Drug-Induced Nephrotoxicity of Commonly Used Drugs: Mechanisms and Prevention

Abstract

Drug-induced nephrotoxicity (DIN) is a frequent, under-recognised cause of acute kidney injury (AKI) and progression to chronic kidney disease (CKD). The kidney’s unique physiology-high perfusion, concentrated solute load, many xenobiotic transporters, and high metabolic demands-renders it particularly vulnerable to injury from therapeutic agents. Common drug classes implicated in nephrotoxicity include non-steroidal anti-inflammatory drugs (NSAIDs), aminoglycosides, radiocontrast media, chemotherapeutics, calcineurin inhibitors, antivirals and antifungals. The mechanisms of injury are heterogeneous, involving intraglomerular haemodynamic alterations, direct tubular cytotoxicity, crystal nephropathy, thrombotic microangiopathy, rhabdomyolysis-mediated injury, and interstitial inflammation. Early recognition of risk factors (e.g., older age, baseline renal impairment, dehydration, polypharmacy) and application of preventive strategies-such as dose adjustment, hydration, monitoring of renal function and novel biomarkers-can significantly reduce the incidence and severity of DIN. This review summarises mechanistic pathways of drug-related nephrotoxicity, examines major nephrotoxic drug classes, considers emerging biomarkers and new prevention strategies, and provides a synthesis of best-practice recommendations.