Romen W
Klin Wochenschr. 1980 Oct 1;58(19):1013-22. doi: 10.1007/BF01476871.
The diabetic glomerulosclerosis as a consequence of the abnormal metabolic state is characterized by an uniform thickening of the glomerular basement membrane (GBM) and an augmentation of the mesangial matrix. Both alterations begin already few years after the onset of the diabetes and are observed in all glomeruli to the same extent (=diffuse type). Later on, nodular deposits of glycoproteins are additionally found in the mesangium (=nodular type). Only these nodules are morphologically specific for the diabetic disorder. In association with both the diffuse and the nodular glomerulosclerosis, insudation of plasma can be seen in the afferent and efferent vessels and the glomerular capillary loops. The mechanism of the increase in the amount of GBM-material is not known, since contradictory data have been reported with regards to both the chemical composition and metabolism of the GBM in human and experimental diabetes. Some postulate that the abnormal deposition of GBM-mateiral is due to an excessive synthesis (anabolic disorder), others argue that a further decrease in the normally slow breakdown and disposal (catabolic disorder) might be responsible. This review presents the different pathogenetic concepts of the glomerulosclerosis and attemps to explain the possible causes for the current discrepancies.
作为异常代谢状态的结果，糖尿病性肾小球硬化症的特征是肾小球基底膜（GBM）均匀增厚和系膜基质增加。这两种改变在糖尿病发病后几年就已开始，并且在所有肾小球中均以相同程度出现（=弥漫型）。后来，在系膜中还发现了糖蛋白的结节状沉积物（=结节型）。只有这些结节在形态学上对糖尿病性疾病具有特异性。与弥漫性和结节性肾小球硬化症相关的是，在入球和出球血管以及肾小球毛细血管袢中可见血浆渗出。GBM物质数量增加的机制尚不清楚，因为关于人类和实验性糖尿病中GBM的化学成分和代谢，已报道了相互矛盾的数据。一些人推测GBM物质的异常沉积是由于过度合成（合成代谢紊乱），另一些人则认为正常情况下缓慢的分解和清除进一步减少（分解代谢紊乱）可能是原因。本综述介绍了肾小球硬化症的不同发病机制概念，并试图解释当前差异的可能原因。
