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Cisplatin-induced Kidney Dysfunction and Perspectives on Improving Treatment Strategies

  • Oh, Gi-Su (Center for Metabolic Function Regulation, Department of Microbiology, Wonkwang University School of Medicine) ;
  • Kim, Hyung-Jin (Center for Metabolic Function Regulation, Department of Microbiology, Wonkwang University School of Medicine) ;
  • Shen, AiHua (Center for Metabolic Function Regulation, Department of Microbiology, Wonkwang University School of Medicine) ;
  • Lee, Su Bin (Center for Metabolic Function Regulation, Department of Microbiology, Wonkwang University School of Medicine) ;
  • Khadka, Dipendra (Center for Metabolic Function Regulation, Department of Microbiology, Wonkwang University School of Medicine) ;
  • Pandit, Arpana (Center for Metabolic Function Regulation, Department of Microbiology, Wonkwang University School of Medicine) ;
  • So, Hong-Seob (Center for Metabolic Function Regulation, Department of Microbiology, Wonkwang University School of Medicine)
  • Received : 2014.11.28
  • Accepted : 2014.12.05
  • Published : 2014.12.30

Abstract

Cisplatin is one of the most widely used and highly effective drug for the treatment of various solid tumors; however, it has dose-dependent side effects on the kidney, cochlear, and nerves. Nephrotoxicity is the most well-known and clinically important toxicity. Numerous studies have demonstrated that several mechanisms, including oxidative stress, DNA damage, and inflammatory responses, are closely associated with cisplatin-induced nephrotoxicity. Even though the establishment of cisplatin-induced nephrotoxicity can be alleviated by diuretics and pre-hydration of patients, the prevalence of cisplatin nephrotoxicity is still high, occurring in approximately one-third of patients who have undergone cisplatin therapy. Therefore it is imperative to develop treatments that will ameliorate cisplatin-nephrotoxicity. In this review, we discuss the mechanisms of cisplatin-induced renal toxicity and the new strategies for protecting the kidneys from the toxic effects without lowering the tumoricidal activity.

Keywords

Acknowledgement

Supported by : National Research Foundation of Korea [NRF]

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