A review of the literature has shown that the role of renin in renal failure is not resolved. It has been invoked as an aggravating factor: decreased renal perfusion releasing large quantities of renin sufficient to cause further renal vasoconstriction. If so, then angiotensin generation and action must occur entirely intrarenally since the vasoconstriction appears to be confined entirely to this vascular bed. It may prove necessary to evaluate the renin-angiotensin system within the kidney rather than peripherally. Elevated renin levels in peripheral plasma are at least as likely to be a consequence of reduced renal perfusion as a cause of it.
The few studies so far undertaken of the renin-angiotensin system in renal failure associated with liver disease are inconclusive. If further studies should ascribe a role to renin in the pathology of renal failure, then it may be possible to treat the condition by pharmacological manipulation of the renin-angiotensin system and thereby prevent some of the more serious consequences of renal failure.
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