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Research Letter
June 2014

Subretinal Drusenoid Deposits Associated With Complement-Mediated IgA Nephropathy

Author Affiliations
  • 1Department of Ophthalmology, New England Eye Center, Vitreoretinal Service, Tufts University School of Medicine, Boston, Massachusetts
JAMA Ophthalmol. 2014;132(6):775-777. doi:10.1001/jamaophthalmol.2014.387

Complement-mediated IgA nephropathy is the most common cause of chronic glomerulonephritis worldwide. The pathogenesis of renal damage is related to complement activation secondary to IgA immune complex deposition in the glomerulus. To our knowledge, this is the first report of IgA nephropathy associated with bilateral subretinal drusenoid deposits (SDDs). A hypothesis for the role of complement is proposed.

A 42-year-old asymptomatic Asian woman was referred for fundus abnormality noted on routine examination. Family history was noncontributory. Medical history was significant for proteinuria and stage III kidney disease secondary to IgA nephropathy diagnosed 2 years previously. Renal biopsy demonstrated mesangial IgA deposition, expansion of the mesangial matrix, and positive direct immunofluorescence for complement C3 and C1q. Oral prednisone therapy was unsuccessful, and long-term treatment with mycophenolate mofetil was initiated.

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