Figure 1.

Pathophysiology of contrast-induced nephropathy (CIN) and promising strategies to preserve kidney function. Iodinated CM has direct cytotoxic effect on endothelial cells and renal tubular epithelial cells, induces vasoconstriction causing hypoxia in the outer medulla, and enhances the generation of reactive oxygen species. These changes influence one another and ultimately lead to kidney injury. Each box contains underlying mechanisms relevant to those three pathways. Hydration is the mainstay of CIN preventive strategies and can reduce harmful effect of CM in all three aspects. Other previously reported preventive measures and pharmaceutical agents are presented with regard to each pathogenic process. * These pharmaceutical agents have been studied in in vitro and in vivo experiments to reduce oxidative stress, that is, to reverse each pathogenic pathway. However, because Nrf2 expression increases during CM-induced oxidative stress as a cytoprotective response, Nrf2 activation is preventive against CIN. ** The preventive role of these agents on CIN is controversial. CM, contrast media; MAPK, mitogen-activated protein kinase; Nox, nicotinamide adenine dinucleotide phosphate oxidase; ROCK, rho-kinase; SIRT1, silent information regulator 1; Nrf2, nuclear factor erythroid 2-related factor 2; RBC, red blood cell.