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Biomed Res Int. 2013;2013:868321. doi: 10.1155/2013/868321. Epub 2013 Dec 29.

Role of reactive oxygen species in pathogenesis of radiocontrast-induced nephropathy.

Author information

1
Department of Nephrology, "Federico II" University of Naples, 80131 Naples, Italy.
2
Department of Health Sciences, "Magna Graecia" University, Catanzaro, Italy.
3
National Cancer Institute G. Pascale, Naples, Italy.

Abstract

In vitro and in vivo studies have demonstrated enhanced hypoxia and formation of reactive oxygen species (ROS) in the kidney following the administration of iodinated contrast media, which play a relevant role in the development of contrast media-induced nephropathy. Many studies indeed support this possibility, suggesting a protective effect of ROS scavenging or reduced ROS formation with the administration of N-acetylcysteine and bicarbonate infusion, respectively. Furthermore, most risk factors, predisposing to contrast-induced nephropathy, are prone to enhanced renal parenchymal hypoxia and ROS formation. In this review, the association of renal hypoxia and ROS-mediated injury is outlined. Generated during contrast-induced renal parenchymal hypoxia, ROS may exert direct tubular and vascular endothelial injury and might further intensify renal parenchymal hypoxia by virtue of endothelial dysfunction and dysregulation of tubular transport. Preventive strategies conceivably should include inhibition of ROS generation or ROS scavenging.

PMID:
24459673
PMCID:
PMC3891610
DOI:
10.1155/2013/868321
[Indexed for MEDLINE]
Free PMC Article
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