The Impact of Genetic Polymorphisms on Cisplatin-Induced Acute Kidney Injury: A Systematic Review

Document Type : Review Article

Authors

1 Department of Clinical Pharmacy Practice, Faculty of Pharmacy, The British University in Egypt, Cairo, Egypt

2 Department of Clinical Pharmacy, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt

3 Department of Clinical Oncology and Nuclear Medicine, Faculty of Medicine, Ain Shams University, Cairo, Egypt

Abstract

Cisplatin is a widely used chemotherapeutic agent effective against various solid tumors, including testicular, ovarian, lung, and bladder cancers. However, its clinical use is often limited by dose-dependent toxicities, with nephrotoxicity being the most concerning side effect. Patients undergoing multiple cycles of cisplatin chemotherapy frequently experience a sustained subclinical reduction in glomerular filtration rate (GFR), which can lead to acute kidney injury (AKI) and negatively impact patient outcomes. According to recent research, genetic variability, specifically, single nucleotide polymorphisms (SNPs), may contribute to interindividual differences in susceptibility to cisplatin-induced nephrotoxicity. This review summarizes current research on SNPs across key genes implicated in cisplatin metabolism, transport, and detoxification processes. It examines the association between specific genetic variations and the incidence and severity of nephrotoxicity in patients undergoing cisplatin therapy. Understanding the intricate molecular pathways and genetic variations associated with cisplatin nephrotoxicity is essential to prevent this adverse effect and guide personalized cisplatin treatment approaches. Further research is essential to validate these SNPs as predictive markers and to explore their potential role in guiding tailored cisplatin therapies.

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