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

Perioperative and anesthetic management of a patient with a diabetes insipidus is reported. A 33 year old man was followed by physical therapy after spinal cord injury. At that time polyuria (4300-8600 ml.day-1) and polydipsia developed. His urine output was controlled by DDAVP (desmopressin) preoperatively. As the result of water restriction test and Carter-Robbins test the diagnosis of complete central diabetes insipidus was doubted preoperatively. We investigated the changes of his perioperative body fluids and endocrine responses. The following conclusions are made: 1) The diagnosis of this case is not renal and true diabetes insipidus, but is probably partial or transient diabetes insipidus. 2) These results indicate that endocrine examinations related to AVP secretion are essential.
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PMID:[Perioperative management of a patient with transient polyuria]. 143 56

The physiological osmoregulatory adaptations of pregnancy include decreased thresholds for both thirst and AVP secretion and increased MCR for AVP. The combined effects of these changes may unmask subclinical DI. In view of the altered relationship between serum osmolality and thirst, caution is required in investigating thirst and polyuria in pregnancy lest an erroneous diagnosis of psychogenic polydipsia be made.
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PMID:Osmoregulatory adaptation in pregnancy and its disorders. 173 61

Familial neurohypophyseal diabetes insipidus in humans is a rare disease transmitted as an autosomal dominant trait. Affected individuals have very low or undetectable levels of circulating vasopressin and suffer from polydipsia and polyuria. An obvious candidate gene for the disease is the vasopressin-neurophysin (AVP-NP) precursor gene on human chromosome 20. The 2 kb gene with three exons encodes a composite precursor protein consisting of the neuropeptide vasopressin and two associated proteins, neurophysin and a glycopeptide. Cloning and nucleotide sequence analysis of both alleles of the AVP-NP gene present in a Dutch ADNDI family reveals a point mutation in one allele of the affected family members. Comparison of the nucleotide sequences shows a G----T transversion within the neurophysin-encoding exon B. This missense mutation converts a highly conserved glycine (Gly17 of neurophysin) to a valine residue. RFLP analysis of six related family members indicates cosegregation of the mutant allele with the DI phenotype. The mutation is not present in 96 chromosomes of an unrelated control group. These data suggest that a single amino acid exchange within a highly conserved domain of the human vasopressin-associated neurophysin is the primary cause of one form of ADNDI.
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PMID:A missense mutation in the vasopressin-neurophysin precursor gene cosegregates with human autosomal dominant neurohypophyseal diabetes insipidus. 174 Jan 4

Nephrogenic diabetes insipidus is characterized by polyuria, hyposthenuria and compensatory polydipsia. With conventional clinical and laboratory examinations the diagnosis can be established and the differential diagnostic diseases excluded. In order to verify the diagnosis, differentiate the condition from central and nephrogenic diabetes insipidus and rule out psychogenic polydipsia, additional laboratory studies are required: of these, the concentration test, modified Carter-Robbins test and AVP stimulation test are described.
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PMID:[The diagnosis of nephrogenic diabetes insipidus in the dog]. 175 71

The antitumor drug celiptium (N2-methyl-9-hydroxyellipticinium) is an ellipticine derivative effective in experimental tumors and in man. The major side effect is nephrotoxicity. The impairment of renal function is studied in rats following a single i.v. dose of 20 mg/kg celiptium and a long-term study (day 2 to day 60). A loss of body weight is noted in celiptium-treated animals between day 4 and day 15, and recovery occurs between day 15 and day 60. Histologic study shows cortical lesions characterized by focal necrosis of proximal tubules without any glomerular, interstitial, and vascular alterations on day 8. It is to be noted that any medullary lesions were not shown. A polyuria and a decreased creatinine clearance are reported on day 8. We were interested in a special study of this polyuria. For this study, rats were water deprived between day 6 and day 8 following celiptium administration. The decrease of urinary osmolality is not recovered after dehydration and exogenous vasopressin derivative (dD AVP) does not correct the renal concentration defect. AVP plasma levels increase after dehydration. These results suggest a pitressino-resistant urinary concentrating inability in celiptium-treated rats.
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PMID:Nephrotoxicity of an ellipticine derivative (N2-methyl-9-hydroxyellipticinium acetate) in rat: a defect of urinary concentrating ability. 178 Apr 92

Lithium therapy is known to reduce the renal responsiveness to arginine vasopressin (AVP: the antidiuretic hormone in man) and a proportion of treated patients develop polyuria and polydipsia. In this study seven nonpolyuric female patients receiving lithium treatment for an affective disorder (lithium group) were age-matched with seven healthy females (control group). The mean response of plasma AVP to osmotic stimulation was significantly enhanced in the lithium group but the mean osmotic threshold for AVP release was unchanged. Thirst appreciation in the lithium group commenced and increased overall at an osmotic stimulus 5 mmol/kg less than the control group. It is suggested that primary thirst does play a role in the expression of lithium-induced polyuria.
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PMID:The effect of lithium therapy on arginine vasopressin secretion and thirst in man. 237 37

Sclerosing peritonitis is a serious complication in patients on long-term peritoneal dialysis; it markedly decreases transport of water and solute across the peritoneal membrane. Although the precise mechanism is unknown, organic compounds (i.e., plasticizers) from plastic tubing and dialysis bags have been suggested to be a cause of the syndrome. The effects of three such compounds on water and sodium transport in vitro were studied in the toad bladder. The compounds studied were didodecylphthalate, dioctylphthalate, and benzylbutylphthalate. After 4 hr incubation in vitro, dioctylphthalate and benzylbutylphthalate significantly inhibited vasopressin-stimulated water flow in toad bladder. Basal water flow was not affected by any of the three compounds. Sodium transport, as measured using short-circuit current, was decreased to an equivalent degree by all compounds; inhibition of short-circuit current was dose dependent and was approximately 30% at 10(-3) M. The onset of action was between 3.5 and 4 hr, and the effect on short-circuit current was not reversible. These results demonstrate that the plasticizers (to which patients of all sorts are commonly exposed) inhibit transport across living membranes. In the toad bladder these compounds decrease sodium transport and maximal water flow. Although other evidence suggests that the cumulative toxic effects of these compounds may play a causal role in sclerosing peritonitis in patients on peritoneal dialysis, our study suggests that chronic exposure to the phthalate acid esters in patients with normal renal function may result in sodium wastage, polyuria, and a concentrating defect resistant to AVP.
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PMID:Effect of phthalate acid esters on transport in toad bladder membrane. 255 Jun 21

This chapter reviews the pathophysiological basis for the mechanisms of polyuria and discusses the causes in detail. A small proportion of patients with CDI are of the idiopathic type, with the majority of causes due to trans-spenoidal surgery, head injury following road traffic accidents, and an autoimmune variant. Indirect methods of investigating polyuria are inaccurate in a significant proportion of cases, and the incorporation of measurements of plasma AVP into a water-deprivation test or hypertonic saline infusion can improve diagnostic accuracy. Non-osmotic tests of AVP secretion are of no value in the differential diagnosis of polyuria. Most patients with CDI can maintain water homeostasis with adequate fluid intake, but desmopressin is a convenient, effective and safe therapy which is recommended on both social and medical grounds. Treatment of NDI remains problematic, as neither thiazide diuretics or indomethacin can completely abolish polyuria, and fluid intake remains of primary importance.
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PMID:Polyuric states in man. 269 45

Two vasopressin antagonists, d(CH2)5[Tyr(Me)2]AVP and dP[Tyr(Me)2]AVP, were given to Wistar rats from postnatal day 1 to 21 in order to investigate the influence on development and later diuresis. The latter antagonist significantly reduced body growth from day 3 postnatally onwards. At postnatal day 35 body, total brain, cerebellar and kidney weights were significantly reduced compared with controls. Diuresis, measured at one month of age, was four- to five-fold higher than the control group. Combined treatment with vasopressin failed to abolish the weight disturbances or polyuria. However, animals treated with the vasopressin antagonist d(CH2)5[Tyr(Me)2]AVP did not show developmental or diuretic deficits. Allometric analysis of brain/body relationship of the young animals indicated a disturbance of brain development by dP[Tyr(Me)2]AVP. Although the body and brain growth retardation induced by dP[Tyr(Me)2]AVP supports the hypothesis of a role for vasopressin in brain ontogeny, it can also be the result of a nonAVP-related toxic effect, since it could not be prevented by concomitant treatment with vasopressin.
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PMID:Neonatal treatment with vasopressin antagonist dP[Tyr(Me)2]AVP, but not with vasopressin antagonist d(CH2)5[Tyr(Me)2]AVP, inhibits body and brain development and induces polyuria in the rat. 322 74

The induction of selective renal medullary damage by 2-bromoethylamine hydrobromide (BEA) results in polyuria and raised blood pressure. In view of the likely elevation of plasma vasopressin we have investigated the role of vasopressin (AVP) in the elevated blood pressure in this model. Plasma vasopressin levels in BEA pretreated rats were raised significantly (2 +/- 0.6 pg/ml vs 0.8 +/- 0.1 in normal rat, P less than 0.05) but not to pressor levels. In addition, pressor responsiveness was investigated in renal medullary damaged rats. There was a reduced response to vasopressin and noradrenaline but no alteration with angiotensin II. A specific V1, receptor AVP antagonist [d(CH2)5Tyr(Me)AVP] produced no fall in blood pressure but returned the noradrenaline dose-response curve to normal. This suggests an interaction between vasopressin and the sympathetic nervous system in this model. Thus there is no evidence that vasopressin contributes to the rise in blood pressure produced by chemical renal medullectomy and other mechanisms have to be sought.
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PMID:Selective renal medullary damage and hypertension in the rat: the role of vasopressin. 352 50


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