Despite more than thirty years of use as a renal vasodilator, low-dose dopamine (2μg/kg/min) has shown no evidence 

of benefit in patients with acute oliguric renal failure. In fact, low-dose dopamine can have deleterious effects on hemodynamics (decreased splanchnic blood flow) immune function (inhibition of T-cell lymphocyte function) and endocrine function (inhibition of thyroid-stimulating hormone release from the pituitary).

     Despite its widespread use, there is no evidence to support the use of low-dose dopamine to prevent or treat ARF, and, therefore, dopamine should be eliminated from routine clinical use for this indication. At first glance, it is difficult to understand why low-dose dopamine does not confer any benefit to patients with, or at risk for, ARF. Low-dose dopamine is effective in increasing renal blood flow and results in increased urine output. Clinicians frequently use “renal dose” dopamine in the hopes that such a maneuver might attenuate renal injury and improve survival. In addition, clinicians often interpret an increase in urinary output as proof that these two assumptions are valid. In reality, dopamine may increase urine output through five separate mechanisms.

     Dopamine stimulates both dopaminergic and adrenergic (both α and β) receptors. As such, dopamine may affect renal blood flow by direct vasodilation (dopamine receptors), by increasing cardiac output (β-receptors) or by increasing perfusion pressure (α-receptors). At low doses, particularly, 2μg/kg/min, the dopaminergic effects tend to predominate, although wide variability seems to exist across patients and clinical conditions. In appropriate clinical settings, any of the mechanisms might increase effective renal plasma flow and thus increase urine output. Under such conditions, the increase in urine output might well be indicative of improved renal function. However, dopamine may also increase urine output by both inhibition of aldosterone release as well as inhibition of sodium-potassium ATPase at the tubular epithelial cell level. The effect of these last two mechanisms is to increase sodium excretion and thereby diuresis. Thus, apart from the direct and indirect effects on the renal vasculature, dopamine increases urine output because it is a diuretic.

     Much of the enthusiasm for the use of this agent comes from the belief that dopamine increases renal blood flow and that such an outcome is desirable. Given that ARF in the critically ill is usually caused by acute tubular necrosis (ATN), it seems paradoxic that an agent that improves renal blood flow is not beneficial. Clearly, the continued popularity of so-called “renal dose” dopamine is the result, in large part, of this seemingly strong physiologic rationale even in the face of multiple negative clinical trials.

    First, most clinicians use so-called “renal-dose” dopamine in the belief that they can improve renal blood flow and that this will restore oxygen delivery to portions of the kidney that are dysoxic. However, it is not clear that ischemic ATN is always the result of a decrease in renal blood flow nor is it clear that increasing renal blood flow will reverse or prevent this injury. The renal medulla is constantly on the brink of dysoxia owing to high demand and low delivery of oxygen. Although dopamine increases outer medullary blood flow in hypovolemic animals, it fails to improve outer medullary dysoxia. In fact, analogous to the situation with radiocontrast, the increased solute delivery to the distal tubular cells produced by the natriuretic effects of dopamine (via inhibition of proximal tubular resorption) might actually increase medullary oxygen consumption and thereby increase the risk of ischemia rather than decrease it. This aspect of renal physiology could explain why agents that increase renal blood flow are not protective. Indeed, this scenario would predict that such agents would actually be deleterious. In fact, two recent studies  suggest that dopamine worsens renal tubular injury secondary to radiocontrast agents and in postcardiac surgery patients despite an increase in renal blood flow.

    Finally, drugs that oppose dopamine activity, such as metoclopramide or haloperidol, are not associated with any adverse renal effects despite widespread use in the same populations where “renal dose” dopamine is often advocated. Indeed, both of these agents effectively negate any the renal vascular effects of low-dose dopamine, yet neither is associated with ARF. Thus, the existing experimental evidence does not provide conclusive support for dopamine and some studies raise concerns that dopamine may even be harmful. These studies also call into question the appropriateness of increasing urine output in the first place.

   In the case of other types of diuretics, converting oliguric to nonoliguric renal failure may provide certain management advantages (e.g. controlling volume overload 

and hyperkalemia) but does not affect overall renal recovery or outcome. Accordingly, on the basis of existing evidence, the use of dopamine to improve renal function cannot be recommended.

    Overall, the physiologic considerations and the considerable clinical data amassed to date argue strenuously against the routine use of “renal dose” dopamine.