Mechanisms, Risk factors and Preventive Measures Associated with Drug-Induced Nephrotoxicity

Review Article

Abstract

Drug-induced nephrotoxicity represents a major clinical challenge, manifesting as both acute kidney injury (AKI) and chronic kidney disease (CKD). Multiple therapeutic agents, including aminoglycosides, nonsteroidal anti-inflammatory drugs (NSAIDs), cisplatin, immunosuppressants, radiocontrast media, and various herbal products can impair renal function through diverse pathophysiological mechanisms. These mechanisms encompass direct tubular toxicity, glomerular injury, interstitial nephritis, vascular compromise, oxidative stress, and crystal nephropathy. The proximal tubules serve as the primary site of injury for many nephrotoxic agents due to their role in drug metabolism and transport. Risk factors such as advanced age, pre-existing kidney disease, dehydration, and concurrent use of multiple nephrotoxic medications increase susceptibility to renal injury. Early recognition of nephrotoxicity involves monitoring serum creatinine, blood urea nitrogen, electrolytes, and novel biomarkers. Prevention strategies include appropriate drug selection, dose adjustment based on renal function, therapeutic drug monitoring, and adequate hydration. Management approaches focus on discontinuing the offending agent when possible, maintaining fluid and electrolyte balance, and implementing renal replacement therapy in severe cases. Recent advances in imaging techniques and biomarker development have enhanced the ability to detect and monitor drug-induced kidney injury. Given the increasing prevalence of kidney disease and the expanding arsenal of potentially nephrotoxic medications, vigilant monitoring and implementation of preventive strategies remain crucial for preserving renal function and optimizing patient outcomes.