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Kidney Week

Abstract: PO0361

Nicotinamide Retains Klotho Expression and Ameliorates Rhabdomyolysis-Induced AKI

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Author

  • Lin, Wenjun, Department of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China, Shanghai, China
Background

Acute kidney injury is a severe complication of rhabdomyolysis. Inflammation plays a critical role in the pathogenesis of rhabdomyolysis-induced AKI. Nicotinamide, a form of vitamin B3 and a precursor of nicotinamide adenine dinucleotide, has been shown potent anti-inflammation effects. Klotho is a tubular highly expressed renoprotective protein. Therefore, we explored the effect of nicotinamide on rhabdomyolysis-induced AKI and the underlying mechanisms.

Methods

We used glycerol-induced rhabdomyolysis mice model to observe the effect of nicotinamide on kidney injury. Western blot, chromatin immunoprecipitation and small interfering RNA were used to evaluate the role of Klotho in nicotinamide-related renoprotection.

Results

The results showed that nicotinamide attenuated kidney injury in rhabdomyolysis. Moreover, nicotinamide effectively blocked the recruitment of NF-kB, NCoR and HDAC1 to the promoter of Klotho and preserved Klotho expression. More importantly, renoprotection effect of nicotinamide was abrogated when Klotho was knockdown by small interfering RNA.

Conclusion

Our study demonstrates that Klotho preservation is essential for the renoprotection effect of nicotinamide and provides a new preventive strategy for rhabdomyolysis-induced AKI.

Funding

  • Government Support – Non-U.S.