Radiocontrast-induced acute renal failure is the third-leading cause of acute renal failure in hospitalized patients in the United States. More than 10 million radiocontrast studies are performed annually in the United States. Of importance, contrast-induced nephropathy, although largely preventable, is associated with 34% mortality. Radiocontrast-induced nephropathy is due to acute tubular necrosis that results from reduced renal perfusion secondary to vasoconstriction, tubular obstruction, and direct tubular toxicity from the contrast medium, which is thought to be mediated by oxygen free radicals. The definition of radiocontrast-induced nephropathy is variable, with some defining it as a greater than 25% increase from baseline serum creatinine and others defining it as an absolute increase of greater than 0.5 mg/dL of creatinine from baseline within 48 hours of exposure to contrast. Because absolute serum creatinine values are an imprecise method for measuring renal function, the calculation of estimated glomerular filtration rate is recommended before and after administration of contrast dye to evaluate for acute renal failure.

The following risk factors predispose patients to nephropathy secondary to radiocontrast agents: pre-existing chronic renal insufficiency, diabetes mellitus, reduced effective circulating volume as in patients with intravascular depletion or heart failure, and the use of large volumes of contrast dye. Most patients who develop radiocontrast-induced nephropathy recover their renal function with no lasting sequelae. The serum creatinine value usually peaks at 3 to 5 days and returns to baseline within 10 days. However, a few patients have a residual requirement for renal replacement therapy. These patients have a reported 2-year survival rate of 18%. In addition, the risk-adjusted odds ratio for death after the development of radiocontrast-induced nephropathy is nearly 5 (p < .01).