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Review
. 2023 Aug 25;8(11):2211-2225.
doi: 10.1016/j.ekir.2023.08.031. eCollection 2023 Nov.

Overview of Antibiotic-Induced Nephrotoxicity

Ruth E Campbell  1 , Chang Huei Chen  1 , Charles L Edelstein  1
Affiliations
Review

Overview of Antibiotic-Induced Nephrotoxicity

Ruth E Campbell et al. Kidney Int Rep. .

Abstract

Drug-induced nephrotoxicity accounts for up to 60% of cases of acute kidney injury (AKI) in hospitalized patients and is associated with increased morbidity and mortality in both adults and children. Antibiotics are one of the most common causes of drug-induced nephrotoxicity. Mechanisms of antibiotic-induced nephrotoxicity include glomerular injury, tubular injury or dysfunction, distal tubular obstruction from casts, and acute interstitial nephritis (AIN) mediated by a type IV (delayed-type) hypersensitivity response. Clinical manifestations of antibiotic-induced nephrotoxicity include acute tubular necrosis (ATN), AIN, and Fanconi syndrome. Given the potential nephrotoxic effects of antibiotics on critically ill patients, the use of novel biomarkers can provide information to optimize dosing and duration of treatment and can help prevent nephrotoxicity when traditional markers, such as creatinine, are unreliable. Use of novel kidney specific biomarkers, such as cystatin C and urinary kidney injury molecule-1 (KIM-1), may result in earlier detection of AKI, dose adjustment, or discontinuation of antibiotic and development of nonnephrotoxic antibiotics.

Keywords: AKI; KIM-1; antibiotics; cystatin C; drug-induced nephrotoxicity; novel biomarkers.

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Figures

Figure 1
Figure 1
Mechanisms of antibiotic-induced nephrotoxicity. ATN, acute tubular necrosis.
See this image and copyright information in PMC

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