The University of Toledo Translation Journal of Medical Sciences 
Nephrology Abstract, Department of Medicine Research Symposium UTJMS 2023 May 5; 11(1):e1-e1 

Disruption of CD40 Results in Significantly 
Attenuated Renal Inflammation Following 
Glycerol-Induced Acute Kidney Injury 
Shungang Zhang, PhD1*, Prabhatchandra Dube, PhD1, Jerrin George, BS1, Xiaoming 
Fan, PhD1, David J. Kennedy, PhD2, Steven T. Haller, PhD2

1Division of Nephrology, Department of Medicine, The University of Toledo, 
Toledo, OH 43614 
2Division of Cardiovascular Medicine, Department of Medicine, The University of 
Toledo, Toledo, OH 43614 

*Corresponding author: Shungang.Zhang@rockets.utoledo.edu

Published: 05 May 2023 

Introduction: We have shown that disruption of the prominent pro-inflammatory receptor CD40 
attenuates renal tubular atrophy and tubular cell death following high salt diet in our CD40 knockout 
(KO) model in addition to significantly reduced renal fibrosis following experimentally induced 
ischemic renal injury. We have also demonstrated significantly reduced pro-inflammatory and pro-
fibrotic signaling in human CD40 KO renal proximal tubule epithelial cells. We performed the following 
study to test the hypothesis that disruption of CD40 significantly attenuates acute kidney injury (AKI). 

Methods: Age matched (8-week-old) C57/BL6 wild-type and C57/BL6 CD40 KO male mice (n=8) 
were administered glycerol (7.5 ml/kg in 50% glycerol) to induce AKI. After 24h, animals were 
euthanized and kidneys were assessed for evidence of renal injury.   

Results: Renal expression of CD40 was increased in the proximal tubules of wild-type mice in response 
to AKI. CD40 KO mice demonstrated reduced renal inflammation compared with wild-type mice 
following AKI. In addition, CD40 KO mice demonstrated significantly attenuated renal cortex gene 
expression of inflammatory markers IL1β, TGFβ1, and the fibrosis marker Col3a1 following AKI 
compared to wild-type (all p<0.05).  

Conclusion: Disruption of CD40 results in significant attenuation of renal inflammation following 
experimentally induced AKI. Our results indicate that disruption of CD40 signaling may be a promising 
therapeutic target for the treatment of AKI. 

https://dx.doi.org/10.46570/utjms.vol11-2023-769 

https://dx.doi.org/10.46570/utjms.vol11-2023-769
mailto:Shungang.Zhang@rockets.utoledo.edu