Ota K, Ota Z, Shikata K, Makino H
Third Department of Internal Medicine, Okayama University Medical School, Japan.
J Diabetes Complications. 1995 Oct-Dec;9(4):285-7. doi: 10.1016/1056-8727(95)80023-8.
To clarify the ultrastructural changes of the glomerular basement membrane (GBM) in diabetic nephropathy, the renal tissues of the patients with diabetic nephropathy were examined by electron microscopy using our newly devised "tissue negative staining method." A fine meshwork structure consisting of fibrils forming the small pores are observed in the normal human GBM. The diameter of these pores was slightly smaller than that of human albumin molecules. The GBM in patients with diabetic nephropathy showed irregular thickening. At higher magnification, cavities and tunnel structures, which were not seen in normal controls, were observed in the thickened GBM. As the diameters of the cavities and tunnels were far larger than the dimensions of albumin molecules, these enlarged structures are considered to allow serum protein molecules to pass through the GBM from the capillary lumen to the urinary space. The present results suggest that the cause of massive proteinuria in diabetic nephropathy is the disruption of the size barrier of the GBM.
为了阐明糖尿病肾病中肾小球基底膜（GBM）的超微结构变化，我们使用新设计的“组织负染色法”通过电子显微镜检查了糖尿病肾病患者的肾组织。在正常人的GBM中观察到由形成小孔的纤维组成的精细网状结构。这些孔的直径略小于人白蛋白分子的直径。糖尿病肾病患者的GBM显示不规则增厚。在更高放大倍数下，在增厚的GBM中观察到正常对照中未见的腔和隧道结构。由于腔和隧道的直径远大于白蛋白分子的尺寸，这些扩大的结构被认为允许血清蛋白分子从毛细血管腔穿过GBM进入尿腔。目前的结果表明，糖尿病肾病中大量蛋白尿的原因是GBM大小屏障的破坏。
