Abstract: PO1902
Association Between Anti-Complement Factor H Antibodies and Renal Outcome in Primary Membranous Nephropathy
Session Information
- Glomerular Diseases: Clinical, Outcomes, and Trials - 2
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1203 Glomerular Diseases: Clinical, Outcomes, and Trials
Authors
- Kagaya, Yu, Department of Nephrology, School of Medicine, Kanazawa Medical University, Uchinada, Japan
- Hayashi, Norifumi, Department of Nephrology, School of Medicine, Kanazawa Medical University, Uchinada, Japan
- Fujimoto, Keiji, Department of Nephrology, School of Medicine, Kanazawa Medical University, Uchinada, Japan
- Adachi, Hiroki, Department of Nephrology, School of Medicine, Kanazawa Medical University, Uchinada, Japan
- Furuichi, Kengo, Department of Nephrology, School of Medicine, Kanazawa Medical University, Uchinada, Japan
- Yokoyama, Hitoshi, Department of Nephrology, School of Medicine, Kanazawa Medical University, Uchinada, Japan
Background
The complement factor H (CFH) regulates activation of the alternative complement pathway. Autoantibodies against CFH have been involved in progressive renal dysfunction in a case with primary membranous nephropathy (MN) (Ronco P. et al. N Eng J Med 2018;379: 2479-81). However, the prevalence and the roles of anti-CFH antibodies in the clinical outcome of MN remains unclear.
Methods
We investigated retrospectively 36 Japanese patients with primary MN (23 males, 13 females; age 64.5 [59-72] years old) and 18 healthy normal controls (8 males, 10 females, age 31 [27-38] years old). Serum anti-CFH antibody titers were measured by enzyme-linked immunosorbent assay (Vidia Vestec, Czech Republic) to evaluate the association between anti-CFH antibody titers and the clinical outcome of MN patients.
Results
Anti-CFH antibody titers were significantly higher in MN patients as compared with normal controls [4.69 (3.69-6.38) RU/mL vs. 0.0 (0.0-0.0) RU/mL, p <0.001]. Twenty-eight patients were classified into the anti-CFH antibody positive group. The other 8 patients were classified into negative group. According to the Kaplan-Meier method, no significant difference was observed in the complete or incomplete remission rate of proteinuria, the incidence of renal dysfunction judged by the 30% reduction of estimated glomerular filtration rate (eGFR) and 50% elevation of serum creatinine (s-Cr) levels between the anti-CFH antibody positive group and the negative group of MN patients, however. In MN patients, anti-CFH antibody titer was selected an independent unfavorable predictor of renal dysfunction in Cox proportional hazards analysis adjusted by age, gender, sCr levels, proteinuria (g/gCr), anti-CFH antibody titer and immunosuppressive therapy (adjusted hazard ratio (HR) 1.344, 95% confidence intervals (CI) 1.038 to 1.741, p=0.025 for 30% reduction of eGFR; adjusted HR 1.930, 95% CI 1.108 to 3.363, p=0.020 for 50% elevation of sCr).
Conclusion
These data suggested that anti-CFH antibodies may be involved in the deterioration of renal function in primary membranous nephropathy.
