1969
DOI: 10.1159/000179720
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Plasma Renin Activity in Acute Renal Insufficiency

Abstract: Plasma renin activity (p.r.a.) was studied in 37 patients with acute renal insufficiency and in 20 healthy subjects. Significant increase of the p.r.a. in the oliguric phase of acute renal failure could be established. The p.r.a. decreased in the diuretic phase of this syndrome. No straight correlation between elevated p.r.a. on the one hand and the degree of hypertension and plasma sodium and potassium on the other hand could be found. The possible role of renin in the development of acute renal insufficiency… Show more

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Cited by 78 publications
(28 citation statements)
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“…First, reninangiotensin and thromboxane activity are known to be increased after ischemic injury to the kidney. Several investigators have measured increases in plasma and renal renin activity in clinical and experimental ARF (13,14,(23)(24)(25). Others have provided evidence that renal thromboxane activity is elevated after ischemia (15, 26).…”
Section: Discussionmentioning
confidence: 99%
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“…First, reninangiotensin and thromboxane activity are known to be increased after ischemic injury to the kidney. Several investigators have measured increases in plasma and renal renin activity in clinical and experimental ARF (13,14,(23)(24)(25). Others have provided evidence that renal thromboxane activity is elevated after ischemia (15, 26).…”
Section: Discussionmentioning
confidence: 99%
“…The rats were returned to metabolic cages receiving water ad lib and a low-potassium diet (ICN Pharmaceuticals, Cleveland, OH) for 72 h and a standard rat chow diet (Wayne Feed, Longmont, CO) thereafter. Peak azotemia occurred between 24 and 48 h after NE infusion. Renal blood flow returned to 70% ofcontrol levels by 24 …”
Section: Methodsmentioning
confidence: 99%
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“…It is possible that renin activation is due to prostaglandin stimulation from kinins; however, there is no direct evidence to support such a process. Angiotensin blockade may reduce the effect of the renin-angiotensin, since the latter has been shown to be stimulated by ischemia (40). However, the protective effect of angiotensin blockade would not explain the initiation of ischemia following endotoxin.…”
Section: Discussionmentioning
confidence: 99%
“…These include: (1) 50% stenosis of the left renal artery which probably wor sened in the 3 years prior to occlusion, thereby providing a constant stimulus for development of collaterals: (2) the demonstration of significant renal blood flow by techne tium studies in the face of total renal artery occlusion, and (3) a hydrostatic pressure of 36 mm Hg in the renal artery distal to the occlusion. The extremely high periph eral vein renin could not be used in differential diagnosis, as renin can be elevated in acute tubular necrosis [13]. It is well documented that the latter can be precipitated by radiocontrast material [3], In retrospect, however, the high renin was due to the decreased hydrostatic pressure on the JGA.…”
Section: Discussionmentioning
confidence: 99%