Drs. Maurovich-Horvat, Bosserdt, and Kofoed contributed equally to this article. This article was published on March 4, 2022, at NEJM.org.

ur understanding of postcontrast acute kidney injury (AKI) (1,2) is limited by the lack of randomized control groups in clinical studies (3). Moreover, a recent reassessment of the risk resulting from exposure to contrast agents has questioned the existence of postcontrast AKI (4). While there is agreement that intra-arterial contrast agent administration can cause AKI (5), retrospective studies suggest that intravenous contrast material administration for CT has a similar risk of AKI to noncontrast CT (6-8). The latter finding was corroborated in a metaanalysis of 28 observational studies comparing CT studies performed with or without intravenous contrast material administration (9), while no randomized clinical trial has yet compared intravenous and intra-arterial contrast agent administration in relationship to AKI (10). Although the exact underlying mechanisms are poorly understood (11), the intravenous route of contrast agent administration may reduce AKI compared with intra-arterial injection (12) by avoiding microembolization from the aorta to the kidneys (13) and reducing peak contrast agent concentration in the renal arteries (14). However, a recent paired cohort study found minimal differences between patients who received both intravenous and intra-arterial contrast agents, with AKI frequencies of 9.9% and 11%, respectively (15). Similar findings with minimal differences in AKI rates were obtained by Karlsberg et al (16) in an intraindividual comparison of CT angiography (7.6%) and peripheral angiography (8.7%). On the other hand, a nonrandomized study showed a higher rate of AKI after catheterization (4.4%) than after CT (1.2%) (17), and large observational studies