Review Article

Reactive Oxygen Species and the Pathogenesis of Radiocontrast-Induced Nephropathy

Heyman, Samuel N. MD^*; Rosen, Seymour MD^†; Khamaisi, Mogher MD, PhD^‡; Idée, Jean-Marc PhD^§; Rosenberger, Christian MD^¶

Author Information

From the *Department of Medicine, Hadassah Hospital, Mt. Scopus and the Hebrew University Medical School, Jerusalem, Israel; †Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA; ‡Department of Medicine, Institute of Endocrinology, Rambam Hospital, The Technion Medical School, Haifa, Israel; §Guerbet Research Division, Aulnay-sous-Bois, France; and ¶Department of Nephrology, Charité University Clinic, Berlin, Germany.

Received December 1, 2009, and accepted for publication, after revision, December 22, 2009.

Supported by the Israeli Science Foundation (1473/08) and the Harvard Medical Faculty Physicians at Beth Israel Deaconess Medical Center, Boston.

Reprints: Samuel N. Heyman, MD, Department of Medicine, Hadassah Hospital, Mt. Scopus, PO Box 24035, Jerusalem 91240, Israel. E-mail: [email protected].

Investigative Radiology 45(4):p 188-195, April 2010. | DOI: 10.1097/RLI.0b013e3181d2eed8

Abstract

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.