Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032617 (polyuria)
 3,056 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fluid management and assessment of organ perfusion in organ donors with hypotonic polyuria remain poorly investigated problems. In our protocol, urinary losses (565 +/- 202 ml/h) were replaced volume for volume by 3.3% dextrose/0.3% natrium chloride solution (Baxter) with 20 mmol/l potassium chloride. Concentrated red blood cells were administered to maintain hematocrit at about 30%, and volume expansion (central venous pressure above 6 mmHg) was obtained by gelatin (haemaccel) infusion. In all donors (n = 9), plasma electrolytes remained within normal limits despite hypotonic polyuria. Suppression of initial plasma renin activity (PRA: 9.7 +/- 3.6 ng/ml per hour) was obtained by subacute volume expansion. In eight donors the hemodynamic status improved, dopamine administration, when used, was discontinued, and PRA decreased (2.3 +/- 0.7 ng/ml per hour; P less than 0.05). The only donor who failed to respond to fluid therapy had increased PRA (24.2 ng/ml per hour). During fluid challenge, an inverse relationship was demonstrated between mean arterial pressure and PRA in all nine donors (r = -0.61; P less than 0.001), while there were no significant changes in blood urea. creatinine, or urine output. It is concluded that in organ donors, proper maintenance of the hemodynamic status and suppression of the renin stress response may be obtained by an adequate fluid management, involving both qualitative restoration and expansion of intravascular volume.
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PMID:Fluid management and plasma renin activity in organ donors. 267 27

The renal function was evaluated by clearance (cl.) method during hypotonic polyuria and successive relative antidiuresis induced by lysine-8-vasopressin (LVP) administration. Four 15 min and two 60 min cl. periods were performed during hypotonic polyuria and antidiuresis, respectively. Glomerular filtration rate was estimated by creatinine cl.; the osmotic cl. (Cosm'CH2O), the absolute and fractional excretions of water, sodium, potassium and chloride were determined by usual methods. The urinary PGE2, 6-keto-(-)PGF1 alpha and TxB2 concentrations were determined by RIA method. The study protocol was applied on 22 healthy women in acute potassium depletion obtained by natriuretic treatment combined with replacement on quantitative basis of net salt and water urinary losses either in normal potassium diet intake (50 meq/d) or in a low one (less than or equal to 10 meq/d). In Group D3 (n = 6) in the presence of a greater potassium cumulative deficit (198.4 +/- 22.2 meq), as compared to normal potassium balance, a significant reduction of kaliemia and a significant increase of PRA were present. During hypotonic poliuria, besides a marked renal potassium conservation, a significant decrease of creatinine cl., fractional chloride reabsorption (apparently at the diluting segments) and of urinary 6KPGF and TxB2 excretions, were observed. Urinary PGE2 excretion was n.s. reduced.
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PMID:[Further research on the role of prostanoids in controlling renal function in humans in normal potassium balance and acute experimental potassium depletion. II: Studies of potassium depletion]. 275 83

A 23-yr-old male patient with normotensive primary aldosteronism is reported. He complained of muscle weakness, polydipsia, and polyuria. His blood pressure was generally 118/60 to 124/70 mm Hg. Serum sodium, potassium and chloride were 152.2.2, and 108 meq/liter, respectively. Arterial blood pH, glomerular filtration rate, renal plasma flow and circulating plasma and blood volumes were normal, and plasma bicarbonate was normal or elevated. PRA was 0.16 ng/ml.h and did not increase significantly after sodium deprivation, ambulation, and iv furosemide injection. Plasma aldosterone was 64.1 ng/100 ml. He showed pressor responses to infused angiotensin II and norepinephrine which were similar to those in normal men. Adrenal scintiscanning after iv injection of [131I]6 beta-iodomethyl-19-nor-cholesterol during dexamethasone administration showed dense uptake on the right adrenal and minimal uptake on the left. Intravenous infusion of angiotensin III at a rate of 20 ng/kg. min for 30 min did not cause an increase in plasma aldosterone. Serum electrolytes became normal after spironolactone but not after dexamethasone. At surgery, the right adrenal, bearing a benign adenoma, was removed. After surgery, blood pressure was unchanged, but all biochemical abnormalities disappeared. The cause of this normotension remains to be elucidated, but the diagnosis criteria of primary aldosteronism should now be partly modified.
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PMID:Normotensive primary aldosteronism: report of a case. 626 53

In 7-week-old male, spontaneously hypertensive rats (SHR) and matched normotensive control rats, Wistar Kyoto Rats (WKY), a bilateral renal denervation was performed. In two additional groups of rats a sham denervation was done (SHRS, WKYS). The animals were then kept in metabolic cages during a 10-day period during which sodium intake, urine volume, urinary sodium excretion, fecal sodium excretion, urinary aldosterone excretion and plasma renin activity were determined. Fractional urinary excretion of sodium was higher in the denervated SHR (p less than 0.1) and WKY (p less than 0.05) during the first 3 days after denervation, but during the following 3-day periods no difference between denervated and sham-operated groups was noted. The difference in fractional urinary excretion of sodium initially was due to a diminished urinary sodium excretion in the sham-operated groups since both SHRS and WKYS exhibited a significant increase between the first and the last 3-day period. Urine volume increased significantly in both SHR and WKY after denervation. Urinary aldosterone excretion on the 7th day after denervation was significantly lower in SHR compared to WKY, but there was no significant difference between the denervated and sham-operated groups. PRA was also significantly lower in SHR but no significant decrease was seen after denervation.
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PMID:Renal denervation and sodium balance in young spontaneously hypertensive rats. 686 67

Criteria for the screening, diagnosis and therapy of primary aldosteronism (PA) were defined on the basis of its symptoms analysis in 40 PA patients. A diagnosis of PA was proved in 4.12% of 970 patients admitted for arterial hypertension. The presence of polyuria, nocturia, neuromuscular disorders, hypertension, hypopotassaemia, alkalosis, elevated urinary potassium excretion, improving after Spironolactone, was most valuable for the purposes of screening. High plasma aldosterone concentration (PAC) and suppressed renin activity (PRA) provided evidence of the presence of PA. The most successful technique to differentiate aldosterone producing adenoma (APA) from idiopathic hyperaldosteronism (IHA) proved to be adrenal phlebography combined with determination of PAC in the adrenal veins. APA was associated with a 5.9 fold higher PAC in the vein of the adenoma - affected adrenal in contrast with a symmetric PAC rise in both adrenal veins in IHA. A paradoxical decrease of PAC occurred in the peripheral blood of most patients with APA after standing up, but 23.8% exhibited the same orthostatic increase as IHA patients. In all APA patients, unilateral adrenalectomy eliminated the symptoms of hyperaldosteronism and improved or cured hypertension. Spironolactone was indicated preoperatively for all surgical candidates, for non-operated APA patients, and for all IHA patients.
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PMID:Primary aldosteronism -- screening, diagnosis and therapy. 702 94

In healthy women we have studied the effects of potassium depletions of different degrees on the generation of some bioregulators of hydro-saline balance. The study has been performed on 20 women in normal potassium balance (N group) and 20 women submitted to potassium depletive treatment by dietary and pharmacological means. On the basis of different patterns of treatment we have obtained three groups i.e. KD1 (n = 8), KD2 (n = 6) and KD3 (n = 6) with potassium cumulative deficit of 160 +/- 43, 198 +/- 22 and 214 +/- 54 mmol, respectively. The renal function was assessed by the clearance method during induced hypotonic polyuria and subsequent moderate antidiuresis induced by low dose infusion of lysine-8-vasopressin. The urinary PGE2, 6-keto-PGF1 (6KPGF) and TxB2 were determined by the RIA method. Moreover, the basal PRA and urinary aldosterone were determined before the renal functional exploration. The data obtained in both KD2 and KD3 groups where renal hypokalemic dysfunctions occurred--indicate that hypokalemia stimulated renin secretion and inhibited the reactivity of renal prostanoid production to the polyuric stimulus. However, in the KD3 group--where the circulating levels of renin, and probably of angiotensin II were the highest--the hypokalemic depression of the synthesis of 6KPGF and TxB2 precursors was attenuated while the synthesis of PGE2 was still inhibited.
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PMID:Studies on renal function in healthy women with different degrees of induced potassium depletion. 1) Hormonal changes relevant to salt and water balance. 815 5