Many different definitions of CN appear in the literature, but it is commonly defined as an acute decline in renal function following the administration of intravenous contrast in the absence of other causes. For research purposes, a definition such as a rise in serum creatinine ≥25 or 50% above the baseline value is often used. Patients with CN typically present with an acute rise in serum creatinine anywhere from 24 to 48 h after the contrast study. Serum creatinine generally peaks at 3 to 5 d and returns to baseline value by 7 to 10 d (2,3,4). The acute renal failure is nonoliguric in most cases (5, 6). Urinalysis often reveals granular casts, tubular epithelial cells, and minimal proteinuria, but in many cases may be entirely bland. Most, but not all, patients exhibit low fractional excretion of sodium (5, 7), The diagnosis of CN is frequently obvious if the typical course of events follows the administration of contrast. However, other causes of acute renal failure, including atheromatous embolic disease, ischemia, and other nephrotoxins should always be considered. This is particularly true if significant renal impairment should occur in patients without risk factors for CN.