ABSTRACT
Vancomycin is a glycopeptides antibiotic which has been approved for clinical use since 1958. It is commonly used for treating mechanism-resistant Staphylococcus aureus (MRSA) infection and is an important antibiotic for treating resistant infection (1, 2). The Killing action of vancomycin is slow and is negatively affected by biofi lm formation, stationary growth phase, large bacterial inoculates, and anaerobic growth conditions (3). Vancomycin is renally eliminated mainly via glomerular fi ltration, and to some extent via active tubular secretion (4). However, it is also associated with some adverse effects, including nephrotoxicity (5). Although the exact mechanism of vancomycin-induced renal toxicity is not well defi ned, current animal data suggest that proximal renal tubular cell necrosis by vancomycin accumulation as mechanism of nephrotoxicity and that oxidative stress might underlie the pathogenesis of vancomycin-induced toxicity (6-11). In most studies, nephrotoxicity has been defi ned as a 0.5 mg/dL elevation in serum creatinine if the initial serum creatinine was ≤3 mg/dL, or a rise of ≥1mg/dL if the initial serum creatinine was ≤ 3 mg/dL (2). The serum trough concentration threshold associated with vancomycin nephrotoxicity
National Institute of Food and Drug Safety Evaluation, Ministry of Food and Drug Safety, Osong Health Technology Administration 363-951, South Korea. aEmail: 0jjy@korea.kr
has been reported to be ≥10-20 mg/L (12-16). Treatment with vancomycin beyond 1 week can increase the incidence of associated nephrotoxicity from 6 to 21%. With more than 2 weeks of vancomycin therapy, the incidence of renal failure may reach up to 30% (12, 15, 17). Fortunately, vancomycininduced nephrotoxicity is usually reversible, with a low incidence of residual damage if the antibiotic is discontinued or if doses are correctly adjusted immediately after the occurrence of renal failure (18).
