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Membranoproliferative glomerulonephritis type II (MPGN type II)/dense deposit disease (DDD) is characterised by electron deposits within the lamina densa of the glomerular basement membrane. Systemic manifestation may include lipodystrophy and a retinopathy characterised by drusenoid deposits.1–3 MPGN type II is caused by overactivation of the alternative complement pathway (C3 Nephritic Factor, Factor H deficiency or functional defects) in the majority of cases.4 Recently, Factor H H402Y has been identified as a major-risk haplotype within the alternative complement pathway.5 In vivo microstructural identification and localisation of these retinal deposits in humans are …
Funding: This study was supported by the NEI (grant 014743) and an RPB Jules and Doris Stein Professorship (JSW).
Competing interests: None.
Patient consent: Obtained
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