Klin Monbl Augenheilkd 1998; 213(10): 252-253
DOI: 10.1055/s-2008-1034983
Diagnostisches Forum

© 1998 F. Enke Verlag Stuttgart

Subretinale Neovaskularisationsmembranen bei Membranoproliferativer Glomerulonephritis Typ II

Subretinal neovascular membranes in membranoproliferative glomerulonephritis type IICarsten Framme, Thomas Herboth, Johann Roider, Horst Laqua
  • Klinik für Augenheilkunde, Medizinische Universität zu Lübeck (Direktor: Prof. Dr. med. H. Laqua)
Further Information

Publication History

Manuskript erstmalig eingereicht am 17.07.1998

in der vorliegenden Form angenommen

Publication Date:
08 February 2008 (online)

Summary

Background So called ‘dense deposits‘ in the retina of a patient suffering from membranoproliferative glomerulonephritis type II (MPGN II) were first demonstrated in 1989. Appearence of subretinal neovascular membranes associated with MPGN II in three patients was described in 1990.

Patient and methods We present a 45-year-old male patient, whose insufficiency of the kidney due to a membranoproliferative glomerulonephritis type II required peritoneal dialysis and later transplantation. In both eyes fundus examination revealed typical disseminated, partly confluencing, drusen-like ‘dense deposits’ and exsudative degeneration of the macula due to subretinal neovascular membranes. Visual acuity was less than 20/400 and visual fields were reduced to small excentrics islands. There was an atrophy of the optic nerve with nearly extinguished VEP in both eyes.

Conclusion Flecked changes of the retina called ‘dense deposits’ associated with membranoproliferative glomerulonephritis type II have to be differentiated in particular from drusen, as well as metabolic-toxic and degenerative retinopathy. Development of subretinal neovascular membranes is attributed to altered retinal pigment epithelium, similar to age-related macular degeneration. An atrophy of the optic nerve associated with this disease has not been described so far. It is possible that vascular damage because of hypertensive changes due to renal dysfunction is the reason for the optic nerve atrophy. With another hypothesis this could be caused by intraocular pressure due to a risen flow of water into the vitreous cavity following the altered osmotic gradient after peritoneal dialysis.

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