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• W4312097220 abstract "To the Editor—We read with interest the article entitled “Nephrotoxicity of vancomycin in combination with beta-lactam agents: ceftolozane-tazobactam vs. piperacillin-tazobactam” [1]. The authors used a unique methodological approach, use of a tazobactam-containing comparator product, to attempt to disentangle the relative importance of the beta-lactam and the beta-lactamase inhibitor in this toxicity evaluation. Their results implicate an association between piperacillin-tazobactam (TZP) and creatinine-defined acute kidney injury (AKI), suggested to be driven by piperacillin. While we applaud the exploration of the relationship between TZP and creatinine, we argue that prospective studies using alternative kidney biomarkers are required to determine the renal safety of the vancomycin-TZP combination, and that it is premature to make clinical decisions on the basis of this article. Like numerous previous studies, Alosaimy et al show that TZP is associated with a higher risk of creatinine-defined AKI versus a comparator beta-lactam. The authors propose a mechanism involving intracellular accumulation of piperacillin mediated via binding of Organic Anion Transporter 1 and Organic Anion Transporter 3 transporters in the proximal tubule. Crucially, however, these same transporters are implicated in the tubular handling of creatinine [2]. Thus, whether this binding results in intracellular accumulation of piperacillin and toxicity, or merely inhibition of creatinine secretion and pseudotoxicity, is unclear. Similar inhibition of creatinine secretion is well described for drugs such as sulfamethoxazole/trimethoprim or probenecid [2–4]. In addition, a recent prospective cohort study showed that vancomycin + TZP was associated with changes in creatinine but not changes in cystatin C, an alternative kidney biomarker not subject to tubular secretion [5]. The biological plausibility of an actual injury event is questionable. Prior animal studies that used urinary kidney injury biomarkers (eg, kidney injury molecule-1 [KIM-1], clusterin, and osteopontin) failed to identify increased injury [2, 6–8] during concurrent TZP and vancomycin therapy. This lack of association has been corroborated with functional experiments in animals that used gold-standard markers of glomerular filtration rate [9]. In the present study [10], the high proportion of stage 1 AKI (which could represent hemodynamic changes and not injury) drove the primary outcome. Coupled with no difference in need for kidney replacement therapy, pseudotoxicity is highly plausible, and an assessment of longer-term kidney outcomes is needed. Consequently, while these data may suggest that piperacillin rather than tazobactam increases serum creatinine, it remains unclear whether injury or dysfunction occurred. We argue that this is the key question that now faces the field." @default.
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• W4312097220 date "2022-12-23" @default.
• W4312097220 modified "2023-09-28" @default.
• W4312097220 title "Nephrotoxin Stewardship Alongside Antimicrobial Stewardship" @default.
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• W4312097220 doi "https://doi.org/10.1093/cid/ciac958" @default.
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