Acute renal failure (ARF) is common in the critically ill and is associated with a high mortality rate. Its pathogenesis is not understood. Because animal models use ischemia to induce experimental ARF, there is the widespread belief that lack of blood flow is responsible for ARF. Low-dose dopamine (LDD) has been shown to increase renal blood flow in animal and in human volunteers. Thus, it has been administered to humans for almost 3 decades in the belief that it would lead to renal arterial vasodilation and increase renal blood flow (RBF). However, the etiology of ARF in critical illness is likely multifactorial, and the contribution of hypovolemia and reduced renal perfusion is unknown. Furthermore, interindividual variation in the pharmacokinetics of dopamine typically results in poor correlation between blood levels and administered dose, making accurate and reliable delivery of LDD difficult. Finally, dopamine is a proximal tubular diuretic that increases Na(+) delivery to tubular cells, thus increasing their oxygen demands. Accordingly, even if LDD were able to preferentially increase RBF, there is no guarantee that it would restore renal parenchymal oxygen homeostasis. More important, 2 meta-analyses and a large double-blind, prospective, multiple-center, randomized controlled trial have failed to demonstrate that dopamine protects the kidney in critically ill patients with ARF. Currently, there is insufficient evidence to support the use of renal-dose dopamine in the intensive care unit.