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Updated: May 5, 2026

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
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Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

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Oxidative Stress-Driven Mechanisms and Biomarkers of Drug-Induced Nephrotoxicity: Translational Insights and

Rizwan Ahamad1, Nida Mubin2, Mohammed Alnukhali3,4

  • 1Department of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi 110062, India.

Antioxidants (Basel, Switzerland)
|May 4, 2026
PubMed

Insights

Drug-induced kidney injury is often caused by oxidative stress disrupting cellular balance. This review explores how reactive oxygen species (ROS) damage kidneys and discusses new antioxidant strategies for prevention.

Area of Science:

  • Nephrology
  • Toxicology
  • Biochemistry

Background:

  • Drug-induced kidney injury (DIKI) is a significant clinical issue linked to various medications.
  • Nephrotoxicity from anticancer, immunosuppressive, and anti-infective drugs is increasingly attributed to oxidative stress.
  • Disruption of redox homeostasis in renal tubular cells leads to cellular damage and functional decline.

Purpose of the Study:

  • To review the mechanisms of oxidative stress in drug-induced nephrotoxicity.
  • To highlight the translational relevance of these mechanisms.
  • To discuss emerging biomarkers and antioxidant strategies for kidney protection.

Main Methods:

  • Literature review of mechanistic insights into drug-induced nephrotoxicity.
  • Focus on oxidative stress and redox homeostasis disruption pathways.
  • Examination of current and emerging therapeutic strategies.

Main Results:

  • Excessive reactive oxygen species (ROS) production overwhelms antioxidant defenses, causing mitochondrial dysfunction and inflammation.
  • Oxidative stress triggers apoptosis, necrosis, microvascular injury, and reduced glomerular filtration rate.
  • Dysregulation of redox-sensitive pathways exacerbates renal vulnerability.

Conclusions:

  • Oxidative stress is a key mediator of DIKI, involving complex cellular signaling pathways.
  • Early detection biomarkers and novel antioxidant/redox-modulating therapies hold promise for preventing kidney injury.
  • Understanding these mechanisms is crucial for preserving kidney function during drug therapy.
Keywords:
acute kidney injuryantioxidant therapychronic kidney diseasedrug-induced nephrotoxicitykidney injury biomarkersmitochondrial dysfunctionoxidative stressreactive oxygen species (ROS)redox signalingrenal tubular injury

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