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Kidney Week

Abstract: FR-PO108

Dexamethasone Pretreatment Prevented Chemotherapy-Induced Acute Renal Failure by Inducing Polymorphonuclear Myeloid-Derived Suppressor Cells

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Qiao, Yi-Dan, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, GuangDong, China
  • Zhao, Li-Yun, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, GuangDong, China
  • Chen, Jie, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, GuangDong, China
  • Zhu, Gao-Hui, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, GuangDong, China
  • Xing, Yan-Fang, the Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, GUANGDONG, China
  • Wu, Xiang-Yuan, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, GuangDong, China
  • Li, Xing, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, GuangDong, China
Background

Chemotherapy for cancer patients leads to renal toxicity which was the main cause for chemotherapy discontinuation. Current preventive measures failed to be successful. Previous studies indicated dexamethasone cured renal diseases. The present study was aimed to reveal the efficacy and mechanism of dexamethasone in preventing chemotherapy induced renal toxicity.

Methods

Cisplatin was utilized to build acute renal failure mice model. Th17, Treg, polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) and monocytic MDSC (M-MDSC) was tested in injured kidney. Dexamethasone pretreatment was used to relieve renal failure with the immune mechanism investigated.

Results

Cisplatin induced acute liver failure confirmed by increased serum creatinine. Th17 cells were increased in injured kidney, with increased PMN-MDSC and decreased Treg cells. Dexamethasone pretreatment decreased serum creatinine and induced PMN-MDSC and Treg in kidney and increased Th17 cells. Gr-1 antibody was utilized to eliminate PMN-MDSC after dexamethasone pretreatment. PMN-MDSC depletion eliminated the efficacy of dexamethasone in relieving renal failure. Dexamethasone induced PMN-MDSC was transferred to mice before cisplatin administration, which decreased serum creatinine. Dexamethasone induced PMN-MDSC suppressed T cell proliferation through reactive oxygen species (ROS) pathway.

Conclusion

Dexamethasone pretreatment relieved chemotherapy induced renal failure by inducing PMN-MDSC, which suppressed Th17 cells and induced Treg cells.