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Cyclophosphamide-Induced Nephrotoxicity and Nephroprotection in Rodent Models: A Systematic Review and Random-Effects

Denis Oberiukhtin¹, Anton Chernitskiy², Desheng Hu^3,4,5

¹Institute of Immunology and Physiology, Ural Branch of the Russian Academy of Science, 106 Pervomaiskaya Street, Ekaterinburg 620049, Russia.

Journal of Xenobiotics

|March 24, 2026

Summary

Cyclophosphamide causes significant kidney damage in rodent models, increasing creatinine and urea levels. While some interventions show promise in reducing oxidative stress, variability hinders definitive conclusions on renoprotective effects.

Keywords:

acute kidney injury apoptosis cyclophosphamide inflammation meta-analysis nephroprotection nephrotoxicity oxidative stress rodent models systematic review

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Area of Science:

Nephrology
Toxicology
Pharmacology

Background:

Cyclophosphamide (CP) is a widely used chemotherapy and immunosuppressant.
Dose-limiting nephrotoxicity is a significant clinical challenge associated with CP treatment.

Purpose of the Study:

To systematically review and meta-analyze in vivo rodent models of CP-induced nephrotoxicity.
To evaluate the efficacy of interventions in mitigating CP-induced renal injury.

Main Methods:

Systematic review of rodent models of CP nephrotoxicity (2010-2025).
Meta-analysis of serum creatinine, serum urea, and renal oxidative stress markers.
Separation of model effects (CP vs. control) and treatment effects (intervention + CP vs. CP-only).

Main Results:

CP significantly increased serum creatinine by 1.059 mg/dL and serum urea by 39.852 mg/dL.
Interventions showed consistent protection against oxidative stress markers (MDA/TBARS, glutathione).
Functional recovery estimates were variable, limited by reporting and heterogeneity.

Conclusions:

CP is a valid preclinical model for studying functional and redox-mediated renal injury.
Multiple intervention classes can partially mitigate CP nephrotoxicity.
Heterogeneity in reporting and study design prevents reliable ranking of renoprotective agents.