Review
Copyright ©The Author(s) 2015.
World J Nephrol. May 6, 2015; 4(2): 196-212
Published online May 6, 2015. doi: 10.5527/wjn.v4.i2.196
Table 2 Clinical studies providing evidence against/in support of clinical use of low dose dopamine
Study designResultsRef.
Against clinical use of low dose dopamineThe Australian and New Zealand Intensive Care Society (ANZICS): multicenter, randomized, double-blind, placebo-controlled324 patients with at least two criteria for the systemic inflammatory response syndrome and clinical evidence of early renal dysfunction: continuous intravenous infusion of low-dose dopamine (2 µg/kg per minute) did not attenuate the peak serum creatinine compared with placebo. There was no statistical difference in mortality between dopamine and placebo armsBellomo et al[119]
Meta-analysis study: 17 studies were randomized clinical trials (n = 854)Low dose dopamine administration did not prevent mortality or the onset of acute renal failure, or the need for haemodialysis in clinically ill patientsKellum and M Decker[120]
Meta-analysis study: 15 randomized controlled studiesDopamine administration did not present beneficial results in terms of serum creatinine changes and incidence of acute renal failure in clinically ill patientsMarik[121]
Sepsis Occurrence in Acutely Ill Patients (SOAP): Cohort, multiple-center, observational studyDopamine administration in shock patients, compared to patients who did not receive it, was associated with 20% increase in ICU and hospital mortality ratesSakr et al[122]
Renal Optimization Strategies Evaluation (ROSE) study: multicenter, double-blind, placebo-controlled randomized clinical trialLow dose dopamine (2 µg/kg per minute) did not enhance decongestion or improved renal function when added to diuretic therapy in 360 patients with acute heart failure and renal dysfunctionChen et al[123]
In support of clinical use of low dose dopamineDopamine in Acute Decompensated Heart Failure (DAD-HF) Trial: randomized clinical trialThe addition of low-dose dopamine (5 μg/kg per minute) to low-dose furosemide (5 mg/h) was associated with improvement in renal function profile and potassium homeostasis at 24 h and it was equally effective as high-dose furosemide (20 mg/h) alone on subjective perception of dyspnoea in 60 patients with acute decompensated heart failureGiamouzis et al[124]
Retrospective clinical studyContinuous infusion of furosemide in addition to low-dose dopamine compared to intermittent boluses of furosemide was less nephrotoxic and carried a lower readmission rate at 30 d in 116 patients with acute decompensated heart failureAziz et al[125]
A prospective single-center randomized double-blind placebo controlled trialThe treatment with high-dose fenoldopam at 1 μg/kg per minute (short-acting D1 agonist) during cardiopulmonary bypass in 80 pediatric patients undergoing cardiac surgery for congenital heart disease significantly decreased urinary biomarkers of acute kidney injury (urinary neutrophil gelatinase-associated lipocaline and cystatin C levels) and also reduced the incidence of acute kidney injury in the postoperative period and the use of diuretics and vasodilatorsRicci et al[126]
Clinical case findingLow doses of ANP (0.0125 μg/kg per minute) with low dose dopamine (1.0 μg/kg per minute) in acute decompensated heart failure increased urine output, decreased heart rate, improved congestion with a reduced brain natriuretic peptide level, reduced serum creatinine and the levels of urinary liver-type fatty acid binding protein -a novel reno-tubular stress marker- and 8-hydroxydeoxyguanosine -an oxidative stress markerKamiya[127]
Prospective randomized clinical studyLow dose dopamine infusion reduces renal tubular injury following cardiopulmonary bypass in 48 patients with normal or near normal baseline renal functionSumeray et al[128]