Contrast-induced nephropathy (CIN) is one of the most common forms of hospital-acquired acute kidney injury (1). The elective or semielective timing of the majority of diagnostic and therapeutic procedures using iodinated contrast allows CIN to be one of the few causes of acute kidney injury that are amenable to implementation of preventive interventions. Numerous potential preventive strategies have been evaluated, including periprocedural administration of saline (2,3) or isotonic bicarbonate solutions (4–7); use of pharmacologic agents including diuretics (2), mannitol (2), natriuretic peptides (8), dopamine (9), fenoldopam (10), theophylline (11,12), and N-acetylcysteine (12–14); and prophylactic renal replacement therapy (15–17). In addition, multiple studies have compared the relative nephrotoxicity of various contrast agents (18–23). In virtually all of these studies, CIN has been defined in terms of small absolute or relative increases in serum creatinine concentration. Implicit in the use of these surrogate end points is the assumption that amelioration of contrast-associated increases in serum creatinine correlates with improved clinical outcomes. The association between CIN and adverse clinical outcomes, including cardiovascular complications and death, has been amply demonstrated in retrospective database analyses and …