SUBRETINAL NEOVASCULAR MEMBRANES IN MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS TYPE-II

Citation
C. Framme et al., SUBRETINAL NEOVASCULAR MEMBRANES IN MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS TYPE-II, Klinische Monatsblatter fur Augenheilkunde, 213(4), 1998, pp. 252-253
Citations number
12
Categorie Soggetti
Ophthalmology
Journal title
Klinische Monatsblatter fur Augenheilkunde
ISSN journal
00232165 → ACNP
Volume
213
Issue
4
Year of publication
1998
Pages
252 - 253
Database
ISI
SICI code
0023-2165(1998)213:4<252:SNMIMG>2.0.ZU;2-7
Abstract
Background So called 'dense deposits' in the retina of a patient suffe ring from membranoproliferative glomerulonephritis type IT (MPGN II) w ere first demonstrated in 1989. Appearence of subretinal neovascular m embranes associated with MPGN II in three patients was described in 19 90. Patient and methods We present a 45-year-old male patient, whose i nsufficiency of the kidney due to a membranoproliferative glomerulonep hritis type II required peritoneal dialysis and later transplantation. In both eyes fundus examination revealed typical disseminated, partly confluencing, drusen-like 'dense deposits' and exsudative degeneratio n of the macula due to subretinal neovascular membranes. Visual acuity was less than 20/400 and visual fields were reduced to small excentri cs islands. There was an atrophy of the optic nerve with nearly exting uished VEP in both eyes. Conclusion Flecked changes of the retina call ed 'dense deposits' associated with membranoproliferative glomerulonep hritis 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 pigm ent epithelium, similar to age-related macular degeneration. An atroph y of the optic nerve associated with this disease has not been describ ed so far. It is possible that vascular damage because of hypertensive changes due to renal dysfunction is the reason for the optic nerve at rophy. With another hypothesis this could be caused by intraocular pre ssure due to a risen flow of water into the vitreous cavity following the altered osmotic gradient after peritoneal dialysis.