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Ann Thorac Surg 2004;78:1337-1338
© 2004 The Society of Thoracic Surgeons
Division of Cardiothoracic Anesthesia and Critical Care Medicine, Department of Anesthesiology, Box 3094, Duke University Medical Center, Durham, NC 27710, USA
swami001{at}mc.duke.edu
Ranucci and associates report a multicenter, prospective cohort study of fenoldopam prophylaxis in cardiac surgical patients at high risk for postoperative acute renal failure (ARF). Fenoldopam was administered in 108 patients prospectively, and data were analyzed against a matched retrospective cohort of 108 control group patients who did not receive the drug. The authors found a significant reduction in incidence of ARF with fenoldopam use, but could not confirm this in a multivariable analysis. However, fenoldopam was found to be an independent renal protective factor in a subgroup of 70 patients with low cardiac output syndrome.
Several studies have attempted to define the importance of postoperative acute nephropathy after cardiac surgery. It has been established beyond doubt that postoperative ARF is a major complication and is strongly associated with death. Although numerous investigators have attempted to protect the kidneys during cardiopulmonary bypass using a variety of agents and techniques, few have lived up to their initial reported potential. Dopamine continues to be the first choice renoprotective agent in cardiac surgical patients, a choice based more on theoretical considerations than evidence. The choice of fenoldopam as a renoprotective drug is based on the same sound principles of dopaminergic A1 receptor agonism: renal vasodilatation during situations of splanchnic vasoconstriction. The expectation is that fenoldopam will deliver in cases in which the vasoconstrictive effects of other inotropic agents may be damaging to the kidneys.
Ranucci and colleagues have shown that in a special subset of their study population with low postoperative cardiac output and high inotrope use, fenoldopam did, in fact, exert a significant renoprotective effect. However, fenoldopam did not seem to exert an equivalent beneficial effect when low cardiac output was not a factor. That may be due to the fact that renal vasodilatation may not provide any added benefit given an appropriate cardiac output. The delivery of inflammatory mediators, microemboli, and aortic atheromatous debris to the kidneys may even be enhanced owing to the increase in renal blood flow. There may also be an undesirable redistribution of intrarenal perfusion due to the vasodilatory effects of fenoldopam. Given this rationale, it is not surprising that the authors could not demonstrate a renal benefit with fenoldopam in the entire study group, which included patients with other renal risk factors, some independent of renal vasoregulatory mechanisms. The beneficial effect, if any, may have been small enough to elude statistical analysis in their sample population. The observed effect size (a reduction of 22% to 11%) has an odds ratio of 2.28, which this study is underpowered to declare as significant. The authors powered their study to detect an odds ratio of 3.6, which was optimistic, and they did not actually see this effect size. Although this was not a randomized trial, the findings are fairly significant. However, these findings must be substantiated in a controlled, randomized clinical trial before fenoldopam can be accepted as the renoprotective agent of choice during cardiac surgery.
Related Article
Ann. Thorac. Surg. 2004 78: 1332-1337.
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