Figure 1.

Pathophysiology of contrast-associated acute kidney injury. Two main mechanisms contribute to the pathogenesis of contrast-associated acute kidney injury: direct cytotoxic effects on tubular and endothelial cells and intrarenal vasoconstriction, favored by an imbalance between vasoconstricting and vasodilating mediators. The medullary hypoxia resulting from renal vasoconstriction further alters the structure and function of renal tubular cells. The increased production of free oxygen species and the consequent increase in oxidative stress aggravate renal vasoconstriction and exert toxic effects on renal tubular cells. In parallel, renal ischemia and local cytotoxic effects aggravate oxidative stress, creating a vicious cycle. The coexistence and mutual stimulation of these mechanisms eventually result in contrast-associated acute kidney injury.