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BioMed Research International
Volume 2013 (2013), Article ID 123589, 8 pages
Review Article

Why Is Diabetes Mellitus a Risk Factor for Contrast-Induced Nephropathy?

1Department of Medicine, Hadassah Hospital, Mt. Scopus and the Hebrew University Medical School, P.O. Box 24035, Jerusalem 91240, Israel
2Department of Nephrology, Charité Campus Mitte, Berlin 10115, Germany
3Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA
4Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA

Received 5 September 2013; Accepted 24 October 2013

Academic Editor: Michele Andreucci

Copyright © 2013 Samuel N. Heyman et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Contrast-induced nephropathy (CIN) remains a leading cause of iatrogenic acute kidney injury, as the usage of contrast media for imaging and intravascular intervention keeps expanding. Diabetes is an important predisposing factor for CIN, particularly in patients with renal functional impairment. Renal hypoxia, combined with the generation of reactive oxygen species, plays a central role in the pathogenesis of CIN, and the diabetic kidney is particularly susceptible to intensified hypoxic and oxidative stress following the administration of contrast media. The pathophysiology of this vulnerability is complex and involves various mechanisms, including a priori enhanced tubular transport activity, oxygen consumption, and the generation of reactive oxygen species. The regulation of vascular tone and peritubular blood flow may also be altered, particularly due to defective nitrovasodilation, enhanced endothelin production, and a particular hyperresponsiveness to adenosine-related vasoconstriction. In addition, micro- and macrovascular diseases and chronic tubulointerstitial changes further compromise regional oxygen delivery, and renal antioxidant capacity might be hampered. A better understanding of these mechanisms and their control in the diabetic patient may initiate novel strategies in the prevention of contrast nephropathy in these susceptible patients.