G J Duke1. 1. Intensive Care Department, The Northern Hospital, Epping, VIC, Australia gduke@tnh.vic.gov.au.
Abstract
OBJECTIVE: To review the role of drugs with potential benefit to renal function in critically ill patients. DATA SOURCES: A review of articles published in peer review journals from 1966 to 1998 and identified through a MEDLINE search on kidney failure. SUMMARY OF REVIEW: Acute renal failure in critically ill patients is characterised by ischaemic injury to the tubule and is potentially preventable. Many agents have been shown to benefit renal function in animal models of acute renal failure, but supporting human data are lacking. There is evidence to support the defence of extracellular volume (with volume loading) and renal perfusion pressure (with pressor agents) but there are no controlled trials. While there are limited data to support the use of mannitol and calcium channel blockers in renal transplantation there are no studies that have confirmed their benefit in critically ill patients. Controlled trials of frusemide, dopamine and mannitol do not support their routine use. All other agents have been inadequately studied. CONCLUSIONS: The common factor in renal dysfunction and acute renal failure is tubular ischaemia. Prevention of this final common pathway is the chief goal of renal protection in critically ill patients. Despite the plethora of potentially beneficial drugs, volume loading and defence of renal perfusion pressure (and renal blood flow) with pressor agents appear to be the only reliable means of renal protection.
OBJECTIVE: To review the role of drugs with potential benefit to renal function in critically illpatients. DATA SOURCES: A review of articles published in peer review journals from 1966 to 1998 and identified through a MEDLINE search on kidney failure. SUMMARY OF REVIEW: Acute renal failure in critically illpatients is characterised by ischaemic injury to the tubule and is potentially preventable. Many agents have been shown to benefit renal function in animal models of acute renal failure, but supporting human data are lacking. There is evidence to support the defence of extracellular volume (with volume loading) and renal perfusion pressure (with pressor agents) but there are no controlled trials. While there are limited data to support the use of mannitol and calcium channel blockers in renal transplantation there are no studies that have confirmed their benefit in critically illpatients. Controlled trials of frusemide, dopamine and mannitol do not support their routine use. All other agents have been inadequately studied. CONCLUSIONS: The common factor in renal dysfunction and acute renal failure is tubular ischaemia. Prevention of this final common pathway is the chief goal of renal protection in critically illpatients. Despite the plethora of potentially beneficial drugs, volume loading and defence of renal perfusion pressure (and renal blood flow) with pressor agents appear to be the only reliable means of renal protection.
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