Chen Y, Qian Y
Department of Endocrine, First Hospital, Beijing Medical University.
Zhonghua Yi Xue Za Zhi. 1995 Sep;75(9):537-9, 574.
The changes of width and anionic sites of glomerular basement membrane (GBM) are considered early changes of diabetic nephropathy. Recent work suggests that the normal barrier to the penetration of renal glomerular basement membrane by anionic plasma proteins may depend in part on the existence of negatively charged sites within the membrane. We evaluated the relationship between the change of width, anionic sites of GBM and transferrinuria in diabetic rats and normal controls in 1, 3, 6 months after administration by STZ. Diabetic rats revealed a thicken GBM (0.40-0.44microns) and reduced anionic sites (16-12/1000nm GBM length) compared with control rats (0.22 microns, 20-22/1000 nm GBM lenth). Transferrinuria was also significantly greater in diabetic rats than normals (P < 0.01). The changes in anionic sites and transferrinuria represented defect of GBM charge barrier in early phase of diabetic nephropathy. Aminoguanidine attenuated the rise in transferrinuria and prevented GBM thickness and loss of anionie sites.
肾小球基底膜(GBM)宽度和阴离子位点的变化被认为是糖尿病肾病的早期变化。最近的研究表明,阴离子血浆蛋白穿透肾小球基底膜的正常屏障可能部分取决于膜内带负电荷位点的存在。我们评估了链脲佐菌素(STZ)给药后1、3、6个月糖尿病大鼠和正常对照中GBM宽度、阴离子位点的变化与转铁蛋白尿之间的关系。与对照大鼠(0.22微米,20 - 22/1000纳米GBM长度)相比,糖尿病大鼠显示GBM增厚(0.40 - 0.44微米)且阴离子位点减少(16 - 12/1000纳米GBM长度)。糖尿病大鼠的转铁蛋白尿也显著高于正常大鼠(P < 0.01)。阴离子位点和转铁蛋白尿的变化代表糖尿病肾病早期GBM电荷屏障的缺陷。氨基胍减轻了转铁蛋白尿的升高,并防止了GBM厚度增加和阴离子位点丢失。