Complement in anti-glomerular basement membrane glomerulonephritis

Pei Zhang¹Kai-Li Shi²Chunlin Gao^3*Feng Xu⁴Li-Li Jia³Ji-Chao Sun⁵

• ¹Department of Pediatrics, Nanjing General Hospital of Nanjing Military Command, Nanjing, China
• ²Department of Pediatrics, Jinling Hospital, Nanjing Medical University, Nanjing, China
• ³Affiliated Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu Province, China
• ⁴National Clinical Research Center for Kidney Disease, Jinling Hospital, Nanjing Medical University, Nanjing, China
• ⁵First Affiliated Hospital of Guangxi University of Chinese Medicine, Nanning, Guangxi Zhuang Region, China

Anti-glomerular basement membrane glomerulonephritis (anti-GBM GN) is a rare autoimmune disease that often progresses to end-stage renal disease (ESRD). Complement activation and anti-GBM GN are closely related, as evidenced by the renal pathological characteristics of patients with anti-GBM GN, which include linear deposition of IgG and C3 along the GBM.Increasing evidence suggests that all three pathways of complement activation may be involved in the pathogenesis and progression of anti-GBM GN. Anti-GBM GN's clinical symptoms are linked to complement-related proteins, which are risk factors that impact the disease's prognosis. This suggests that complement activation and activity may be the primary causes of renal damage in anti-GBM GN. Therefore, biomarkers of complement activation can identify anti-GBM GN cases that may progress to severe renal damage, and complement inhibition may become a new strategy for the clinical treatment of anti-GBM GN.