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A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion
Published on: February 2, 2021
Pathophysiology of Contrast-Induced Acute Kidney Injury
Remy W F Geenen1, Hylke Jan Kingma2, Aart J van der Molen3
1Department of Radiology, Medisch Centrum Alkmaar, Wilhelminalaan 12, Alkmaar 1815 JD, Netherlands.
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.
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