Cisplatin-Induced Nephrotoxicity and Renoprotective Strategies

Cisplatin is a cornerstone chemotherapeutic agent whose clinical efficacy is often limited by its dose-dependent nephrotoxicity. Following systemic administration, cisplatin accumulates in proximal tubular epithelial cells, where it induces reactive oxygen species (ROS) generation, DNA damage and mitochondrial dysfunction. These primary insults trigger inflammatory cascades, tubular apoptosis and necrosis, culminating in acute kidney injury (AKI) and, in repeated courses, chronic kidney disease. Conventional prevention relies on rigorous hydration, diuresis and electrolyte supplementation, but these measures are not universally protective and may pose logistical challenges. Recent advances seek to preserve antitumour potency while mitigating renal injury through targeted antioxidant formulations, anti-inflammatory agents, transporter modulation and genetic interventions. Emerging nanosystems, natural product adjuvants and small-molecule regulators of key signalling pathways offer renewed promise for safeguarding renal function without compromising cisplatin’s cytotoxicity against malignancies.

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Cisplatin-Induced Nephrotoxicity and Renoprotective Strategies publication trend

The graph below shows the total number of articles in cisplatin-induced nephrotoxicity and renoprotective strategies across all publications each year (not limited to Nature Index journals).

Technical terms

Acute kidney injury (AKI): Sudden decline in renal function marked by reduced glomerular filtration and elevated serum creatinine.

Reactive oxygen species (ROS): Highly reactive molecules derived from oxygen that can damage cellular lipids, proteins and DNA.

Apoptosis: Programmed cell death characterised by caspase activation and DNA fragmentation.

Proximal tubular epithelial cells: Kidney cells in the nephron segment responsible for reabsorption and a primary site of cisplatin accumulation.

Nrf2: Nuclear transcription factor that induces expression of antioxidant response elements.

NF-κB: Transcription factor central to the regulation of inflammatory cytokine production.

References

1. Protective effect of spore oil-functionalized nano-selenium system on cisplatin-induced nephrotoxicity by regulating oxidative stress-mediated pathways and activating immune response. Journal of Nanobiotechnology (2023).
2. Molecular mechanisms of cisplatin-induced nephrotoxicity: a balance on the knife edge between renoprotection and tumor toxicity. Journal of Biomedical Science (2019).
3. Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury. International Journal of Molecular Sciences (2019).
4. Natural products: potential treatments for cisplatin-induced nephrotoxicity. Acta Pharmacologica Sinica (2021).
5. Mechanisms of Cisplatin-Induced Acute Kidney Injury: Pathological Mechanisms, Pharmacological Interventions, and Genetic Mitigations. Cancers (2021).