A lthough the clinical features of contrast-induced nephropathy (CIN) have been well described for some time (1,2), during the past 15 yr, interest among physicians on the subject of CIN has dramatically increased. A PubMed search of the phrase "contrast-induced nephropathy" between 1990 and 2007 produced 347 citations. During the past 5 yr alone, there were 290 citations, 159 of which appeared since 2006 (3).Intravascular administration of contrast is widely known to be a common cause of hospital-acquired acute kidney injury (AKI). In 1983, Hou et al. (4) prospectively evaluated 2216 patients with hospital-acquired AKI and found decreased renal perfusion and major surgery to be the leading causes of AKI. Contrast medium (CM) was the next most common cause, accounting for 12% of cases of AKI, and was associated with an in-hospital mortality of 6%. In 1987, Shusterman et al. (5) demonstrated that CM was one of four major factors contributing to hospital acquired AKI (the others being volume depletion, congestive heart failure, and aminoglycosides).The exact risk for CIN is difficult to determine. It is widely known that in patients with normal renal function, even in the presence of diabetes, the risk for CIN is Յ1 to 2% (1). In patients with chronic kidney disease (CKD), it is also well accepted that the risk for CIN is significantly increased and rises in proportion to the severity of underlying renal impairment (1,6,7). Another established observation is that the coupling of CKD and diabetes dramatically increases the risk for CIN compared with that observed for CKD alone (6). Recent studies on CIN in "high-risk" patients have demonstrated a wide range of incidences from 1 to 45% (8,9). Reasons for this wide variation in CIN risk include study differences in the number and severity of underlying risk factors, definition of CIN used, prospective or retrospective collection of data, exclusion or nonexclusion of patients with other AKI etiologies, timing of the baseline serum creatinine (SCr) relative to hydration administration, type and amount of CM used, type and amount of hydration, and presence or absence of other prophylactic measures. Unfortunately, the consequence of these multiple factors makes it difficult to state with reasonable accuracy the clinical risk for CIN in a "high-risk" patient. Additional problems caused by the apparently observed wide range of CIN incidences are methodologically inadequate comparisons of studies for the value of procedural or prophylactic strategies to minimize CIN risk and prospective, randomized, controlled trials that are underpowered to answer the question for which they were designed.Despite the uncertainty of the incidence of CIN in "high-risk" patients, there are a number of reasons to believe that CIN will be an increasing cause of hospital-and outpatient-acquired AKI. Use of intravascular contrast is widespread and continues to expand. In 2003, 80 million doses of CM were administered worldwide (10,11). As of 2004, 3.3 million coronary angiograms, 25.7 million c...