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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of raised plasma renin and angiotensin-II concentrations in the development of acute renal failure in man was examined in patients in shock from various causes and in patients in whom hypotension was used to promote haemostasis. Ten of the thirteen patients in shock had raised angiotensin-II concentrations in peripheral blood and acute renal failure manifested by oliguria, increasing serum-creatinine, a urine osmolality of less than 400 mos-mol/kg and a urine/plasma osmolality ratio of less than 1-5. Although patients who were hypotensive for periods of 1 h 45 min to 4 h to promote haemostasis during surgery had similarly raised plasma-renin activity and angiotensin-II concentrations in peripheral venous blood, they did not have acute renal failure. It is concluded that high plasma-angiotensin-II concentrations do not explain the pathogenesis of acute renal failure in patients in shock.
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PMID:Plasma renin and angiotensin II in acute renal failure. 6 36

In 19 patients with acute renal failure the plasma renin activity and aldosterone were determined in the phase of anuria and oliguria. A highly increased plasma renin activity was found while aldosteronemia was only moderately raised. No significant correlation was demonstrated between plasma renin activity and aldosterone while a negative correlation was found between aldosteronemia and plasma sodium and bicarbonates concentrations. Lack of significant correlation between plasma renin activity and aldosteronemia in cases of acute renal failure suggests that factors other than renin participate in the regulation of aldosterone secretion in these patients.
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PMID:Aldosteronemia in patients with acute renal failure. 18 68

After a minor abdominal traumatism, M. B., 53 years of age, presents a sudden and acute edematous syndrome. Cardiac, renal, hepatic, nutritional and thyroid etiologies ares rapidly eliminated. A cavography and lymphography reveal the integrity of the drainage pathways. The idiopatic cyclic edematous syndrome is therefore evoked by few clinical details (diurnal weight gain, diurnal oliguria...). Exploration of the renin - angiotensin - aldosterone system, the Landis test and the marked radioactive serum albumin test attest to the exaggeration of capillary permeability. Likewise, it was discovered in this patient, a Klinefelter syndrome which was, until now, unknown. This case poses interesting pathogenic problems since the idiopathic cyclic edematous syndrome is a predominantly feminine disease. Only a few cases were described in the masculine sex and, to our knowledge, this syndrome has never been associated with Klinefelter syndrome.
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PMID:[Idiopathic cyclic edema in Klinefelter syndrome (author's transl)]. 22 26

Urinary renin activity (URA) was measured by radioimmunoassay in sequential studies of 5 patients with acute renal failure (ARF) and in 13 normal volunteers. URA was elevated during the oliguric phase of ARF and fell to low levels prior to resolution of oliguria. Plasma renin activity (PRA) varied approximately in response to changes in intravascular volume status. In normal volunteers, the very low URA values did not change following furosemide-induced increases in PRA. A simple, rapid, and accurate method is described for the measurement of URA in humans by radioimmunoassay of angiotensin I generated during incubation of urine with homologous plasma substrate. The urinary enzyme exhibited the same properties as purified human renal renin and the incubation product appeared identical to angiotensin I standard. Renin activity in urine was directly proportional to enzyme concentration and no evidence was obtained for interference from other proteolytic activities or from inhibitors or promoters of renin in urine.
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PMID:Measurement of urinary renin activity by radioimmunoassay: sequential studies in acute renal failure in man. 64 43

Acute renal failure is a pathogenetically heterogenous syndrome. Only in a small number of patients with acute renal failure anuria or oliguria is caused by morphological alterations of the glomeruli, renal blood vessels or tubuli. In the majority of patients with acute renal failure the cause of oliguria or anuria are haemodynamic changes which are the expression of a physiological tubulo-glomerular feedback mechanism. The participation anuria/oliguria is probable, but not proved with certainty. A scheme of the pathogenesis of anuria/oliguria of the renin-angiotensin system in the development of in the acute renal failure is presented based on recent renovasographic, haemodynamic and micropuncture technique.
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PMID:[Pathophysiology of acute non-inflammatory kidney failure]. 68 27

Indomethacin inhibits the synthesis of prostaglandin and the release of renin. These effects were studied in normal rabbits and rabbits with two-kidney Goldblatt hypertension (2KGH) and one-kidney Goldblatt hypertension (1KGH) by giving daily intravenous injections of indomethacin (3mg/kg after two initial doses of 9 mg/kg), and in appropriate control rabbits given diluent phosphate buffer without indomethacin. In normal rabbits, indomethacin significantly decreased immunoreactive plasma prostaglandin E-like substance (IPGE) and plasma renin activity (PRA). Indomethacin did not change plasma creatinine (PCr) or mean blood pressure but it decreased renal blood flow (RBF) and glomerular filtration rate (GFR). In 2KGH rabbits, responses depended on the level of renal function and, to a lesser extent, on the level of PRA. In six of10 2KGH rabbits in which hypertension developed without significant changes in PRA, IPGE, PCr, RBF, and GFR, indomethacin produced changes similar to those seen in normals. In the other four rabbits, development of 2KGH was accompanied by increased PRA, increased IPGE, and decreased RBF and GFR, and indomethacin produced renal failure, oliguria, malignant hypertension, and death within 5 days. In 1KGH rabbits, indomethacin decreased IPGE, PRA, and renal function but increased mean blood pressure. These observations suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.
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PMID:The effect of indomethacin blockade of prostaglandin synthesis on blood pressure of normal rabbits and rabbits with renovascular hypertension. 83 Apr 37

Renal ischemia of 90 min duration provokes initial oliguria and hyperazotemia; however, in rats with high diuresis, with or without renal renin depletion, protection against acute renal failure is observed in this model. The protection is directly proportional to the diuresis.
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PMID:[Protection against acute renal insufficiency by means of forced diuresis in an ischemic rat model]. 92 53

In 19 patients with acute renal insufficiency the plasma renin activity (PRA) and the aldosteronaemia were determined during the phase of anuria and oliguria. Significantly elevated PRA values were found while plasma aldosterone was only moderately elevated in the blood plasma. Apart from this a significantly negative correlation between the aldosterone level and the sodium and bicarbonate concentrations in the blood plasma were found. The lack of a significant positive correlation between PRA and plasma aldosterone levels suggests the participation of factors other than renin in the regulation of the aldosterone secretion in patients with acute renal insufficiency.
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PMID:[Aldosteroneia in acute kidney failure]. 93 3

Three patients with severe hypertension and rapidly progressive oliguric renal failure who required dialysis were found by aortography to have bilateral renal artery occlusion or stenosis. Each had peripheral arteriosclerosis or an abdominal bruit. Following renal artery reconstructive surgery, all three patients recovered nearly normal renal function in 3 to 12 weeks, though mild hypertension persisted in two patients. The common findings of a normal-sized kidney with collateral blood flow and nearly normal histological features were predictive of recovery of renal function. Prolonged postoperative oliguria in two patients may have been due to increased preglomerular vascular resistance mediated by the renin-angiotensin system.
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PMID:Reversible renal failure following bilateral renal artery occlusive disease. Clinical features, pathology, and the role of surgical revascularization. 94 90

1. Indomethacin inhibits prostaglandin synthesis and interferes with renin release; these effects were studied in rabbit renovascular hypertension. 2. Ten intravenous injections (3 mg day-1 kg-1 after two initial doses of 9 mg/kg) of indomethacin were given daily to ten normal rabbits, ten rabbits with two-kidney Goldblatt hypertension (2KH), tension (1KH). Twelve appropriate control rabbits received diluent phosphate buffer without indomethacin. Plasma renin activity and plasma prostaglandin E2 were measured by radioimmunoassay. 3. In the normal group, indomethacin significantly decreased plasma prostaglandin E2 (1-15 to 0-2 ng/ml, SEM 0-2; P less than 0-01) and plasma renin activity (20 to 3 ng h-1 ml-1, SEM 1, P less than 0-01). Plasma creatinine increased slightly but the mean blood pressure was not significantly changed by indomethacin. 4. Six of ten rabbits with 2KH showed results similar to those in the normal rabbits. In four of ten rabbits in which development of 2KH was accompanied by increments in plasma renin activity (18 to 31-5 ng h-1 ml-1, SEM 3 and 4 respectively; P less than 0-01) and plasma prostaglandin E2 (1-2 to 3-4 ng/ml, SEM 0-2 and 0-4 respectively; P less than 0-05), treatment with indomethacin produced renal failure (plasma creatinine increasing to 7-6 mg/100 ml), oliguria, malignant hypertension (mean blood pressure, 168 mmHg, SEM 7-7) and death within 5 days. 5. In 1KH, indomethacin decreased plasma renin activity and plasma prostaglandin E2, but caused increased mean blood pressure (102 to 121 mmHg, SEM 4 and 6 respectively; P less than 0-01) and decreased renal function (plasma creatinine 0-9 +/- 0-04 to 3-5 +/- 1 mg/100 ml, SEM 0-04 and 1 respectively; P less than 0-01). 6. Aggravation of hypertension was conditioned by pre-existing levels of renal function and, to a lesser extent, by plasma renin activities. 7. These results suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.
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PMID:Effects of indomethacin in rabbit renovascular hypertension. 107 20


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