variety of tissues including the kidney. Vasopressin plays an important role in regulation of water metabolism, and under normal conditions the kidney collecting duct is extremely sensitive to vasopressin. Vasopressin stimulates the synthesis of aquaporin 2 (AQP2) in kidney collecting duct principal cells. Studies in Brattle Boro rats which are vasopressin deficient, revealed low levels of AQP2 in association with extreme polyuria. After vasopressin treatment for 5 days AQP2 levels increased threefold. Using rat models with nephrogenic diabetes insipidus (NDI) we have demonstrated that AQP2 expression is down regulated in association with polyuria, suggesting that reduced levels of AQP2 may be a general factor in acquired forms of NDI from a variety of reasons. The polyuria and urinary concentrating defects associated with an abnormal nightly-increase in AVP in patients with nocturnal enuresis may partly be due to a lack of vasopressin-mediated AQP2 expression since treatment with desmopressin in these patients have normalised their nocturnal urine production.

Animals↗
PubMed1977

Transient diabetes insipidus with elevated serum osmolarity associated with 'benign' febrile illness.

A 38-year-old physician developed polyuria and hypodipsia four days after the onset of an upper respiratory tract infection. Subsequent investigation showed a concentration defect with dehydration that partially corrected with vasopressin injection (Pitressin) administration compatible with partial central diabetes insipidus (DI). Skull roentgenograms, EEG, and lumbar puncture were normal. The polyuria and hypodipsia slowly resolved without treatment. Normal urinary concentration ability was achieved by the 48th day, but a residual elevation in serum osmolarity persisted for one year. Review of the literature failed to show previous documentation of transient DI with elevated serum osmolarity from an acute, febrile illness. The mechanism is speculative, but may be related to a subclinical encephalitis. The true frequency of this syndrome and its relationship to the frequent observation of transient polydipsia and polyuria in "benign" febrile illness remains to be determined.

Acute Disease↗
PubMed2006

Proteomic identification of alterations in metabolic enzymes and signaling proteins in hypokalemic nephropathy.

Hypokalemic nephropathy caused by prolonged K(+) deficiency is associated with metabolic alkalosis, polydipsia, polyuria, growth retardation, hypertension, and progressive tubulointerstitial injury. Its pathophysiology, however, remains unclear. We performed gel-based, differential proteomics analysis of kidneys from BALB/c mice fed with high-normal-K(+) (HNK), low-normal-K(+) (LNK), or K(+)-depleted diet for 8 wk (n = 6 in each group). Plasma K(+) levels were 4.62 +/- 0.35, 4.46 +/- 0.23, and 1.51 +/- 0.21 mmol/L for HNK, LNK, and KD mice, respectively (p < 0.0001; KD vs. others). With comparable amounts of food intake, the KD mice drank significantly more water than the other two groups and had polyuria. Additionally, the KD mice had growth retardation, metabolic alkalosis, markedly enlarged kidneys, renal tubular dilation, intratubular deposition of amorphous and laminated hyaline materials, and tubular atrophy. A total of 33 renal proteins were differentially expressed between the KD mice and others, whereas only eight proteins were differentially expressed between the HNK and LNK groups, as determined by quantitative intensity analysis and ANOVA with Tukey's post hoc multiple comparisons. Using MALDI-MS and/or quadrupole-TOF MS/MS, 30 altered proteins induced by K(+)-depletion were identified as metabolic enzymes (e.g., carbonic anhydrase II, aldose reductase, glutathione S-transferase GT41A, etc.), signaling proteins (14-3-3 epsilon, 14-3-3 zeta, and cofilin 1), and cytoskeletal proteins (gamma-actin and tropomyosin). Some of these altered proteins, particularly metabolic enzymes and signaling proteins, have been demonstrated to be involved in metabolic alkalosis, polyuria, and renal tubular injury. Our findings may lead to a new road map for research on hypokalemic nephropathy and to better understanding of the pathophysiology of this medical disease when the functional and physiological significances of these altered proteins are defined.

Animals↗
PubMed1981

Proteinuria in the acutely diabetic rat and its response to insulin treatment.

The development of proteinuria and its response to insulin therapy in acute experimental diabetes was examined in 11 female rats by sequentially measuring 24 h excretion of glucose and total protein before diabetes, during 5-37 days of acute streptozotocin diabetes, during and after 7-14 days of continuous subcutaneous insulin administration. Induction of diabetes promptly resulted in marked polyuria (78 +/- 9 ml/24 h), and glycosuria (6.6 +/- 0.7 g/24 h), while proteinuria quadrupled (from 4.7 +/- 0.7 to 18.8 +/- 1.8 mg/24 h, p less than 0.001). Concurrent with amelioration of polyuria and glycosuria by insulin treatment, proteinuria decreased strikingly (8.5 +/- 1.2 mg/24 h, p less than 0.001) Polyuria and glycosuria resumed after discontinuing continuous subcutaneous insulin, and proteinuria promptly returned to pretreatment levels (19.0 +/- 2.5 mg/24 h). Similarly decreased proteinuria (8.8 +/- 0.9 mg/24 h) recurred in five rats retreated with insulin after 100 days of diabetes. Elevated proteinuria was not associated with lysozymuria or consistent changes in glomerular filtration rate. The rapid fluctuations in proteinuria attending acute diabetes and its effective treatment suggest that metabolic aberrations of diabetes may directly effect renal handling of proteins.

Acute Disease↗
PubMed1999

Fluid balance therapy of nocturia in women.

Nocturia is a common and troublesome symptom in otherwise healthy elderly men and women. Nocturnal polyuria (an excessive nighttime urine output) has been documented to be a common finding in healthy men with lower urinary tract symptoms. It is also a presenting feature of various medical conditions, such as renal failure, hypercalcemia and diabetes. Fluid balance therapy is an option in those whose nocturia is secondary to nocturnal polyuria. If a reduction in fluid intake fails to reduce nocturnal frequency a variety of drug treatments may be beneficial. Several studies have confirmed the efficacy of intranasal DDAVP, a synthetic analog of antidiuretic hormone, in both healthy patients and those with neuropathic bladders, although fluid overload and hyponatremia are potential side effects. Other drug treatments include early evening diuretics, such as frusemide or bumetanide. More recently imipramine has shown therapeutic benefit in young adults with enuresis, and might prove to be useful in the elderly with nocturnal polyuria.

Adult↗
PubMed2006

Nocturia: "do the math".

PURPOSE: We reviewed the definition and etiologies of nocturia, offering the current diagnostic procedures and standards of care. MATERIALS AND METHODS: We reviewed recent published literature regarding nocturia, along with current paradigms for diagnosis and management. RESULTS: Nocturia is common as a limited occurrence but troublesome if the patient regularly experiences more than 2 episodes during sleep hours. The 4 principle etiologies associated with nocturia (nocturnal polyuria, decreased nocturnal bladder capacity, mixed polyuria, and global polyuria) may be easily differentiated through mathematical analysis of a 24-hour bladder diary. CONCLUSIONS: Nocturia is highly treatable in many patients. Identification of the precise type and its cause enable clinicians to minimize the inconvenience and sleep deprivation associated with nocturia.

Age Distribution↗
PubMed2006

Urinary calcium excretion in healthy children and children with primary monosymptomatic nocturnal enuresis.

PURPOSE: We investigated the role of urinary Ca excretion in monosymptomatic nocturnal enuresis, and defined normality and intra-individual variability in Ca excretion in healthy children. MATERIALS AND METHODS: We included 46 Danish children with desmopressin resistant nocturnal enuresis and 96 healthy controls. We performed fractional urine collections at home during 2 days in controls or during hospitalization in children with enuresis. Urine volume, osmolality, and Ca and creatinine measurements were performed and Ca-to-creatinine ratios were calculated and compared between groups. Based on nocturnal urine output children with enuresis were characterized as having polyuria (nocturnal urine volume greater than 130% of expected bladder capacity) or not having polyuria. RESULTS: We did not find any differences in controls compared with children with enuresis who did not and did have nocturnal polyuria in daytime Ca excretion (mean +/- SE 0.121 +/- 0.012, 0.078 +/- 0.014 and 0.095 +/- 0.020 mg/mg creatinine), nighttime Ca excretion (0.115 +/- 0.011, 0.092 +/- 0.019 and 0.139 +/- 0.029 mg/mg creatinine) or 24-hour Ca excretion (0.118 +/- 0.011, 0.083 +/- 0.014 and 0.106 +/- 0.020 mg/mg creatinine, respectively). Urinary Ca excretion was not influenced by patient age, sex or body weight and, furthermore, we did not find evidence of diurnal variation. However, we observed considerable intra-individual variability in diurnal, nocturnal and total 24-hour urinary Ca-to-creatinine ratios. CONCLUSIONS: These observations contradict several previous reports and speculations on a role of Ca in the pathogenesis of nocturnal enuresis.

Adolescent↗
PubMed2005

D-amino-acid oxidase is involved in D-serine-induced nephrotoxicity.

D-serine is nephrotoxic in rats. Based on circumstantial evidence, it has been suspected that D-amino-acid oxidase is involved in this nephrotoxicity. Since we found that LEA/SENDAI rats lacked D-amino-acid oxidase, we examined whether this enzyme was associated with D-serine-induced nephrotoxicity using the LEA/SENDAI rats and control F344 rats. When d-propargylglycine, which is known to have a nephrotoxic effect through its metabolism by D-amino-acid oxidase, was injected intraperitoneally into the F344 rats, it caused glucosuria and polyuria. However, injection of d-propargylglycine into LEA/SENDAI rats did not cause any glucosuria or polyuria, indicating that D-amino-acid oxidase is definitely not functional in these rats. D-serine was then injected into the F344 and LEA/SENDAI rats. It caused glucosuria and polyuria in the F344 rats but not in the LEA/SENDAI rats. These results indicate clearly that D-amino-acid oxidase is responsible for the D-serine-induced nephrotoxicity.

Alkynes↗
PubMed2002

Vasopressin and hypercalciuria in enuresis: a reappraisal.

OBJECTIVE: To test the hypotheses that vasopressin deficiency or hypercalciuria are important in polyuric and non-polyuric bedwetting, as nocturnal polyuria is a pathogenetic factor in enuresis responsive to antidiuretic therapy with desmopressin. SUBJECTS AND METHODS: Vasopressin deficiency has been implicated as a cause of nocturnal polyuria, but measurements of vasopressin in plasma have given contradictory results, because the hormone is released in pulses. Urinary levels reflect the secretion over longer periods. Hypercalciuria has also been proposed as a pathogenetic factor. Twenty-eight enuretic children who responded to desmopressin therapy with or without added anticholinergic agents (diuresis-dependent enuresis, DE), 15 children with therapy-resistant enuresis (not diuresis-dependent, NDE) and 51 continent controls were assessed. Urinary vasopressin, calcium and osmolality were measured in the morning after a 12-h thirst provocation. Urine production was recorded for 2 days. RESULTS: Because most data were not normally distributed, the values are expressed as the median (range). There were no differences in urine osmolality; i.e. con-trols 919 (636-1232), DE 849 (462-1149), NDE 968 (664-1191) mOsml/kg); vasopressin, controls 34 (8-983), DE 26 (9-295), NDE 50 (9-116) pmol/L; or calcium excretion (expressed as the calcium/creatinine ratio), controls 0.16 (0.01-0.71), DE 0.14 (0.04-0.67), and NDE 0.23 (0.03-0.69). The DE group produced more urine, at 18.4 (9.2-52.5) mL/kg/day, than the other groups, i.e. control 12.7 (8.3-42.8) and NDE 12.1 (6.3-36.8) mL/kg/day (P = 0.008). CONCLUSION: All enuretic children with nocturnal polyuria do not have vasopressin deficiency. The urinary calcium excretion does not differ between enuretic and dry children.

Adolescent↗
PubMed1999

Pathophysiology and treatment of enuresis in adults.

Monosymptomatic nocturnal enuresis (MNE) in children is partly the result of inadequate reduction in the rate of urine output at night. This nocturnal polyuria is due to the lack of a rise in the anti-diuretic hormone, arginine vasopressin (AVP), and can be reduced or eliminated by treatment with desmopressin at bedtime. Since there is a 1% incidence of MNE among adults, this study investigated the circadian pattern of solute and water balance in nine young adult enuretics before and during desmopressin therapy and compared the results with nine-age- and sex-matched, healthy controls. Before treatment, enuretics and controls had similar total fluid intake, urine output, urine osmolality, plasma osmolality, plasma total protein, mean arterial pressure and plasma AVP. The circadian pattern of fluid intake was also normal in enuretics. This abnormality could not be attributed to a deficiency of plasma AVP or an increase in solute excretion, since both variables were similar to controls. Rather, their nocturnal polyuria appeared to be due to a marked nocturnal reduction in renal sensitivity to the antidiuretic effect of vasopressin. In seven enuretics, restudied during treatment with desmopressin (10-30 micrograms o.d.), circadian urine output was normal and enuresis was absent. These results indicate that: (i) The circadian pattern of urine output in healthy adults is largely due to a nocturnal decrease in solute excretion rather than a rise in plasma AVP; (ii) The subset of adults with persistent MNE also have nocturnal polyuria as a result of insensitivity to the antidiuretic action of AVP; (iii) These defects can be corrected by treatment with desmopressin.

Adult↗
PubMed1985

Dietary self-selection patterns of rats with mild diabetes.

Rats were allowed a free selection of a diet from among separate sources of protein, fat and carbohydrate or were fed a composite diet formulated to approximate the nutrient composition of a commonly used nonpurified diet. Immediately after streptozotocin injections, diabetic rats displayed polyuria, polydipsia and glycosuria as well as elevated fasting plasma glucose levels and glucose intolerance indicative of mild diabetes. Diabetic rats allowed a free choice tended to consume more protein and consumed significantly less carbohydrate than nondiabetics. This pattern of nutrient choice was associated with a reduction of diabetic signs including reduced polyuria, polydipsia and glycosuria. Diabetic rats permitted to choose their diets were not hyperphagic and maintained a slow but steady rate of body weight gain, accompanied by a sparing of body fat stores. In contrast, diabetic rats consuming the composite diet experienced no improvement in diabetic status; these rats displayed a deterioration of fasting plasma glucose, severe polydipsia, polyuria and glycosuria as well as hyperphagia and wasting of fat stores. These data demonstrate that when mildly diabetic rats are given the opportunity to select their own diets, they choose a diet that leads to improvement of their diabetic status.

Animals↗
PubMed2006

Polynocturia in chronic kidney disease is related to natriuresis rather than to water diuresis.

BACKGROUND: Nocturnal polyuria has been well known in renal insufficiency. Recently, we found that as renal function deteriorated in chronic kidney disease (CKD), natriuresis was enhanced during the night with nocturnal blood pressure elevation. In the present study, we investigated whether nocturnal polyuria in CKD was due to the inability to concentrate urine, as previously proposed, or based on osmotic diuresis mainly by natriuresis. METHODS: In 27 CKD patients, circadian rhythms of urinary sodium, potassium, urea and osmolar excretion rates (U(Na)V, U(K)V, U(urea)V, U(osm)V) as well as of urinary volume (V) and free-water clearance (C(H(2)O)) were estimated during both daytime (6:00 to 21:00) and nighttime (21:00 to 6:00). Then, the night/day ratios of these parameters were analysed in relation to creatinine clearance (C(cr)) as a marker of glomerular filtration rate. RESULTS: C(cr) had significantly negative relationships with night/day ratios of V (R = -0.69; P < 0.0001), U(osm)V (R = -0.54; P = 0.004) and U(Na)V (R = -0.63; P = 0.0005), but no correlation with night/day ratios of C(H(2)O) (R = -0.33; P = 0.1), U(K)V (R = -0.29; P = 0.1) or U(urea)V (R = -0.31; P = 0.1). Linear and multiple regression analysis identified nocturnal natriuresis rather than urea excretion as an independent determinant of nocturia. CONCLUSION: As renal function deteriorated, nocturnal polyuria was seen, being consistent with classical recognition. Furthermore, this increase in nocturnal urine volume seemed related to osmotic diuresis mainly by natriuresis rather than to water diuresis or urea excretion.

Blood Pressure↗
PubMed1991

Primary hyperparathyroidism and coexisting nephrogenic diabetes insipidus: rapid postoperative correction.

Shortly after diagnosis of primary hyperparathyroidism, a patient had serum hyperosmolality, polyuria, isosthenuria, profound potassium depletion, and elevated plasma antidiuretic hormone levels, all consistent with nephrogenic diabetes insipidus. After parathyroidectomy, serum calcium and serum osmolality levels fell concurrently. Profound potassium deficits did not recur. We propose that (1) hypercalcemia produced a concentrating defect and polyuria; (2) renal tubular acidosis and polyuria combined to produce severe potassium depletion; (3) hypokalemia potentiated the nephrogenic diabetes insipidus caused by hypercalcemia; and (4) postoperative disappearance of the diabetes insipidus confirmed its reversible, purely metabolic causes.

Diabetes Insipidus↗
PubMed2005

Clinical observations of the effect of antidiuretic hormone on nocturia in elderly men.

OBJECTIVE: To evaluate the effect of desmopressin on nocturia, based on patients' subjective scoring of nocturia, as desmopressin is widely used to treat nocturnal enuresis and nocturnal polyuria. PATIENTS AND METHODS: We investigated a specific subgroup of 28 men with benign prostate obstruction and nocturia who were treated with desmopressin. Patients with nocturnal polyuria were excluded. All the patients were refractory to treatment with antimuscarinics or anticholinergics, e.g. oxybutynin, tolterodine, and propantheline bromide. We assessed the effect of desmopressin using a quantitative nocturia score and analysed its synergistic effect with alpha-blockers. RESULTS: The mean frequency of nocturia was 6.1 before desmopressin and most (86%) patients had an improvement in nocturia within 1-12 weeks of treatment with desmopressin. There was a 43% reduction in nocturia after using desmopressin (P < 0.001). The correlation coefficient between the number of nocturnal voids and the reduction in nocturia after treatment with desmopressin was 0.756, indicating that the more severe the nocturia, the more effective was desmopressin. CONCLUSIONS: Desmopressin is effective for refractory nocturia in elderly men with no nocturnal polyuria, and has limited side-effects.

Adult↗
PubMed1987

Atrial natriuretic peptide in spontaneous tachycardias.

Because anecdotal reports suggest that concentrations of atrial natriuretic peptide are raised during tachycardias, plasma immunoreactive atrial natriuretic peptide concentrations were measured in 34 consecutive patients when tachycardia was diagnosed and again five and 15 minutes after conversion to sinus rhythm. Plasma atrial natriuretic peptide concentrations were raised in all but four patients, and were higher in patients with known heart disease than in those without. The concentrations were higher with ventricular tachycardia than with atrial fibrillation or supraventricular tachycardia, and in acute versus chronic tachycardia. There was only a weak positive relation between ventricular rate and atrial natriuretic peptide (r = 0.31); but there was a closer inverse correlation between atrial natriuretic peptide and systolic arterial pressure (r = -0.60). Conversion to sinus rhythm was associated with a definite fall in plasma atrial natriuretic peptide concentrations. Despite very high baseline concentrations of atrial natriuretic peptide only two patients reported polyuria. It is likely that atrial pressure rather than ventricular rate determines atrial natriuretic peptide release during tachycardia. Despite the absence of polyuria in all but two patients in this study atrial peptides could still contribute to, or cause, the polyuria of tachycardias.

Adult↗
PubMed1981

Vasopressin function in familial cranial diabetes insipidus.

A family suffering from cranial diabetes insipidus, that extends over 4 generations, is described. Inheritance of polyuria was autosomal dominant. Vasopressin function was studied in members of the last 2 generations, 4 of whom had polyuria. Osmoregulation of vasopressin secretion was assessed by infusion of hypertonic saline. Plasma vasopressin remained undetectable in one patient, while 2 others had very blunted vasopressin responses to osmotic stimulation. Three non-osmotic stimuli were applied. Controlled hypotension produced by trimetaphan infusion and insulin-induced hypoglycaemia did not increase plasma vasopressin but apomorphine-induced nausea caused a minimal rise in plasma vasopressin to 0.7 pg/ml. Polyuria and thirst resolved with antidiuretic therapy in all patients studied. Congenital absence of vasopressin as in Brattleboro rats is unlikely to account for diabetes insipidus in this disorder since small increases in vasopressin have been demonstrated in these patients. In view of previous post-mortem findings, familial cranial diabetes insipidus is most likely to be due to degeneration of vasopressin-synthesizing neurones.

Adult↗
PubMed1994

Vasopressin V1 and V2 receptors in diabetes mellitus.

Diabetes mellitus causes hypertonicity, increased plasma arginine vasopressin (AVP), polydipsia, and polyuria. Downregulation of AVP V2 receptors may contribute to the polyuria through diminished V2 receptor-mediated free water retention. After 2 wk of streptozotocin-induced diabetes mellitus, the diabetic rats had raised plasma glucose, AVP, and osmolality levels (P < 0.001) compared with nondiabetic controls (Sham). Insulin treatment (4 U long-acting insulin sc, daily) partially lowered these values (P < 0.01). There was a reduction in the number of renal and hepatic V1 receptors in the diabetic and diabetic+insulin animals compared with the sham animals (P < 0.05). The receptor affinity remained unchanged. In parallel, there was a reduction in maximum AVP-activated total inositol phosphate production in the liver and kidney of the diabetic and diabetic+insulin animals compared with the sham animals (P < 0.05). The density and affinity of renal V2 receptors and AVP-stimulated adenosine 3',5'-cyclic monophosphate production in the diabetic and diabetic+insulin animals were unchanged compared with the sham. These results demonstrate differential regulation of AVP receptors and suggest that downregulation of renal V2 receptors does not contribute to the polyuria of diabetes. In contrast, downregulation of V1 receptors might contribute to diminished V1 receptor-mediated biological responses to AVP seen in diabetes mellitus.

Animals↗