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Abstract: PO1823

Retinal Drusen and Atrophy in Focal and Segmental Glomerulosclerosis: A Complement-Mediated Disease?

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation

Authors

  • Harraka, Philip Adam, The University of Melbourne Department of Medicine, Northern Health, Melbourne, Victoria, Australia
  • Mack, Heather G., The University of Melbourne Department of Sugery (Ophthalmology), Melbourne, Victoria, Australia
  • Colville, Deb J., The University of Melbourne Department of Medicine, Northern Health, Melbourne, Victoria, Australia
  • Barit, David, The University of Melbourne Department of Medicine, Northern Health, Melbourne, Victoria, Australia
  • Langsford, David, The University of Melbourne Department of Medicine, Northern Health, Melbourne, Victoria, Australia
  • Pianta, Timothy J., The University of Melbourne Department of Medicine, Northern Health, Melbourne, Victoria, Australia
  • Savige, Judith A., The University of Melbourne Department of Medicine, Northern Health, Melbourne, Victoria, Australia
Background

Retinal drusen are small yellow-white deposits typically found in age-related macular degeneration but also with dense deposit disease, lupus nephritis, IgA disease, and membranous and post-streptococcal glomerulonephritis. Drusen and glomerular immune deposits result from complement activation, are similar in composition and share a subepithelial location. Focal and segmental glomerulosclerosis (FSGS) is a heterogeneous clinicopathological entity in which immune deposits comprising IgM and C3 may be seen. This study investigated a cohort of individuals with FSGS for retinal drusen.

Methods

This was a cross-sectional observational case-control study of individuals with FSGS recruited from a general renal clinic in an Australian tertiary-care metropolitan hospital. Previous structural renal disease and glomerulonephritis were noted. Two-field colour fundus images were assessed by two trained graders for drusen count, location and size using the Wisconsin Age-Related Maculopathy Grading Grid. Central drusen counts ≥10 were considered abnormal. Retinal atrophy and pigmentation were recorded by a retinal expert.

Results

Forty-nine individuals with FSGS were compared with 49 matched controls. Mean age was 55 ± 14 years and 29 (59%) were male. One (2%) with FSGS had co-existent structural renal disease, two (4%) had thin basement membrane nephropathy and three (6%) had syndromic FSGS. Twenty-five (51%) had reached end-stage kidney failure, and 16 (33%) had transplants. Central drusen count was 9 ± 25 in FSGS and 3 ± 8 in controls with normal renal function (p=0.02). Central drusen counts ≥10 were present in nine patients with FSGS (18%) and four controls (8%) (p=0.23). Seven of these nine (78%) were younger than 60 years which excluded age-related macular degeneration. Medium-sized drusen (>63µm) were more common in FSGS (20, 41%) than controls (10, 20%) (p=0.048). Retinal atrophy was present in 9 with FSGS (18%) and no controls (p=0.003).

Conclusion

Drusen are more abundant and larger in FSGS than controls. Drusen reflect complement activation and their similarities in composition and subepithelial location with glomerular immune deposits suggests that some of the mechanisms underlying drusen are also relevant to FSGS. Retinal atrophy occurs more often in FSGS and may reflect podocyte loss.