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Related Experiment Video

Updated: Oct 10, 2025

Retinal Pathophysiological Evaluation in a Rat Model

Retinal Pathophysiological Evaluation in a Rat Model

Published on: May 6, 2022

Retinal findings in glomerulonephritis.

Heather G Mack^1,2,3, Deborah J Colville^1,2, Phillip Harraka⁴

¹Department of Surgery (Ophthalmology), University of Melbourne, Melbourne, Australia.

Clinical & Experimental Optometry

|December 8, 2021

Summary

This summary is machine-generated.

Dense deposit disease, a rare kidney condition, is linked to complement system overactivity and retinal abnormalities like drusen. This review explores complement pathway roles in kidney and eye diseases, including C3 glomerulonephropathy.

Keywords:

C3 glomerulonephropathy complement drusen glomerulonephritis renal

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Last Updated: Oct 10, 2025

Retinal Pathophysiological Evaluation in a Rat Model

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Assessment of Kidney Function in Mouse Models of Glomerular Disease

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Published on: June 30, 2018

Area of Science:

Immunology
Ophthalmology
Nephrology

Background:

The complement system, integral to innate immunity, comprises classical, lectin, and alternative pathways.
Dense deposit disease (DDD) involves complement factor H mutations and alternative pathway overactivity, causing glomerulonephritis and retinal abnormalities.
Retinal abnormalities, including drusen, are observed in DDD and other glomerulonephritides linked to complement pathway dysregulation.

Purpose of the Study:

To review retinal abnormalities associated with glomerulonephritis across all three complement activation pathways.
To discuss the reclassification of DDD as C3 glomerulonephropathy and its implications for retinal manifestations.
To present the first report of drusen in a patient with C3 glomerulonephritis and a specific complement factor H variant.

Main Methods:

Literature review of complement system pathways and associated renal and retinal diseases.
Discussion of C3 glomerulonephropathy classification and pathogenic mechanisms.
Case report of a patient with C3 glomerulonephritis and homozygous complement factor H variant V62I.

Main Results:

Drusen and other retinal abnormalities occur in glomerulonephritis involving all three complement pathways, with varying onset, etiology, and visual threat.
DDD is reclassified as a form of C3 glomerulonephropathy.
A patient with C3 glomerulonephritis and a homozygous complement factor H variant V62I presented with retinal drusen.

Conclusions:

Complement pathway dysregulation significantly impacts both renal and ocular health.
Understanding these links is crucial for diagnosing and managing patients with glomerulonephritis and associated retinal conditions.
Optometric management and complement-based therapies offer potential strategies for visual preservation.