Drug-induced Nephrotoxicity: An Updated Review of Pharmacotherapy based on Monotherapy and Polypharmacy

Introduction: Kidney damage, which presents with various manifestations and mechanisms, may result from drug-induced nephrotoxicity (ranging from mild to advanced), affecting glomerular and tubular function, filtration, and the integrity of both tubules and glo-meruli. Objective: This article aims to provide an updated review of drug-induced nephrotoxicity. Methods: This is a focused literature review using keywords relevant to the topic in PubMed, Scopus, and Web of Science. The reference lists of appropriate articles published up to 11 June 2025 were examined to identify significant papers relevant to the aim of the investiga-tion. Comprehensive, high-quality, and well-informed articles were selected and used for this review (n = 100). Results: Transporter defects, apoptosis, and mitochondrial injury may be caused by cidofovir, adefovir, and tenofovir. Acyclovir, indinavir, and foscarnet can lead to acute kidney injury through crystal nephropathy due to intratubular obstruction. Nephrotoxicity is associated with polypharmacy involving isoniazid, rifampicin, and pyrazinamide in anti-tuberculosis regi-mens. Polypharmacy with aminosalicylates, steroids, antibiotics, immunosuppressants, and biological agents prescribed for inflammatory bowel disease may also lead to drug-induced nephrotoxicity. Antibiotics and drugs such as acetaminophen and aspirin can cause acute in-terstitial nephritis. Tacrolimus and cyclosporine are nephrotoxic, and this effect may be dose-dependent and reversible or, in some cases, irreversible in the long term. Discussion: Due to its economic and therapeutic implications, drug-induced nephrotoxicity remains an important issue in pharmacotherapy. To assess kidney toxicity, measurement of the following should be considered: (1) urine proteins and enzymatic activity, (2) proteinuria, (3) kidney injury molecule-1, (4) neutrophil gelatinase-associated lipocalin, (5) type IV col-lagen, and (6) clusterin. Conclusion: Information on the pathogenic mechanisms of renal injury, patient- and drug-related risk factors, and preventive measures should be combined with vigilance and early intervention in the context of nephrotoxic drugs. For improved management of drug-induced nephrotoxicity, the use of relevant biomarkers to monitor kidney function is recommended and may be advantageous.