Biopsy-Proven Acute Tubular Necrosis due to Vancomycin Toxicity

Farheen Shah-Khan,Marc H Scheetz,Cybele Ghossein

doi:10.4061/2011/436856

Farheen Shah-Khan, Marc H Scheetz + Show 1 more

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https://doi.org/10.4061/2011/436856

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Abstract

Vancomycin (VAN) has been associated with acute kidney injury (AKI) since it has been put into clinical use in the 1950's. Early reports of AKI were likely linked to the impurities of the VAN preparation. With the advent of the more purified forms of VAN, the incidence of AKI related to VAN were limited to acute interstitial nephritis (AIN) or as a potentiating agent to other nephrotoxins such as Aminoglycosides. VAN as the sole etiologic factor for nephrotoxic acute tubular necrosis (ATN) has not been described. Here, we report a case of biopsy-proven ATN resulting from VAN.

Highlights

Vancomycin (VAN) has been associated with acute kidney injury (AKI) since it has been put into clinical use in the 1950’s
With the advent of the more purified forms of VAN, the incidence of AKI related to VAN were limited to acute interstitial nephritis (AIN) or as a potentiating agent to other nephrotoxins such as Aminoglycosides
The beneficial effect of some antioxidants like DL-α lipoic acid, Melatonin, Ginkgo biloba and milrinone have been shown to reduce the renal damage, suggesting the involvement of free radicals in renal damage [26]. While it is unclear if VAN-associated acute tubular necrosis is preventable, these data argue for prompt serum VAN monitoring given the rapid functional decline of patient nephrologic function even before the patient was scheduled to receive the 4th dose of therapeutically dosed VAN

Summary

Case Report

Vancomycin (VAN) has been associated with acute kidney injury (AKI) since it has been put into clinical use in the 1950’s. The PICC line was removed, and antibiotic therapy initiated with piperacillin-tazobactam and VAN. With a volume of distribution estimated at approximately 0.6 L/kg of actual body weight and a VAN clearance estimated to be at least 120 mL/min [3], the patient was expected to achieve an initial VAN trough of approximately 8 mg/L with steady state troughs above 10 mg/L with a dosing scheme of 2000 mg given every 12 hours. As pharmacokinetic estimates in patients above their average body weight exhibit substantial variability, the patient was initiated on the aforementioned dose with a measured VAN trough planned antecedent to the fourth dose (to capture steady-state concentrations). The following day, the serum creatinine was 3.62 mg/dL He became oligo-anuric with a urine output of 50 cc in 24 hours. The VAN serum concentration done on day 4 was 64.7 mg/L, and hemodialysis was initiated for volume overload. His creatinine improved to 1.2 mg/dL over the few weeks

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