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Letter
A microstructural retinal analysis of membrano-proliferative glomerulonephritis type II
  1. C Gerth1,
  2. R J Zawadzki2,
  3. C Licht3,
  4. J S Werner2,
  5. E Héon1,4
  1. 1
    Department of Ophthalmology and Vision Sciences, The Hospital for Sick Children and The University of Toronto, Canada
  2. 2
    Department of Ophthalmology & Vision Science and Section of Neurobiology, Physiology & Behavior, University of California, Davis, USA
  3. 3
    Department of Nephrology, The Hospital for Sick Children, Toronto, Canada
  4. 4
    Program of Genetics and Genomic Biology, The Hospital for Sick Children, Toronto, Canada
  1. E Héon, University of Toronto and Hospital for Sick Children, Department of Ophthalmology and Vision Sciences, 555 University Avenue, Toronto, ON, M5G 1X8, Canada; eheon{at}attglobal.net

https://doi.org/10.1136/bjo.2007.122549

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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 …

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    Footnotes

    • 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