KDIGO Clinical Practice Guideline for Acute Kidney Injury
Dopamine for the prevention or treatment of AKI: Recommendations and Rationale

Chapter 3.5: Vasodilator therapy: dopamine, fenoldopam, and natriuretic peptides

Dopamine for the prevention or treatment of aki

Dopamine was once commonly used for renal protection in the critically ill. However, with multiple negative studies, including a randomized, double-blind, placebo-controlled trial of adequate size and power,²⁰⁷ its use has been abandoned by most. Low-dose dopamine administration (1–3 µg/kg/min) to healthy individuals causes renal vasodilation, natriuresis, and increased GFR; because of these effects, it has been given as prophylaxis for AKI associated with radiocontrast administration, repair of aortic aneurysms, orthotopic liver transplantation, unilateral nephrectomy, renal transplantation, and chemotherapy with interferon.²⁰⁸ The majority of prevention trials with low-dose dopamine have been small, inadequately randomized, of limited statistical power, and with end-points of questionable clinical significance. Furthermore, recent data suggest that the renal vasodilatory effect of dopamine found in healthy populations is not preserved in patients with AKI. Using Doppler ultrasound, Lauschke et al.²⁰⁹ found that dopamine significantly increased renal vascular resistance in AKI patients. Kellum and Decker²¹⁰ found no benefit of dopamine for prevention or therapy of AKI in an adequately-powered meta-analysis, and Marik²¹¹ found no benefit in a systematic review.

There is also limited evidence that the use of dopamine to prevent or treat AKI causes harm. Although the meta-analysis by Friedrich et al.,²¹² found no significant increase in adverse events or evidence of harm from low-dose dopamine, there is significant literature demonstrating adverse effects of dopamine, even at low doses. It can trigger tachyarrhythmias and myocardial ischemia, decrease intestinal blood flow, cause hypopituitarism, and suppress T-cell function.²⁰⁸ Taken together with the lack of positive trials to support the use of dopamine for AKI prevention or therapy, the aforementioned potential deleterious effects of this drug provide additional arguments for abandoning its use entirely for the prevention and therapy of AKI.

Rationale

In their meta-analysis, Friedrich et al.,²¹² did not specifically separate prophylactic trials from trials where dopamine was used therapeutically in patients with established AKI, because many of the original trials failed to do so.²¹⁰ The authors analyzed 61 randomized or quasi-randomized controlled trials of low-dose dopamine, and found no improvement of survival (Figure 11), no decrease in dialysis requirement (Figure 12), no improvement in renal function, and improved urine output only on the first day of dopamine therapy.²¹² Similarly, although there were trends towards transiently greater urine output, lower SCr, and higher GFR in dopamine-treated patients on day 1 of therapy (but not days 2 and 3), there was no evidence of a sustained beneficial effect on renal function. In an earlier systematic review, Kellum et al.,²¹⁰ performed an analysis of studies that reported incidence of AKI as an outcome, which developed in 15.3% in the dopamine arms and 19.5% in the control arms (RR 0.79 [0.54–1.13]). Similar to the earlier analysis by Kellum et al., restriction of the Work Group’s analysis to prevention trials did not disclose any benefit of dopamine vs. placebo therapy. Similarly, analysis of adequate trials restricted to patients treated for AKI does not suggest a benefit of dopamine therapy. Specifically, a relatively large randomized, placebo-controlled trial in 328 critically ill patients with early AKI sufficiently powered to detect a small benefit was reported.²⁰⁷ There was no effect of low-dose dopamine on renal function, need for dialysis, ICU or hospital length of stay (LOS), or mortality (Suppl Table 4). Taken together, these analyses found no evidence that dopamine therapy is effective in the prevention or treatment of AKI.