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In this randomized, double-blind, placebo-controlled clinical study from the Australia and New Zealand Intensive Care Study (ANZICS) clinical trial group, they questioned the use of the widely practiced, but never proven, role of low-dose dopamine therapy "to protect renal function" or "to improve renal blood flow." Over a period of three years, more than 300 patients in New Zealand and Australia were randomized to receive either a placebo infusion or a dopamine infusion at 2 mg kg-1 min-1. Inclusion criteria were the presence of a central venous catheter, two or more features of the systemic inflammatory response syndrome (SIRS) during a 24-hour period, and at least one indicator of early renal dysfunction. The latter included a urine output averaging less than 0.5 mL/kg/h for four hours or more, a serum creatinine concentration more than 150 mmol/L (1.69 mg/dL) in the absence of premorbid renal dysfunction, or a rise in serum creatinine concentration of more than 80 mmol/L (0.9mg/dL) in less than 24 hours in the absence of creatinine kinase more than 5000 IU/L or myoglobin in the urine.
Patients who were younger than 18 years, who had a recent episode of acute renal failure in the previous three months, and those with renal transplants were excluded. After randomization, patients were given an infusion of either dopamine or placebo, and all care providers including physicians and nurses were blinded. There were two interim safety analyses, and the study had a 90% power to detect a 25% difference in creatinine rise between the two groups. There were 161 patients in the low-dose dopamine group and 163 in the placebo group. The groups were comparable in terms of age, disease severity, mean arterial pressure, creatinine levels at baseline, and use of nephrotoxic agents or diuretics during their stay. Both groups received the study drug or placebo infusion for about five days.
There was no difference in the urine output, the rise in serum creatinine, or the use of renal replacement therapy. There were equal numbers of arrhythmias in both groups. Dopamine infusion had to be stopped due to arrhythmia in seven patients. (Lancet 2000;356:2139-2143.)
Having had a chance to review the literature on this topic not long ago, I have to admit that this article provides what is perhaps the only evidence-based information we have in the field of dopamine therapy. The disease spectrum in this study was similar to what is encountered in most ICUs. The indications for starting dopamine therapy in the study are similar to those that most proponents of this therapy would agree. One can only hope that the proponents of this unproven therapy would also agree to the findings. Dopamine was no better than placebo in terms of "renal protection." Of more interest, it did not even have much natriuresis effect.
Hopefully, the results of this large, randomized, controlled study will have an effect on the widespread use of an unproven therapy so widely prevalent in ICUs around the world. The use of dopamine, especially "renal dose" dopamine, has been controversial for a long time. This therapy was based on observations in healthy volunteers in which some increases in renal blood flow and urine output were noted. However, what happens in healthy volunteers is not necessarily the same as is observed in disease states, as the physiology likely changes. The only subgroup of patients in whom dopamine has been shown to be somewhat effective is following cardiac surgery in the presence of decreased renal function. That particular group was not represented in the present study. Overall, it seems safe to conclude that, for most patients in ICU, "there is nothing like renal dose dopamine."