Mesangial lesions and focal glomerular sclerosis in the aging rat.
Mesangial lesions and focal glomerular sclerosis in the aging rat.
复制标题
老年大鼠的系膜病变和局灶性肾小球硬化。
DOI：
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发表时间：
1975
期刊：
影响因子：
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通讯作者：
Stilmant Mm
中科院分区：
文献类型：
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作者：
Couser Wg;Stilmant Mm
局灶性肾小球硬化(FGS)的发病机制及其与蛋白尿和特发性肾病综合征的关系尚不清楚。SD大鼠尿蛋白排泄量随年龄增长而增加。50%的12月龄动物和90%的24月龄动物是蛋白尿(大于20毫克)。每天)。大量蛋白尿老年大鼠表现为肾病综合征典型的生化改变，但肾功能无明显损害。3个月、6个月和12个月龄无蛋白尿的动物在一些肾小球的偶有小叶有IgM的系膜沉积，并有轻微的系膜增生。4只12月龄蛋白尿症大鼠肾小球系膜弥漫性4+IgM沉积，基底膜增厚，上皮细胞足突融合，无FGS。系膜IgM沉淀物在酸性缓冲液中洗脱，不固定补体。6只12月龄蛋白尿症大鼠肾小球局部和节段性硬化，伴有与Bowman‘s囊粘连、泡沫细胞、管腔内嗜酸性粒细胞沉积和毛细血管壁皱缩。这些损害在24个月大的动物中更为严重。24个月龄无蛋白尿的大鼠没有检测到FGS。在无FGS的蛋白尿和非蛋白尿动物中，系膜摄取胶体碳是正常的。在无FGS的蛋白尿和非蛋白尿动物中，系膜摄取胶体碳是正常的，而在有FGS的蛋白尿动物中，胶体碳摄取减少。在老年大鼠，蛋白尿和系膜IgM沉积明显先于局灶性硬化性肾小球病变的发展，其组织学和超微结构特征类似于人的FGS。FGS蛋白尿症大鼠肾小球系膜吞噬功能普遍受损，提示这种损害可能是肾小球通透性持续增加和蛋白尿持续增加所致的系膜超负荷和功能障碍所致。
: The pathogenesis of focal glomerular sclerosis (FGS) and its relation to proteinuria and idiopathic nephrotic syndrome are unknown. Urine protein excretion in Sprague-Dawley rats increased with age. Fifty per cent of 12-month and 90 per cent of 24-month-old animals were proteinuric (greater than 20 mg. per day). Heavily proteinuric old rats manifested biochemical changes characteristic of nephrotic syndrome without significant loss of renal function. Three-month, 6-month, and nonproteinuric 12-month-old animals had mesangial deposits of IgM in occasional lobules of some glomeruli and slight mesangial hyperplasia. Four proteinuric 12-month-old rats had diffuse 4+ deposits of IgM in the mesangium of most glomeruli, basement membrane thickening and epithelial cell foot process fusion without FGS. The mesangial IgM deposits eluted in acid buffer and did not fix complement. Six proteinuric 12-month-old rats had focal and segmental areas of glomerular sclerosis with adhesions to Bowman's capsule, foamy cells, intraluminal eosinophilic deposits and capillary wall wrinkling and collapse. These lesions were more advanced in 24-month-old animals. Nonproteinuric 24-month-old rats did not have detectable FGS. Mesangial uptake of colloidal carbon was normal in proteinuric and nonproteinuric animals without FGS. Mesangial uptake of colloidal carbon was normal in proteinuric and nonproteinuric animals without FGS and reduced in proteinuric animals with FGS. In the aging rat the development of proteinuria and mesangial IgM deposition apparently precede development of a focal sclerotic glomerular lesion with histologic and ultrastructural features similar to FGS in man. The generalized impairment of mesangial phagocytic function in proteinuric rats with FGS suggests that this lesion may result from mesangial overload and dysfunction consequent to the persistent increase in glomerular permeability and proteinuria.