Review of vancomycin-induced renal toxicity: an update

Abstract

Abstract:In recent times the use of larger doses of vancomycin aimed at curbing the increasing incidence of resistant strains of Staphylococcus aureus has led to a wider report of acute kidney injury (AKI). Apart from biological plausibility, causality is implied by the predictive association of AKI with larger doses, longer duration, and graded plasma concentrations of vancomycin. AKI is more likely to occur with the concurrent use of nephrotoxic agents, and in critically ill patients who are susceptible to poor renal perfusion. Although most vancomycin-induced AKI cases are mild and therefore reversible, their occurrence may be associated with greater incidence of end-stage kidney disease and higher mortality rate. The strategy for its prevention includes adequate renal perfusion and therapeutic drug monitoring in high-risk individuals. In the near future, there is feasibility of renoprotective use of antioxidative substances in the delivery of vancomycin.

Effect of perioperative sodium bicarbonate administration on renal function following cardiac surgery for infective endocarditis: a randomized, placebo-controlled trial

“…Furthermore, prolonged use of nephrotoxic antibiotics preoperatively, and administration of contrast media shortly before cardiac surgery, adds to the risk of AKI by enhancing proinflammatory oxidative stress [16, 24]. Sodium bicarbonate administration produces blood and urine alkalization and may slow pH-dependent Haber-Weiss free-radical production, thereby attenuating reactive oxygen species-mediated tubular injury [11, 24, 25].…”

“…After a pilot study reported that with sodium bicarbonate infusion there was a reduced incidence of AKI after cardiac surgery [8], numerous clinical trials evaluated its renoprotective efficacy in different types of surgery and patients, yielding conflicting results [12–15]. Considering the massive oxidative stress associated with systemic inflammation and prolonged use of nephrotoxic antibiotics in patients with IE [16], the abilities of sodium bicarbonate to attenuate oxidative stress may prove especially helpful in preventing AKI in these patients. However, most previous studies investigating the renal effects of sodium bicarbonate have excluded patients with systemic infection, and no study has heretofore been conducted solely in patients with IE.…”

p53 activates miR-192-5p to mediate vancomycin induced AKI

“…Therefore, one guideline suggested a dose of 15–20 mg/ml VAN. However, emerging data to achieve these treatment targets carry a substantial risk for nephrotoxicity89. Although some authors reported that the mechanism of VAN nephrotoxicity is similar to that of gentamicin, it remains unclear irrespective of numerous studies over the past several decades.…”

Vancomycin-Associated Acute Kidney Injury with a Steep Rise in Serum Creatinine

“…Until the late 1970s, vancomycin was not widely used because of a widespread concern that the original preparations contained nephrotoxic impurities. This concern was validated by a reduction in vancomycin-associated (VA) acute kidney injury (AKI) that followed a technological improvement in the fermentation process, which led to a 95% level of product purity by 1985 [1-3]. Subsequently, most reports of AKI associated with vancomycin were described in the context of concomitant administration of other known nephrotoxic drugs, such as aminoglycosides [4, 5].…”