A 48-year-old man presents to the Emergency Department and complains of new onset of chest pain with exertion. He has a history of tobacco use, hypercholesterolemia, type 2 diabetes mellitus, and chronic renal disease (baseline serum creatinine concentration [SCr] 1.7 mg/dL; estimated glomerular function [eGFR] 47 mL/min per 1.73m2). Initially, he undergoes coronary computed tomography (CT) angiography, which demonstrates >75% narrowing of the proximal left anterior descending coronary artery. The next day he undergoes coronary catheterization with successful drug-eluting stent placement to an 80% stenosis of the left anterior descending coronary artery. He receives a total of 211 mL contrast agent (320 mgI/mL; 67.52 g iodine) from both examinations. His SCr level increases to a peak of 2.4 mg/dL at 48 hours after percutaneous intervention, returning to baseline over the next 72 hours. He recovers uneventfully. The treating physicians diagnose him with postinterventional contrast-induced nephropathy (CIN). After the introduction of iodinated contrast agents in the last century, their use was promptly linked to acute kidney injury (AKI).1 The presumed causal relationship between contrast medium (CM) exposure and AKI has since been axiomatic in clinical care, with substantial implications for patient management in the context of contrast-enhanced imaging. Indeed, fear of contrast-induced AKI is one of the most frequent reasons why CM is withheld from patients and thus frequently compromises the diagnostic information gained from imaging. Despite the nearly universal concern about the risks of CIN, several recent large-scale studies have questioned the general concept of CIN and the relationship between CM administration, AKI, and worsened clinical outcome.2,3 In fact, AKI may occur at similar rates in matched control groups of patients undergoing CT scanning with and without CM administration.4,5 Therefore, a clear differentiation between AKI due to other causes and true CIN …