Contrast-induced nephropathy occurs in 2-10% of patients exposed to intravascular radiographic contrast agents and results in significant morbidity and mortality. Although the exact mechanism of this disorder has not been fully elucidated, contrast nephropathy is probably due to a combination of decreased renal medullary blood flow, resulting in medullary ischemia, and direct toxicity to renal tubules. Contrast nephropathy is most commonly defined as either a >25% increase or a >0.5 mg/dL rise in serum creatinine level within 48 hours of contrast medium exposure. Baseline characteristics associated with an increased risk for development of contrast nephropathy include the presence of baseline renal dysfunction, diabetes mellitus, congestive heart failure, volume depletion, and concomitant administration of nephrotoxic drugs. Many strategies have been investigated in an effort to prevent the occurrence of renal dysfunction following contrast media exposure. Intravenous hydration has been shown to significantly decrease the incidence of nephropathy in high-risk patients. However, trials of several prophylactic pharmacologic interventions have been mostly disappointing, including the administration of calcium channel antagonists, diuretics, dopamine, endothelin receptor antagonists and fenoldopam. The use of N-acetylcysteine has been shown in some trials to decrease the incidence of contrast nephropathy in patients with a baseline renal dysfunction, and should currently be strongly considered in this high-risk patient subgroup in addition to hydration. Our purpose is to review the contemporary literature regarding contrast-induced renal dysfunction and present an evidence-based approach for prevention of this complication.