Acute kidney injury (AKI) is a complex clinical syndrome with a spectrum of clinical manifestations and outcomes (1); characterized by the deterioration of renal function over a period of hours to days, resulting in the failure of the kidney to eliminate nitrogenous waste products and to maintain fluid and electrolyte homeostasis (2). The Acute Dialysis Quality Initiative group developed a definition for AKI based on risk, injury, failure, loss of kidney function, and end-stage kidney disease, collectively known as the RIFLE criteria, which classify the stages of AKI disease (3,4).

The frequency of AKI among hospitalized patients is approximately 25%; however, it can reach 50% in adult patients who undergo cardiac surgery (8,9). Acute kidney injury has been noted to be associated with increased length of stay, admission to the intensive care unit, and a 2-fold increase in mortality (8,10). Vives et al (11) proposed that postoperative AKI is complex and multifactorial and that interventions relying on serum creatinine levels are often initiated too late.

Pharmacological and non-pharmacological interventions aimed at preventing postoperative AKI have been previously described. Pharmacological interventions to prevent cardiopulmonary bypass (CPB)-associated AKI have had limited success, whereas there are generally accepted non-pharmacological interventions. The non-pharmacological interventions, largely surgical and protective techniques, include the timing of transfused blood, maintaining baseline preoperative hemoglobin/hematocrit levels, and using pulsatile CPB (11). Current pharmacological interventions include the use of angiotensin-converting enzyme inhibitors, aspirin, statins, dexmedetomidine, erythropoietin, and diuretics (11). More commonly studied interventions are the use of N-acetylcysteine, dopamine, and fenoldopam