Abstract

Vancomycin, discovered in 1953 and widely used today, has a nephrotoxic potential that has long been debated. The frequency of renal involvement is variable and can range from 5% to 30% depending concomitant risk factors: overdose, chronic kidney disease, obesity, hypovolemia, and use of other nephrotoxic drugs as aminoglycosides. Its association with piperacillin–tazobactam also appears to increase the risk of nephrotoxicity. This hypothesis should be confirmed experimentally. Vancomycin-induced oxidative stress in tubular cells and intraluminal cast formation are the two physiopathological mechanisms explaining its nephrotoxicity. Vancomycin may induce acute tubular injury and rapid decline in renal function. These lesions are often reversible when the infusion is discontinued, but sometimes chronic kidney failure may ensue. As vancomycin is widely used and the current tendency is to increase target trough levels, it is necessary to identify risk factors in order to reduce its risk of nephrotoxicity.

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