• A D Bersten and A W Holt.
• Department of Critical Care Medicine, Flinders Medical Centre, Flinders University, Adelaide, Australia.
• New Horiz. 1995 Nov 1; 3 (4): 650-61.

AbstractDespite the often multifactorial nature of renal insults in critically ill patients, inadequate renal blood flow (RBF) is common and frequently causes a reduction in the glomerular filtration rate (GFR). Renal autoregulation acts to maintain both the RBF and GFR constant across a broad range of renal perfusion pressure (RPP) levels; however, the lower limit of this range (approximately 80 mm Hg for RBF, and 10-15 mm Hg higher for GFR) is often above the RPP achieved in critically ill patients. Furthermore, renal autoregulation is often lost, resulting in a linear pressure-flow relationship in the "at-risk" kidney. Consequently, maintenance of an adequate RPP level is needed to optimize RBF. While this may require the use of vasopressor catecholamines with their attendant risk of renal vasoconstriction and a reduction in RBF, both laboratory studies and clinical data suggest that such reactions rarely occur with intravenous infusions of these drugs, and that RBF and renal function usually improve when RPP is augmented during shock. Preliminary data, using nitric oxide (NO.) synthase inhibitors to augment blood pressure, showed a detrimental effect on renal perfusion, perhaps due to the central role of NO. in the normal vasoregulation of the kidney. Dopaminergic agonists have been commonly used as renal vasodilators; however, their actions are complex and include a proximal tubular diuretic effect, renal vasodilation, and systemic hemodynamic effects. Their specific action to increase RBF and GFR has not been demonstrated in clinically relevant studies and no prospective randomized study has shown a reduction in the incidence of renal impairment or acute renal failure.

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