Prevention of vancomycin induced nephrotoxicity: a review of preclinical data
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REVIEW ARTICLE
Prevention of vancomycin induced nephrotoxicity: a review of preclinical data Sepideh Elyasi & Hossein Khalili & Shima Hatamkhani & Simin Dashti-Khavidaki
Received: 8 June 2012 / Accepted: 4 September 2012 # Springer-Verlag 2012
Abstract Purpose Several strategies have been proposed for the prevention of vancomycin-induced nephrotoxicity. Here, we review available evidence supporting the respective strategies. Method Data were collected by searching the Scopus, PubMed, and Medline databases and the Cochrane database of systematic reviews. The key words used as search terms were “vancomycin,” “nephrotoxicity”, “renal failure,” “renal damage,” “nephroprotective,” “renoprotective”, and “prevention.” Prospective or retrospective observational animal studies that evaluated the effects of a modality for the prevention of vancomycin-induced nephrotoxicity was included. Results and conclusion Animal studies show beneficial effects of various antioxidants, such as erdosteine, vitamin E, vitamin C, N-acetylcysteine, caffeic acid phenethyl ester, and erythropoietin, in the prevention of vancomycin-induced nephrotoxicity. However, before these agents can be used in clinical practice, their potential benefits must be confirmed in future randomized controlled human studies. Keywords Vancomycin . Nephrotoxicity . Prevention
Introduction Vancomycin is a glycopeptide antibiotic commonly used for treating methicillin-resistant Staphylococcus aureus (MRSA) infections. However, it is also associated with a number of adverse effects, including nephrotoxicity [1–5]. Vancomycin S. Elyasi : H. Khalili (*) : S. Hatamkhani : S. Dashti-Khavidaki Department of Clinical Pharmacy, Faculty of Pharmacy, Tehran University of Medical Sciences, P.O.Box: 14155/6451, 1417614411 Tehran, Iran e-mail: [email protected]
is currently the antibiotic of choice for serious infections caused by multi-resistant Gram-positive organisms, such as MRSA, methicillin resistant coagulase-negative staphylococci, and Enterococcus faecium [6, 7]. The incidence of vancomycin-induced nephrotoxicity (VIN) has been reported to be between 5 and 35 % [1, 3, 5–12]. This broad range for the rate of VIN reflects the different criteria used to detect renal injury. To provide consistency in future studies, novel criteria, namely the AKIN (Acute Kidney Injury Network) criteria, have been proposed for defining VIN. Using the AKIN criteria, Minejima et al. reported the incidence of AKI to be 19 % of patients following vancomycin therapy [13]. Although the exact mechanism of VIN is not well defined, current animal data suggest that vancomycin has oxidative effects on the proximal renal tubule [14–20] and that the use of antioxidants can prevent VIN [14, 18, 19]. The role of free radicals and oxidative stress in VIN has been documented in animal studies [15, 21–25], and it has also been shown that vancomycin can change the energy-dependent renal reabsorption function of the proximal tubule and alter mitochondrial function [17, 26, 27]. Based on these animal data, r
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