UMLS:C0032617 - FACTA Search

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

The interaction between moderate salt depletion and urinary excretions of prostanoids (PGE2,6-keto-PGF1 alpha and TxB2), as well as the effective role of the activated renin-angiotensin system (RAS), in the control of renal function and urinary prostanoid excretions have been investigated in healthy women. Salt depletion (SD, n = 8) was induced by low sodium chloride dietary intake (< or = 60 mmol per day) and combined treatment with natriuretic and potassium sparing drugs. The cumulative sodium deficit was 381 +/- 55 mmol. The renal function and urinary excretion of prostanoids were evaluated during hypotonic polyuria (oral water load) and subsequent moderate antidiuresis (lysine-8-vasopressin (LVP) low-dose infusion). Basal plasma renin activity (PRA) and urinary aldosterone excretion were determined, before the water load, in both the SD group and control studies in normal balance of sodium and potassium (N, n = 20). Paired studies were performed in the absence and in the presence of enalapril in the same SD group, as well as in a subgroup, with normal sodium and potassium balance, previously studied (N3, n = 6). In the SD vs. N group, significantly higher values of PRA and urinary aldosterone excretion were found. The renal antinatriuretic mechanism was activated and the diuretic response to water load depressed. During polyuria, the urinary 6-keto-PGF1 alpha and TxB2 excretions were significantly higher, probably reflecting an increase in the renal synthesis of their precursors. During the late LVP infusion, the urinary PGE2 excretion was also significantly increased, in absence of significant differences in urinary flow rate. In both SD and N3 groups, enalapril decreased the mean arterial pressure (MAP). Despite the decrease in MAP, not significantly different in SD vs. N3 group, the drug did not significantly affect the creatinine clearance. Also, the urinary prostanoid excretions were not significantly affected by enalapril. However, in the SD group, but not in the N3 group, the drug was effective in significantly decreasing the absolute and fractional excretions of sodium and chloride. Moreover, the plasma potassium concentration significantly decreased, despite the concurrent decrease in urinary potassium excretion. The data suggest that: (1) in salt depletion, the prostanoid release from the renal cortical structures was stimulated; (2) the renal prostanoid synthesis, either activated (sodium depletion) or not (normal sodium and potassium balance), was not affected by the RAS pharmacological blockade in the short-term; (3) in salt depletion, the RAS blockade recruited a homeostatic mechanism responsible for the improved renal salt conservation, as well as for the redistribution of potassium between the extra- and intra-cellular compartments.
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PMID:Effective role of the renin-angiotensin system in the control of prostanoid synthesis and renal function in healthy women with moderate salt depletion. 886 76

Polyuria is an important symptom or sign because of its potential severity, diverse causes, and interesting pathophysiology. Whereas polyuria induced by water diuresis is reasonably well understood and easily recognized by clinicians, that produced by solute diuresis is more likely to cause confusion. In this article, we focus on solute diuresis as a cause of polyuria, review the classification and pathophysiology of polyuria, and describe the clinical and laboratory studies useful for the evaluation of the polyuric patient. A stepwise, logical approach is provided (1) to determine whether a patient has a water diuresis, a solute diuresis, or both (concurrently), and (2) if a solute diuresis is present, to determine if it is caused by electrolytes (eg, sodium chloride sodium bicarbonate), by nonelectrolytes (eg, glucose, urea), or by both. How to assess these possibilities and to determine the specific cause of the diuresis is discussed in detail. Three representative case examples are provided. Selected causes of a solute diuresis also are reviewed.
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PMID:The polyuria of solute diuresis. 912 3

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.
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PMID:Effects of experimental salt depletion on urinary prostanoid excretions in normal women. 961 Aug 48

This baby boy was born after a pregnancy complicated by severe polyhydramnios at a gestational age of 28 weeks. Analysis of the amniotic fluid had shown a high chloride content, but normal concentrations of sodium, potassium, and calcium. After birth he displayed extreme polyuria, severe renal sodium and chloride loss, and marked hypercalciuria. Five weeks after birth, his sodium chloride loss turned into renal potassium loss, along with a marked decrease in urine output. All these features are characteristic of the neonatal variant of Bartter syndrome. He was discharged after 11 weeks with oral supplements of sodium chloride, potassium gluconate, and 500 ml of fluid. The follow-up for a period of 6 years showed a surprising evolution: he has no hypokalemic alkalosis, no polyuria, and no hypercalciuria; growth and development are within the normal ranges and, at the time of writing, he is a healthy boy needing no medication and with no medical problems whatsoever.
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PMID:Neonatal Bartter syndrome: spontaneous resolution of all signs and symptoms. 963 34

The effective role played by prostanoids in the control of renal function has been investigated in healthy women with salt depletion. Salt depletion (SD2 group, n = 6) was induced by low sodium chloride dietary intake (< or = 60 mmol per day) and combined treatment with natriuretic and potassium-sparing drugs. At the end of the depletive treatment, the cumulative sodium deficit was 513 +/- 56 mmol. The renal function and urinary excretions of prostaglandin (PG) E2, 6-keto-PGF1 alpha (6KPGF) and thromboxane (Tx) B2 were evaluated during hypotonic polyuria. The basal values of plasma sodium and potassium concentrations, plasma renin activity (PRA) and urinary aldosterone excretion were determined before the induction of hypotonic polyuria. Paired studies were performed in the absence (control) and presence of indomethacin both in the SD2 group and in a previously studied group (N2, n = 6) of healthy women in normal sodium and potassium balance. Women in normal balance received 100 mg i.m. of indomethacin, salt-depleted women received only 50 mg (because 100 mg of the drug produced a prolonged anuria). In the SD2 vs. N2 group in the absence of treatment the following significant differences were found: (a) higher basal values of PRA and urinary aldosterone excretion; (b) higher urinary excretions of 6KPGF and TxB2 but not of PGE2; (c) lower values of urinary flow rate, creatinine clearance, absolute and fractional excretions of sodium and chloride, plasma osmolality and plasma electrolyte concentrations. The effects of the indomethacin have been assessed as percentage variations by using paired data for each experimental group. In the SD2 vs. N2 group the reduction in urinary excretions of 6KPGF, TxB2 and potassium as well as in creatinine clearance were not significantly different. On the other hand, the following were significantly different: (a) the lower reduction in PGE2 excretion; (b) the higher reduction in urinary flow rate and in CH2O; (c) the reductions in absolute and fractional excretions of sodium and chloride, and the increase in plasma potassium concentration, significant in the SD2 group but not in the N2 group. The data suggest that: (1) when stimulated by salt depletion the renal biosynthetic pathways of PGI2 and TxA2 showed greater sensitivity to indomethacin inhibition; (2) the effects of the neurohormonal systems activated by salt depletion were either modulated or mediated by renal prostanoids.
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PMID:Renal prostanoids: physiological relevance in healthy salt-depleted women. 1006 64

The acute effects on urinary prostanoid excretion and on renal function induced by pharmacological inhibition of either the angiotensin-converting enzyme or of the cyclooxygenase system, respectively, have been studied in healthy salt-depleted women. Two experimental groups were studied during salt depletion, SD1 (n=8) and SD2 (n=6). Salt depletion was obtained by combining a low sodium chloride dietary intake (< or =60 mmol per day) with natriuretic and potassium sparing treatment. Paired studies were performed in the absence and in the presence of enalapril (SD1 group) or indomethacin (SD2 group). In both paired studies renal function was estimated by the clearance (cl.) method and the urinary concentrations of PGE2, 6-keto-PGF1alpha and TXB2 were estimated by RIA during sustained hypotonic polyuria (induced by oral water load). Enalapril did not influence urinary excretion of prostanoids. Its main significant effects were: (a) a reduction in mean arterial pressure (MAP); (b) an increase in free-water cl. (C(H2O)) and a reduction in osmolar cl. (Cosm); (c) a reduction in the absolute and fractional urinary excretions of sodium and chloride; and (d) a reduction in both the plasma concentration and urinary excretion of potassium. The urinary flow rate and the creatinine cl. were not significantly affected. Indomethacin reduced urinary excretion of prostanoids and in addition it produced the following significant effects: (a) a reduction in urinary flow rate, C(H2O) and Cosm values, and in absolute and fractional urinary excretions of sodium and chloride; and (b) an increase in plasma potassium concentration. MAP, creatinine cl. and urinary potassium excretion were not significantly affected. With regard to the main parameters, both enalapril and indomethacin exerted similar effects on urinary sodium and chloride excretion but opposite effects on C(H2O) and plasma potassium concentration. In conclusion, after enalapril in a salt-depleted state, the functional expression of acute angiotensin II deprivation was partially masked by the activation of a homeostatic system responsible both for improvement in renal salt conservation and for facilitated cellular potassium uptake. After indomethacin in the same setting, the results were consistent with a differential role of prostanoids in modulating or mediating the activities of neuro-hormonal agonists.
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PMID:Renal function and urinary prostanoid excretions in salt-depleted women: comparative effects of enalapril and indomethacin treatments. 1032 27

We present the eldest case ever reported of central diabetes insipidus (DI) associated with infundibulo-neurohypophysitis. A 77-year old woman, who complained of recent development of excessive thirst, polyuria and polydipsia, was referred to our hospital. The daily urine volume was markedly increased to 6 L. DDAVP administration effectively reduced urine volume and increased urine osmolality. The loading test using high-osmolar sodium chloride showed impaired excretion of vasopressin discordant with plasma osmolar changes. The anterior pituitary function was normal. Pituitary magnetic resonance imaging (MRI) showed thickening of the pituitary stalk and a lack of high-intensity signal of the neurohypophysis on T1-weighted images, suggestive of lymphocytic infundibulo-neurohypophysitis. The thickness of pituitary stalk on MRI improved 6 months later. DI was controlled with DDAVP for 40 days. This was followed by stabilization of the daily urine volume to less than 2.5 L without DDAVP. Our case is the eldest case of central DI associated with infundibulo-neurohypophysitis. The rapid remission of pituitary changes on MRI provides an insight that spontaneously partial remission of central DI may occur, resulting in transient polyuria and polydipsia.
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PMID:An elderly patient with transient diabetes insipidus associated with lymphocytic infundibulo-neurohypophysitis. 1067 Jul 63

Endotoxin (lipopolysaccharide; LPS) and mercury are nephrotoxic compounds of food safety concern. Endotoxin is a product of cell walls of gram negative bacteria. Humans are constantly exposed to LPS through food, water and air. Food is the main source of mercury exposure for humans. Endotoxin potentiates the toxicity of a number of xenobiotics, but its interaction with nephrotoxic heavy metals has not been investigated. We tested the hypothesis that endotoxin enhances mercury-induced nephrotoxicity. Thirty-two, 41-43-day-old, male Sprague-Dawley rats were allocated randomly to four groups of eight rats each as follows: group I received 0.9% sodium chloride, group II received 2.0 mg of Escherichia coli 0128:B12 LPS kg(-1) once, group III received 0.5 mg mercuric chloride kg(-1) once, and group IV received 2.0 mg E. Coli 0128:B12 LPS kg(-1) once 4 h before receiving 0.5 mg mercury chloride kg(-1) once. Mercury, LPS and 0.9% sodium chloride were all injected IV through the tail vein. Rats were monitored for 48 h after mercury injection. Serum creatinine, urea nitrogen, and polyuria were significantly increased in rats given LPS plus mercury relative to those given either agent alone or saline (P</=0.05). The most severe morphologic lesions were found in rats given LPS plus mercury, which also had significantly greater renal mercury concentration than those given mercury alone (P < or = 0. 05). In conclusion, LPS potentiated mercury-induced nephrotoxicity.
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PMID:Potentiation of mercury-induced nephrotoxicity by endotoxin in the Sprague-Dawley rat. 1096 5

Pregnancies with fetuses affected with the Bartter syndrome, an autosomal recessive disorder of hyperreninism and hyperaldosteronism, are complicated by early onset of polyhydramnios which results in preterm deliveries. We have assessed biochemical changes in amniotic fluid and the mother's blood with a view to early diagnosis. Aldosterone levels of both amniotic fluid and the mother's blood were found to be increased at 27 weeks of gestation, while electrolyte levels did not differ significantly from those reported earlier for controls. After birth the baby suffered from polyuria with hyponatremia, hypomagnesemia and hypercalciuria which could be controlled by treatment with sodium chloride and magnesium. Elevated aldosterone thus might be a useful marker for early diagnostic purposes.
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PMID:Elevated aldosterone in amniotic fluid and maternal blood has diagnostic potential in pregnancies complicated with a fetus of Bartter syndrome. 1626 Aug 79

Lesions in the median eminence (ME) produce a well-known neurological model of polydipsia and polyuria in rats. The effect of food availability (ad lib/deprivation) on the polydipsic/polyuric behaviour of animals was tested. As expected, all lesioned rats developed strong polyuria and polydipsia during the first postoperative 24h. This effect was maintained during day 2 when food was available ad lib (experiment A), but both polyuria and polydipsia were abolished when animals were deprived of food during the next 24h (day 3). Animals deprived of food from the first post-operative day (experiment B) showed a significant reduction in the initial polyuria and polydipsia (day 1) on day 2, but these effects were again observed on day 3 when food was available ad lib. Finally, when food-deprived animals were able to choose between a 1.5% sodium chloride solution and water (experiment C), they preferentially chose (82% of total liquid consumed) the hypertonic saline solution (day 1); during the next 24h (day 2), when only water was available, the polyuric/polydipsic effect was abolished but returned when food became available ad lib on day 3. Hence, the polyuria/polydipsia effect produced by ME lesions appears to be consistent during the first 24h but might later be related to the availability of standard food and is completely abolished under food deprivation conditions. Preference for the hypertonic solution supports the volemic component of this syndrome and demonstrates the need for appropriate amounts of hypertonic nutrients to be consumed during the first 24h.
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PMID:NaCl preference and water intake effects of food availability in median eminence polydipsia. 1883 6

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