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BioMed Research International
Volume 2014 (2014), Article ID 236930, 21 pages
Review Article

Pharmacological Strategies to Prevent Contrast-Induced Acute Kidney Injury

Nephrology Unit, Department of Medicine, Faculty of Medicine, Thammasat University (Rangsit Campus), Klong Luang, Pathumtani 12121, Thailand

Received 19 October 2013; Revised 3 January 2014; Accepted 7 January 2014; Published 26 February 2014

Academic Editor: Michele Andreucci

Copyright © 2014 Pattharawin Pattharanitima and Adis Tasanarong. 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 acute kidney injury (CI-AKI) is the most common iatrogenic cause of acute kidney injury after intravenous contrast media administration. In general, the incidence of CI-AKI is low in patients with normal renal function. However, the rate is remarkably elevated in patients with preexisting chronic kidney disease, diabetes mellitus, old age, high volume of contrast agent, congestive heart failure, hypotension, anemia, use of nephrotoxic drug, and volume depletion. Consequently, CI-AKI particularly in high risk patients contributes to extended hospitalizations and increases long-term morbidity and mortality. The pathogenesis of CI-AKI involves at least three mechanisms; contrast agents induce renal vasoconstriction, increase of oxygen free radicals through oxidative stress, and direct tubular toxicity. Several strategies to prevent CI-AKI have been evaluated in experimental studies and clinical trials. At present, intravascular volume expansion with either isotonic saline or sodium bicarbonate solutions has provided more consistent positive results and was recommended in the prevention of CI-AKI. However, the proportion of patients with risk still develops CI-AKI. This review critically evaluated the current evidence for pharmacological strategies to prevent CI-AKI in patients with a risk of developing CI-AKI.