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Query: UMLS:C0032617 (polyuria)
 3,056 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diffusional and osmotic water permeability of collecting ducts in isolated papillae of rats' kidneys were measured in papillae taken from normal and lithium pretreated rats. The diffusional water permeability of collecting ducts in papillae from normal rats in the absence of ADH was 4.1 +/- 0.2 (S.E.M.) (n = 18) muM s-1 increasing to 7.2 +/- 0.6 mum s-1 with ADH. Values obtained with lithium (10 mM) in the medium, perfusate or both and in papillae taken from lithium pretreated rats did not differ significantly from the above. The cyclic AMP content of the papillae taken from normal rats was 83 +/- 6 pm mg protein in the absence of ADH and increased to 196 +/- 12 (n = 13) with 500 mu units ml-1 ADH. Lithium 10 mM in the medium did not alter this response. Papillae from lithium pretreated rats had a similar basal level of cyclic AMP but the increment in a lithium (10 mM) medium after ADH was significantly less. These results indicate that the impaired water handling of lithium treated rats is probably not due to a failure of the membrane to increase its permeability to water after ADH. Though lithium does alter the production of cyclic AMP this is not believed to be important regarding any alteration in water permeability. We believe it is probable that lithium interferes with sodium chloride transport at some more proximal nephron segment thereby producing the syndrome of polyuria.
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PMID:The effect of lithium on the permeability response induced in the collecting duct by antidiuretic hormone. 18 85

A large radiodense calculus in the left renal pelvis of a 22-month-old, male Great Dane disappeared one month following surgical removal of two struvite (magnesium ammonium phosphate) calculi from the right renal pelvis. The dog's urine likely became undersaturated with struvite for a sufficient period to permit dissolution of the renal calculus. Several factors may have contributed to the decrease in urine struvite concentration, including eradication of a urease-producing Proteus sp from the urinary tract and induction of polydipsia and compensatory polyuria by oral administration of sodium chloride.
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PMID:Dissolution of a struvite nephrolith in a dog. 43 42

Polyuria in a herd of forty-five dairy cattle was the chief complaint in the first case. Polydipsia was the principle sign in a second case involving one dairy cow. Less conspicuous clinical findings included salt hunger, pica, weight loss and decreased milk production. Clinicopathologic investigation included monitoring the concentrations of sodium, potassium and chloiride in urine, parotid saliva and plasma. These analyses indicated a primary sodium deficiency which responded to sodium chloride ad libitum.
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PMID:Salt (sodium) deficiency in dairy cattle: polyuria and polydipsia as prominent clinical features. 123 30

Lithium administration raises the minimum sodium requirement of the organism. Lithium treated-rats drink spontaneously a hypertonic sodium chloride solution and thereby protect themselves against the toxic effects of lithium. In the present paper it was studied whether the consumption of sodium chloride can be used as a quantitative measure of the sodium requirement. Rats given different amounts of lithium with food for about 2 months were given free access to water and a 0.46 M NaCl solution, and the 24-h intake of the latter was followed. It was found that the consumption of hypertonic sodium chloride increased with the lithium dosage and the serum lithium level. The consumption showed the following characteristics: (a) It was sufficient to prevent death from lithium poisoning. (b) When access to hypertonic chloride was discontinued for 48 h, the rats lost body weight; the body weight was reestablished within 1 h when the rats again had access to sodium chloride solution. (c) When sufficient amounts of sodium were given with the food, the lithium-treated rats drank no more sodium chloride solution than did the control rats. (d) When lithium administration was discontinued, the consumption of sodium chloride solution fell within 10 days to the control level. (e) The lithium-treated rats developed polyuria, but this was not the cause of the extra intake of sodium chloride. (f) The lithium-treated rats did not drink more of the hypertonic sodium chloride solution than was necessary to cover the minimum sodium requirement. The results indicate that the intake of hypertonic sodium chloride solution can, in fact, be used as a measure of the minimum sodium requirement in lithium-treated rats.
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PMID:Current determination of lithium-induced minimum sodium requirement in rats. 125 Sep 44

I. Time has come to distinguish "Bartter syndrome" from "Bartter disease". The latter is an autosomal recessive renal tubulopathy which manifests itself mostly during infancy and childhood. II. Bartter disease is caused neither by a primary renal potassium loss nor by a primary renal hyperprostaglandinism. All evidence is in favor of a defect in the chloride pump located at the thick ascending limb of Henle's loop. III. The most severe expression of Bartter disease is its neonatal form which is characterized by polyhydramnios, premature delivery and a life threatening sodium chloride loss during the early weeks of life. It takes several weeks before sodium wasting turns into renal potassium wasting. IV. Polyhydramnios not associated with echographically detectable fetal malformation is highly suggestive of Bartter disease. Prenatal diagnosis is based on the combination of fetal polyuria and elevated chloride in the amniotic fluid. V. In this setting the administration of indomethacin is useless and even dangerous from the 32nd week of gestation on. Similarly, indomethacin should not be given to the newborn Bartter patient for the first weeks and months of life. Treatment at that stage consist mainly of the administration of large amounts of fluid and sodium chloride. VI. Indomethacin can be used as soon as children with Bartter disease stop growing normally and preferably after the age of 18 months when kidney maturation is established. The daily dose should not exceed 2.5 mg/kg body weight. VII. Hypercalciuria is part of (the neonatal form of) Bartter disease and it is so severe that nephrocalcinosis seems to be the rule. This hypercalciuria is the direct consequence of the chloride reabsorption defect in Henle's loop. Research is needed to find an adequate solution to this problem.
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PMID:[The neonatal form of Bartter's syndrome: current findings in etiology and physiopathology]. 141 86

A male preterm infant of 32 weeks of gestation with history of severe polyhydramnios during pregnancy presented soon after birth with polyuria with initial sodium chloride loss subsequently followed by increasing potassium loss. After manifestation of hypokalaemia, hypochloraemia, alkalosis and high urinary prostaglandin concentrations, the diagnosis of the neonatal variant of Bartter's syndrome was made. The treatment consisted of administered of large amounts of fluid with sodium chloride and potassium supplementation and indomethacin (1.5 to 2 mg/kg per day).
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PMID:[Neonatal variant of Bartter syndrome]. 161 56

The protective effect of acetazolamide or sodium chloride loading on cisplatin nephrotoxicity was investigated in rats. After a single dose of cisplatin (5 mg kg-1 i.p.) kidney function was studied after 5, 28 and 84 days. Acetazolamide (75 mg kg-1 i.p.) was administered as a single dose prior (30 min) to the cisplatin injection. By the time of cisplatin administration, the rats were sodium depleted except the sodium-loaded group. Five days after the cisplatin administration all rats received a regular rat chow for the rest of the experiment. Cisplatin alone caused renal failure that could be observed for up to 12 weeks (ClCr 0.32 +/- 0.13 vs. 0.62 +/- 0.06 ml min-1 x 100 g BW-1) with polyuria (UVol 41.2 +/- 4.5 vs. 18.4 +/- 4.6 ml 24 h-1). Pretreatment with acetazolamide was the most protective manoeuvre tested. Five days after cisplatin, kidney function was significantly better than in rats treated with cisplatin alone (ClCr 0.21 +/- 0.06 vs. 0.03 +/- 0.01 ml min-1 x 100 g BW-1), after 28 days the only sign of nephrotoxicity was polyuria (UVol 28.9 +/- 3.7 vs. 19.0 +/- 2.6 ml 24 h-1) after 84 days no differences could be observed at all. Sodium chloride loading was less protective on cisplatin nephrotoxicity. Impaired renal function could still be observed after 12 weeks (ClCr 0.41 +/- 0.05 vs. 0.62 +/- 0.06 ml min-1 x 100 g BW-1) with no difference in comparison with the rats treated with cisplatin alone. However, since 12 rats died in the group having received cisplatin alone and only one rat in the high-salt group, sodium chloride loading is regarded as being advantageous over sodium depletion on cisplatin nephrotoxicity.
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PMID:Long-term effects of acetazolamide and sodium chloride loading on cisplatin nephrotoxicity in the rat. 211 87

Authors describe the simultaneous occurrence of ascites due to liver cirrhosis and diabetes insipidus in a patient with consistently normal urine volume. The diagnosis of diabetes insipidus has been proved by the water deprivation test combined with the administration of dDAVP as well as by serial determinations of plasma arginine vasopressin levels before and during infusion of hypertonic sodium chloride solution. Authors discuss the differential-diagnostic difficulties of the case and consider the mechanisms playing a role in the abolishment of diabetic polyuria by hepatic disease.
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PMID:Simultaneous occurrence of diabetes insipidus and ascites due to liver cirrhosis: clinical and pathophysiological studies. 224 24

The effect of lithium administration on urine eletrolyte excretion is controversial with reports of increased, unaltered and reduced excretion rates of sodium, potassium, calcium, magnesium and inorganic phosphate. Therefore rats treated with daily intraperitoneal lithium chloride for 3 weeks were studied and were found to have marked fluctuations in electrolyte excretion when compared to untreated rats. Although lithium-treated rats were always polyuric, urinary sodium, potassium and calcium excretion was significantly elevated immediately following intraperitoneal lithium but their excretion rates then returned towards normal. Magnesium excretion was initially unaltered by lithium administration (6.8 +/- 1.3 compared with 7.3 +/- 1.7 mumol/100 g/8 h) but then decreased (2.5 +/- 0.5 with 7.8 +/- 1.1 mumol of magnesium/100 g/8 h; p less than 0.01) during the final collection period. A persistent phosphaturia also occurred with lithium treatment (122 +/- 5 compared with 92 +/- 6 mumol/100 g body weight/24 h). Despite these significant changes in renal electrolyte transport with lithium administration, similar changes were also noted in rats similarly treated with equimolar doses of sodium chloride although polyuria did not occur. Thus it is postulated that lithium ions exert their effect on renal electrolyte transport in a similar manner to that of sodium.
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PMID:Lithium administration and urinary electrolyte excretion in the rat. 632 37

Nephrogenic diabetes insipidus (NDI) occurred in a 43-year-old woman who had received lobenzarit disodium for the treatment of rheumatoid arthritis (RA). Her urine output was initially 3 l/day and urine osmolarity was 203 mOsm/l. Based on a sodium chloride loading test and a vasopressin loading test, she was diagnosed as having lobenzarit-induced NDI. Seven days after the cessation of the use of lobenzarit disodium, polydipsia and polyuria disappeared, and the vasopressin test showed a normal response. These findings suggest that lobenzarit induces a reversible form of NDI as a side effect. The reports of lobenzarit-induced NDI in Japan during the past seven years are also reviewed.
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PMID:Nephrogenic diabetes insipidus induced by lobenzarit disodium treatment in patients with rheumatoid arthritis. 868 99


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