Journal
INVESTIGATIVE RADIOLOGY
Volume 45, Issue 4, Pages 188-195Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/RLI.0b013e3181d2eed8
Keywords
reactive oxygen species; hypoxia; kidney; radiologic contrast media; kidney failure; acute
Funding
- Israeli Science Foundation [1473/08]
- Harvard Medical Faculty Physicians at Beth Israel Deaconess Medical Center, Boston
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Experimental findings in vitro and in vivo illustrate enhanced hypoxia and the formation of reactive oxygen species (ROS) within the kidney following the administration of iodinated contrast media, which may play a role in the development of contrast media-induced nephropathy. Clinical studies indeed support this possibility, suggesting a protective effect of ROS scavenging or reduced ROS formation with the administration of N-acetyl cysteine 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.
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