Dopamine and Renal Salvage in the Critically Ill Patient

Abstract

Dopamine is a catecholamine used widely in critically ill patients and those undergoing major surgery, often as a ‘renal protective’ agent. Direct renal vasodilatation with ‘low-dose’ dopamine is the widely accepted basis for its use – hence the term ‘renal dose’ dopamine. However, recent evidence has revealed that the renal effects of this agent are far more complex. Moreover, some of these effects may be undesirable in the ‘at-risk’ kidney. The increased renal blood flow (RBF) of dopamine may be largely attributable to its inotropic (myocardial) action, even with low doses (i.e. < 5 μg/kg/min). Similar increases in RBF can also be demonstrated with other (non-dopaminergic) inotropes. The early evidence for direct renal vasodilatation in response to dopamine has been brought into question by more recent research. The diuresis and natriuresis commonly seen following dopamine administration is now known to be due to a direct renal tubular (or ‘diuretic’) action. Furthermore, increasing knowledge regarding the pathophysiology of acute (ischaemic) renal failure, including RBF and the concept of ‘oxygen supply and demand’ in relation to tubular function, suggests that dopamine may mask important signs of renal ischaemia. Whether or not dopamine is truly beneficial to renal function currently remains unanswered. As it stands however, there is sufficient evidence to question its routine use in the setting of renal dysfunction in the critically ill patient.