Wehner H, Kösters W, Strauch M, Staudenmeir M
Virchows Arch A Pathol Anat Histol. 1980;388(2):137-54. doi: 10.1007/BF00430683.
Glomerular changes develop in rats with streptozotocin diabetes. The structure of these lesions (nodular and diffuse glomerulosclerosis, mesangial cell proliferation, basement membrane thickening, glomerular aneurysms, fibrinoid caps, glomerular adhesions) is described in the present paper and the effect of normalization of metabolism by islet transplantation on the glomerular changes is studied with histological, immunohistological and morphometric methods. Isogenous islets were transplanted into the portal vein of streptozotocin-diabetic rats after diabetes of 7 months' duration. The kidneys of normal, diabetic and transplanted animals of the same age were studied 2.5 months later. Studies of the kinetics of immunocomplexes in the mesangium were also performed. The renal changes (glomerulosclerosis, mesangial cell proliferation) were largely reversible after islet transplantation and the blood glucose level and glucose tolerance were normalized. In the diabetic animals the delayed uptake and elimination of immunocomplexes in the mesangium was normalized after the transplantation. It is possible, that the cause of the lesions is a functional disturbance of the mesangium induced by insulin deficiency and/or hyperglycaemia.
链脲佐菌素诱导的糖尿病大鼠会出现肾小球病变。本文描述了这些病变的结构(结节性和弥漫性肾小球硬化、系膜细胞增殖、基底膜增厚、肾小球动脉瘤、纤维蛋白样帽、肾小球粘连),并采用组织学、免疫组织学和形态计量学方法研究了胰岛移植使代谢正常化对肾小球病变的影响。在糖尿病持续7个月后,将同基因胰岛移植到链脲佐菌素诱导的糖尿病大鼠的门静脉中。2.5个月后,对相同年龄的正常、糖尿病和移植动物的肾脏进行了研究。还对系膜中免疫复合物的动力学进行了研究。胰岛移植后,肾脏病变(肾小球硬化、系膜细胞增殖)在很大程度上是可逆的,血糖水平和糖耐量恢复正常。在糖尿病动物中,移植后系膜中免疫复合物摄取和清除延迟的情况得到了正常化。病变的原因可能是胰岛素缺乏和/或高血糖引起的系膜功能障碍。