Why the study?
Does low-dose dopamine improve renal function in critically ill patients?
Does low-dose dopamine improve renal function in critically ill patients?
This review challenges the traditional use of 'renal dose' dopamine, highlighting that it may not offer direct renal protection and could mask renal ischemia in critically ill patients.
Questions routine low-dose dopamine for renal protection in critical illness; leaves open whether targeted trials can clarify net effects on ischaemia.
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. less than 5 micrograms/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.
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Duke et al. (1992) studied this question.
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