Journal of Stress Physiology & Biochemistry, Vol. 22 No. 2 2026, pp. 20-27 ISSN 1997-0838
Original Text Copyright (cc) 2026 by  Raut, Dhurvey, Nagwanshi and Joshi



REVIEW
Full text in PDF Download to Citation Manager Permanent url
         

Cyclophosphamide-Induced Nephrotoxicity: A Mini-Review

Chhayala Raut 1, Varsha Dhurvey 2, Aashikkumar Nagwanshi 3 and Dharita Joshi 4

1 P.G. Student, Department of Zoology, RTM Nagpur University, Nagpur-440033, MS (India)
2 Professor, Department of Zoology, RTM Nagpur University, Nagpur-440033, MS (India)
3 Assistant Professor, Department of Zoology, RTM Nagpur University, Nagpur-440033, MS (India)
4 Research Scholar, Department of Zoology, RTM Nagpur University, Nagpur-440033, MS (India)

*E-Mail: djdharita@gmail.com


Received March 12, 2026


Cyclophosphamide (CP) is a widely used alkylating chemotherapeutic and immunosuppressive drug for treating malignancies, autoimmune disorders, and renal diseases. However, its clinical use is limited by nephrotoxicity caused by toxic metabolites such as phosphoramide mustard and acrolein. These metabolites induce oxidative stress, inflammation, mitochondrial dysfunction, and apoptosis in renal tissues. CP administration results in elevated renal biomarkers including serum creatinine, blood urea nitrogen, cystatin-C, KIM-1, and NGAL, along with severe histopathological damage. Activation of inflammatory cytokines and NF-κB pathways further aggravates renal injury. Various antioxidants and pharmacological agents have shown potential renoprotective effects.

Key words:    Cyclophosphamide, Nephrotoxicity, Oxidative stress, Renal biomarkers, Inflammation, Apoptosis

Back to issue content