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BioMed Research International
Volume 2014 (2014), Article ID 249810, 10 pages
Review Article

Molecular Mechanisms of Renal Cellular Nephrotoxicity due to Radiocontrast Media

1Department of Health Sciences, Nephrology Unit, “Magna Graecia” University, I-88100 Catanzaro, Italy
2Department of Nephrology, “Federico II” University, I-80131 Naples, Italy
3IRCCS Centro Neurolesi “Bonino Pulejo”, I-98124 Messina, Italy
4Department of Drug Sciences and Health Products, University of Messina, I-98168 Messina, Italy

Received 18 October 2013; Revised 9 December 2013; Accepted 24 December 2013; Published 18 March 2014

Academic Editor: Elizabeth N. Pearce

Copyright © 2014 Ashour Michael 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.


Modern iodinated radiocontrast media are all based on the triiodinated benzene ring with various chemical modifications having been made over the last few decades in order to reduce their toxicity. However, CIN remains a problem especially in patients with pre-existing renal failure. In vitro studies have demonstrated that all RCM are cytotoxic. RCM administration in vivo may lead to a decrease in renal medullary oxygenation leading to the generation of reactive oxygen species that may cause harmful effects to renal tissue. In addition, endothelin and adenosine release and decreased nitric oxide levels may worsen the hypoxic milieu. In vitro cell culture studies together with sparse in vivo rat model data have shown that important cell signalling pathways are affected by RCM. In particular, the prosurvival and proproliferative kinases Akt and ERK1/2 have been shown to be dephosphorylated (deactivated), whilst proinflammatory/cell death molecules such as the p38 and JNK kinases and the transcription factor NF-κB may be activated by RCM, accompanied by activation of apoptotic mediators such as caspases. Increasing our knowledge of the mechanisms of RCM action may help to develop future therapies for CIN.