Glomerular C1q deposition and serum anti-C1q antibodies in anti-glomerular basement membrane disease

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• 作者：Shui-yi Hu (1) (2) (3)
  Xiao-yu Jia (1) (2) (3)
  Xiao-wei Yang (1) (2) (3)
  Feng Yu (1) (2) (3)
  Zhao Cui (1) (2) (3)
  Ming-hui Zhao (1) (2) (3) (4)
  
• 关键词：Anti ; glomerular basement membrane disease ; Complement ; Classical pathway ; C1q ; Anti ; C1q antibody
• 刊名：BMC Immunology
• 出版年：2013
• 出版时间：December 2013
• 年：2013
• 卷：14
• 期：1
• 全文大小：217 KB
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• 作者单位：Shui-yi Hu (1) (2) (3)
  Xiao-yu Jia (1) (2) (3)
  Xiao-wei Yang (1) (2) (3)
  Feng Yu (1) (2) (3)
  Zhao Cui (1) (2) (3)
  Ming-hui Zhao (1) (2) (3) (4)
  
  1. Renal Division, Department of Medicine, Peking University First Hospital, Beijing, China
  2. Institute of Nephrology, Peking University, Beijing, China
  3. Key Laboratory of Renal Disease, Ministry of Health of China; Key Laboratory of Chronic Kidney Disease, Prevention and Treatment, Ministry of Education, Beijing, China
  4. Peking-Tsinghua Center for Life Sciences, Beijing, China
  
• ISSN：1471-2172

文摘

Background Anti-glomerular basement membrane (GBM) disease is a well-known antibody-induced autoimmune disease. A few patients have glomerular C1q deposition, but it is usually absent on renal histopathology. The role of C1q deposition in kidney injury is unclear. Recently, anti-C1q antibodies are demonstrated to be pathogenic in the target organ damage of many autoimmune diseases, by facilitating C1q deposition and enhancing complement activation via classical pathway. In the current study, we investigated the associations between anti-C1q antibodies in sera and C1q deposition in kidney of patients with anti-GBM disease. Results It was shown that the severity of kidney injury was comparable between patients with and without C1q deposition, including the prevalence of oliguria/auria, the median percentage of crescents in glomeruli and the mean concentration of serum creatinine. Serum anti-C1q antibodies were detected in 15/25 (60%) patients with a low titer. The prevalence of C1q deposition in kidney was comparable between patients with and without serum anti-C1q antibodies (26.7% vs. 30.0%, p-gt;-.05). No association was found between anti-C1q antibodies and the severity of kidney injury. Conclusions The classical pathway of complement may not play a pathogenic role in the kidney injury of human anti-GBM disease. Anti-C1q antibodies could be detected in more than half of patients, which need further investigations.