Pathophysiology of Contrast-Induced Acute Kidney Injury.

Passing contrast media through the renal vascular bed leads to vasoconstriction. The perfusion decrease leads to ischemia of tubular cells. Through ischemia and direct toxicity to renal tubular cells, reactive oxygen species formation is increased, enhancing the effect of vasoconstrictive mediators and decreasing the bioavailability of vasodilative mediators. Reactive oxygen species formation leads to oxidative damage to tubular cells. These interacting pathways lead to tubular necrosis. In the pathophysiology of contrast-induced acute kidney injury, low osmolar and iso-osmolar agents have theoretic advantages and disadvantages; however, clinically the difference in incidence of contrast-induced acute kidney injury has not changed.