Abstract: TH-PO0407
Perirenal Adipose Tissue Contributes to the Development of Nephritis in Lupus-Prone NZB/W F1 Mice
Session Information
- Glomerular Diseases: Autoimmune Diseases
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology
Authors
- Cheong, Lai Yee, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
- Zhang, Danting, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
- Xie, Ruiyan, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
- Chiu, Christy, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
- Wu, Chun Hei Kevin, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
- Chan, Tak Mao Daniel, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
- Yap, Yat Hin Desmond, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
Background
Lupus nephritis (LN) - a key organ involvement in systemic lupus erythematosus (SLE), is characterized by aberrant systemic and local immune reactions. Peri-renal adipose tissue (PRAT) represents an immunological hub in close proximity to the kidneys that secretes adipocytokines and inflammatory mediators to cause chronic kidney disease progression. The pathogenic role of PRAT in LN remains unclear.
Methods
Female NZB/W F1 mice (at the age of 20 weeks, before the onset of nephritis) were subjected to surgical removal of PRAT (PRATx) or sham operation. Urine protein-to-creatine ratio (UPCR), circulating anti-dsDNA level and kidney histopathological changes were evaluated. Total RNA was extracted from PRAT of NZB/W F1 mice without proteinuria (control) and those exhibiting significant proteinuria for 8 weeks (active LN) for bulk RNA-sequencing.
Results
Mice that underwent PRATx exhibited significantly reduced proteinuria, glomerular inflammation, intra-renal immune cell infiltration, and kidney fibrosis compared to sham-operated controls, but with no difference in circulating anti-dsDNA levels. Differentially expressed genes (DEGs) in PRAT from active LN mice were highly enriched in immune-related pathways (especially B cell receptor signalling) when compared to controls.
Conclusion
PRATx before the onset of nephritis ameliorates renal manifestations in lupus-prone mice, and the effects appear to be localized. Further mechanistic and translational studies are needed to elucidate the role of PRAT-derived B cell immunity in renal pathology.