Overview of Antibiotic-Induced Nephrotoxicity

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.

Automated summary

Drug-induced nephrotoxicity is a common cause of acute kidney injury in hospitalized patients, leading to increased morbidity and mortality. Antibiotics are a major culprit, causing various forms of kidney damage. Novel biomarkers can aid in early detection, optimization of treatment, and prevention of nephrotoxicity.