gms | German Medical Science

VI. International Symposium on AMD – Age-Related Macular Degeneration – Emerging Concepts – Exploring known and Identifying new Pathways

11. - 12.09.2015, Baden-Baden

The level of complement activation varies between the stages of AMD degeneration

Meeting Abstract

  • Yara Lechanteur - Nijmegen
  • T. Schick - Cologne
  • J.M.M. Groenewoud - Nijmegen
  • L. Ersoy - Cologne
  • S. Liakopoulos - Cologne
  • A.I. den Hollander - Nijmegen
  • C.B. Hoyng - Nijmegen
  • B.J. Klevering - Nijmegen

VI. International Symposium on AMD – Age-Related Macular Degeneration – Emerging Concepts – Exploring known and Identifying new Pathways. Baden-Baden, 11.-12.09.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. Doc15amd04

doi: 10.3205/15amd04, urn:nbn:de:0183-15amd041

Veröffentlicht: 1. Oktober 2015

© 2015 Lechanteur et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe



Background: Overactivation of the complement system plays an important role in the development of AMD. This study was conducted to learn about levels of complement activation in different stages of AMD and how this may be influenced by genes and treatment.

Methods: We included 797 patients and 946 controls from the EUGENDA database. Patients were classified as early, intermediate or advanced AMD, the latter subdivided in geographic athropy (GA), active choroidal neovascularization (CNV) or inactive CNV. Serum complement activation (defined as the C3d/C3 ratio) was measured in all participants. General linear models were used to evaluate the association between complement activation and AMD stages, single nucleotide polymorphisms (SNPs) and anti-VEGF treatment.

Results: Mean complement activation was lowest in controls (P<0.05 compared to all AMD groups except for inactive CNV). The highest levels were observed in GA and intermediate AMD. Three SNPs in CFH, CFB and C3 were significantly associated with complement activation. After dividing the participants in two groups based on genetic risk (≥4 or ≤3 risk alleles) we could only replicate the association between AMD stage and complement activation in the high risk group. In addition, we also observed that patients with anti-VEGF treatment in the last three months had lower complement activation levels (P = 0.036).

Conclusions: Our findings show that complement activation varies among the AMD stages and is highest in patients with intermediate AMD and GA. These differences seem most prominent in cases with a high genetic predisposition. Also, patients who received anti-VEGF were found to have lower C3d/C3 levels, suggesting that anti-VEGF lowers complement activation. Our results suggest that complement activation in AMD is a dynamic process. These data could have implications for the optimal window of treatment with complement inhibitors and suggest that genetic testing is warranted in these patients prior to treatment.