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Department of Anesthesia and Intensive Care Medicine; University of Udine; Udine Italy; giorgio.dellarocca{at}uniud.it
In Response:
Recently, there have been several publications regarding renal protection and the limitations of renal dose dopamine. The results found by Lema et al. (1) in cardiac surgical patients have not been confirmed. Lassnigg et al. (2) demonstrated that continuous infusion of renal-dose dopamine failed to exert any advantage over placebo for renal vasodilatation in well hydrated patients after cardiac surgery. Carcoana et al. (3) found that dopamine administered to patients undergoing cardiopulmonary bypass, rather than being a protective drug in the setting of cardiopulmonary bypass, increased the ß2 microglobulin excretion rate, which may be a measure of renal tubular dysfunction. A systematic review of all the studies published until mid-2000, found that the use of small-dose dopamine for the treatment of prevention of acute renal failure cannot be justified on the basis of available evidence and should be eliminated from routine clinical use (4). In a recent meta-analysis of 15 studies containing 970 subjects, Marik et al. (5) found that the incidence of renal dysfunction was 31% in the small-dose dopamine group compared with 33% in the control group. The study concluded that dopamine has no renal vasodilator effect; moreover, considering the potential side effects of the drug, there is no justification for the continued use of small-dose dopamine as a renal vasodilator drug. Holmes et al. (6) found that, in addition to the lack of renal efficacy, small-dose dopamine worsens splanchnic oxygenation, impairs gastroenteric function, impairs the endocrine and immunologic systems, and blunts ventilatory drives.
Finally, the Australian and New Zealand Intensive Care Society Clinical Trials Group (7), in a large phase III double-blind randomized controlled trial, sought to resolve the long-standing debate. This study found no difference between the effect of placebo and small-dose dopamine on clinical markers of glomerular filtration rate in a large group of critically ill patients with early renal dysfunction.
The meaning of "high vasoconstrictive tone" in our article may lead to a possible explanation of the controversial results found in the renal-dose dopamine when all animal models of renal failure used either high norepinephrine infusion or total occlusion of renal artery to produce renal failure (8). However, in most clinical situations, kidneys never experience such an extreme vasoconstriction and, under these conditions, dopamine exerts its effects by acting on both DA1 and DA2 receptors, resulting in a decrease in renal blood flow, glomerular filtration rate, and sodium excretion (9). People undergoing liver transplantation may present many reasons to develop acute renal failure; cyclosporine causes renal vasoconstriction and reduces renal blood flow that may contribute to chronic and acute nephrotoxicity. In the setting of endogenous and exogenous vasoconstrictive pattern, fenoldopam is an independent protective factor against acute renal failure requiring renal replacement therapy (10). It is reasonable to hypothesize that the prerenal vasodilating effect of fenoldopam may effectively counteract the splanchnic vasoconstriction generally considered as a major determinant of acute renal failure (11,12). In conclusion, Lema et al. stated "if renal vasodilation is necessary to preserve renal function, it still remains controversial." The essential elements of perioperative renal preservation are optimization of fluid status and cardiovascular performance, maintenance of renal perfusion, and avoidance of nephrotoxins (13–15).
References
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