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BioMed Research International
Volume 2014 (2014), Article ID 358136, 15 pages
http://dx.doi.org/10.1155/2014/358136
Review Article

Contrast Media Viscosity versus Osmolality in Kidney Injury: Lessons from Animal Studies

Institute of Physiology and Center for Cardiovascular Research, Charité-University Medicine Berlin, Campus Mitte, Hessische Straße 3-4, 10115 Berlin, Germany

Received 18 October 2013; Accepted 29 December 2013; Published 23 February 2014

Academic Editor: Richard Solomon

Copyright © 2014 Erdmann Seeliger 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.

Abstract

Iodinated contrast media (CM) can induce acute kidney injury (AKI). CM share common iodine-related cytotoxic features but differ considerably with regard to osmolality and viscosity. Meta-analyses of clinical trials generally failed to reveal renal safety differences of modern CM with regard to these physicochemical properties. While most trials’ reliance on serum creatinine as outcome measure contributes to this lack of clinical evidence, it largely relies on the nature of prospective clinical trials: effective prophylaxis by ample hydration must be employed. In everyday life, patients are often not well hydrated; here we lack clinical data. However, preclinical studies that directly measured glomerular filtration rate, intrarenal perfusion and oxygenation, and various markers of AKI have shown that the viscosity of CM is of vast importance. In the renal tubules, CM become enriched, as water is reabsorbed, but CM are not. In consequence, tubular fluid viscosity increases exponentially. This hinders glomerular filtration and tubular flow and, thereby, prolongs intrarenal retention of cytotoxic CM. Renal cells become injured, which triggers hypoperfusion and hypoxia, finally leading to AKI. Comparisons between modern CM reveal that moderately elevated osmolality has a renoprotective effect, in particular, in the dehydrated state, because it prevents excessive tubular fluid viscosity.