Using low dose dopamine at 0-2-2-5 micrograms kg-1 per minute ("renal dose") for both the prevention and treatment of acute renal failure is common. Yet randomised trials have shown it is of no benefit either as prevention in high risk postoperative patients or as treatment in established acute renal failure. The effects of a dopamine infusion are complicated because it acts on a number of different receptors that have opposing actions. The action of dopamine is not constant throughout its dose range (see a fuller description in Chapter 6). Stimulation of a receptors causes systemic vasoconstriction and the blood pressure rises; pi receptors increase contractility of the heart, p2 receptors reduce afterload, and dopamine (DA) receptors cause renal and splanchnic vasodilatation. Dopamine acts on all these receptors. In addition, there are two major subgroups of DA receptor: DA1 receptors are in the renal and mesenteric circulation; DA2 receptors are in the autonomic ganglia and sympathetic nerve endings and inhibit noradrenaline release. Dopamine and its synthetic sister dopexamine have been used extensively to theoretically improve renal blood flow and therefore function. Dopexamine is also used to improve splanchnic blood flow in certain postoperative situations.
Dopamine causes a diuresis and natriuresis independent of any effect on renal blood flow by inhibiting proximal tubule Na-K-ATPase (via DA1 and DA2 stimulation). So the effect we see with low dose dopamine is a diuresis - not a change in creatinine clearance. In one randomised prospective double-blind trial, 23 patients at risk for renal dysfunction were given either dopamine at 200 micrograms per minute, dobutamine at 175 micrograms per minute, or 5% dextrose. Dopamine increased urine output without a change in creatinine clearance and dobutamine caused a significant increase in creatinine clearance by increasing cardiac output without an increase in urine output. This illustrates the difficulty of using urine output as a surrogate marker for renal function.
Critically ill patients have reduced dopamine clearance and may consequently have higher plasma levels than anticipated, so it is not correct to assume that low dose dopamine is acting only on the renal circulation. In one study, there was a 27-fold variability in the range of plasma dopamine levels. In some individuals, infusion of "renal dose" dopamine results in plasma levels in the a-receptor range. This leads to side effects such as tachyarrhythmias and increased afterload. In summary, there is no evidence to justify the use of dopamine to prevent or treat acute renal failure.
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