DRUG-INDUCED ACUTE KIDNEY INJURY: INCIDENCE, PATHOPHYSIOLOGICAL MECHANISMS, AND PROGNOSTIC FACTORS – A COMPREHENSIVE REVIEW

Drug-induced acute kidney injury (DI-AKI) is an important and potentially preventable complication of pharmacotherapy, particularly among hospitalized, critically ill, and patients receiving multiple nephrotoxic medications.[1,2] Drugs can produce acute kidney injury through diverse mechanisms, including renal haemodynamic alterations, direct tubular toxicity, acute tubulointerstitial nephritis, crystal nephropathy, rhabdomyolysis, thrombotic microangiopathy, and immune-mediated renal injury.[1,3,4] Previous reviews have predominantly focused on individual nephrotoxic drugs, conventional mechanisms, or selected renal biomarkers.[²-⁵] The present review aims to provide a more integrated and contemporary assessment by correlating specific drug classes with their mechanisms of renal injury, clinical patterns, risk factors, diagnostic approaches, biomarkers, prevention, and management strategies. Particular attention is given to conventional biomarkers such as serum creatinine and blood urea nitrogen, which may identify renal functional decline relatively late, and to emerging biomarkers including kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, N-acetyl-β-D-glucosaminidase, clusterin, and osteopontin.[5-8] Recent evidence also highlights the increasing role of biomarker panels, proteomics, metabolomics, artificial intelligence, and personalized approaches in the early recognition and monitoring of drug-induced renal injury.[⁶˒⁷] In addition, newer approaches to defining and classifying DI-AKI may improve the identification of renal injury before substantial functional deterioration occurs.[⁸˒⁹] Unlike earlier reviews that primarily describe nephrotoxic agents or individual mechanisms, this review integrates drug-specific injury patterns with emerging biomarkers, risk stratification, pharmacovigilance, and preventive strategies. Such an integrated approach may facilitate earlier recognition, individualized management, and reduction of drug-related renal morbidity.