Pathophysiology of Contrast-Induced Acute Kidney Injury

Remy W F Geenen; Hylke Jan Kingma; Aart J van der Molen

doi:10.1016/j.iccl.2014.03.007

Pathophysiology of Contrast-Induced Acute Kidney Injury

Interv Cardiol Clin. 2014 Jul;3(3):363-367. doi: 10.1016/j.iccl.2014.03.007. Epub 2014 Jun 28.

Authors

Remy W F Geenen¹, Hylke Jan Kingma², Aart J van der Molen³

Affiliations

¹ Department of Radiology, Medisch Centrum Alkmaar, Wilhelminalaan 12, Alkmaar 1815 JD, Netherlands. Electronic address: r.w.f.geenen@mca.nl.
² Department of Clinical Pharmacy, Stichting Apotheek der Haarlemse Ziekenhuizen, Boerhavelaan 24, Haarlem 2035 RC, Netherlands.
³ Department of Radiology, Leiden University Medical Center, Albinusdreef 2, Leiden 2333 ZA, Netherlands.

PMID: 28582221
DOI: 10.1016/j.iccl.2014.03.007

Abstract

Contrast-induced acute kidney injury (CI-AKI) refers to acute kidney injury (AKI) after intravenous or intra-arterial administration of contrast media (CM). The 2 key mechanisms related to AKI are acute tubular necrosis and prerenal azotemia. Although the pathophysiology of AKI is complex, modern frameworks show that AKI has 3 major pathways: hemodynamic injury, systemic inflammation, and toxic injury. In the pathophysiology of CI-AKI, 3 major distinct, but potentially interacting pathways are recognized: hemodynamic effects, increase in oxygen free radicals, and direct CM molecule tubular cell toxicity. This article reviews the pathophysiology of CI-AKI by describing and explaining these pathways.

Keywords: Contrast media adverse effects; Contrast media toxicity; Contrast-induced acute kidney injury; Contrast-induced nephropathy.

Publication types

Review