Framme C, Herboth T, Roider J, Laqua H
Klinik für Augenheilkunde, Medizinische Universität zu Lübeck.
Klin Monbl Augenheilkd. 1998 Oct;213(4):252-3. doi: 10.1055/s-2008-1034983.
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.
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.
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.
1989年首次在一名患有II型膜增生性肾小球肾炎(MPGN II)的患者视网膜中发现所谓的“致密沉积物”。1990年描述了3例与MPGN II相关的视网膜下新生血管膜的出现。
我们报告一名45岁男性患者,其因II型膜增生性肾小球肾炎导致肾功能不全,需要进行腹膜透析,后来接受了移植手术。双眼眼底检查发现典型的散在性、部分融合的、类似玻璃膜疣的“致密沉积物”,以及由于视网膜下新生血管膜导致的黄斑渗出性变性。视力低于20/400,视野缩小为小的偏心岛状。双眼视神经萎缩,视觉诱发电位几乎消失。
与II型膜增生性肾小球肾炎相关的视网膜斑点状改变即“致密沉积物”,必须特别与玻璃膜疣、代谢性中毒性和退行性视网膜病变相鉴别。视网膜下新生血管膜的形成归因于视网膜色素上皮的改变,类似于年龄相关性黄斑变性。迄今为止,尚未描述与该疾病相关的视神经萎缩。肾功能不全导致的高血压变化引起的血管损伤可能是视神经萎缩的原因。另一种假设是,腹膜透析后渗透压梯度改变,导致水流入玻璃体腔,眼压升高,从而引起视神经萎缩。