Abstract
The precise mechanisms underlying contrast-induced acute kidney injury (CI-AKI) are not well understood. Intracellular Ca2+ overload is considered to be a key factor in CI-AKI. Voltage-dependent Ca2+ channel (VDC) and Na+/Ca2+ exchanger (NCX) system are the main pathways of intracellular Ca2+ overload in pathological conditions. Here, we review the potential underlying mechanisms involved in CI-AKI and discuss the role of NCX-mediated intracellular Ca2+ overload in the contrast media-induced renal tubular cell injury and renal hemodynamic disorder.
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