Fig. 1
Pathophysiology of CIN. Pathogenesis of CIN consists of 3 mechanisms; direct effect, indirect effect, and generation of ROS. Direct effects include, direct cytotoxicity of CM to nephron leading to cellular apoptosis or necrosis and tubular injury. Indirect effects are that CM could alter renal hemodynamics, leading to intrarenal vasoconstriction, contributing to medullary hypoxia. This mechanism is mediated by the increase in vasoconstrictive mediators including renin, angiotensin II, and endothelin along with the decreasing of vasodilatory mediators including nitric oxide and PGI2. Lastly, CM can generate ROS and also reduce antioxidant enzyme activity as a result of various complex mechanisms which result in oxidative stress, leading to progression of impaired renal function. CIN, contrast-induced nephropathy; CM, contrast media; PGI2, prostaglandin I2; ROS, reactive oxygen species