The precise mechanisms underlying contrast-induced acute kidney injury (CI-AKI) are not well understood. Intracellular Ca(2+) overload is considered to be a key factor in CI-AKI. Voltage-dependent Ca(2+) channel (VDC) and Na(+)/Ca(2+) exchanger (NCX) system are the main pathways of intracellular Ca(2+) overload in pathological conditions. Here, we review the potential underlying mechanisms involved in CI-AKI and discuss the role of NCX-mediated intracellular Ca(2+) overload in the contrast media-induced renal tubular cell injury and renal hemodynamic disorder.