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Kidney Week

Abstract: TH-PO1118

Expression of CPT1α in Human Kidney Biopsy Samples Predicts the Deterioration of Renal Function and Progression of Tubulointerstitial Fibrosis

Session Information

Category: CKD (Non-Dialysis)

  • 1902 CKD (Non-Dialysis): Clinical, Outcomes, and Trials

Authors

  • Fang, Yi, Second Affiliated Hospital, Nanjing Medical University, Nanjing, China
  • Yuan, Qi, Nanjing Medical University, Jiangsu Nanjing, China
  • Yang, Junwei, Second Affiliated Hospital, Nanjing Medical University, Nanjing, China
Background

Fatty acids are the preferred energy source for proximal tubule cells, defective fatty acid oxidation (FAO) leads to intracellular lipid accumulation, which plays an important role in the pathogenesis of kidney fibrosis. CPT1α is the rate limiting enzyme for FAO. In this study, we investigated whether expression of CPT1α in human biopsy samples predicts the progression of renal disease.

Methods

This was a retrospective cohort study enrolled 30 patients in our hospital from May 2015 to December 2015.The clinical data were collected and renal biopsy samples were immunhistochemically stained with CPT1α. Lipid droplets accumulation was detected by Oil Red O staining. Interstitial fibrosis was evaluated by Masson’s trichrome staining. The association of CPT1α with lipid droplets accumulation, degree of renal fibrosis and decline rate of eGFR was investigated.

Results

In kidney biopsy samples, lipid droplets accumulation suggested damage in fatty acid metabolism. Expression of CPT1α was decreased in fibrosis area. Moreover, CPT1α level was negatively correlated to area of lipid droplet deposition and the area of fibrosis (fig. 1). Furthermore, expression of CPT1α is negatively correlated with the decline of eGFR per year.

Conclusion

These results suggest that expression of CPT1α in human kidney biopsy samples may predict the decline of renal function and progression of renal interstitial fibrosis. CPT1α may service as a novel biomarker for prognosis of renal disease.

Funding

  • Government Support - Non-U.S.