Washizawa K, Kasai S, Mori T, Komiyama A, Shigematsu H
Department of Paediatrics, Shinshu University School of Medicine, Matsumoto, Japan.
Pediatr Nephrol. 1993 Feb;7(1):1-5. doi: 10.1007/BF00861549.
The relationship of glomerular anionic sites to proteinuria was examined ultrastructurally in human nephrotic syndrome. The anionic sites were analysed morphometrically in patients with minimal-change nephrotic syndrome (MCNS, 11 patients) and in other glomerulonephritides complicated with nephrotic syndrome (4 patients) by the high-iron diamine-thiocarbohydrazide-silver proteinate method. The anionic sites in MCNS patients in remission (7 patients) were normal. In contrast, the anionic sites in nephrotic patients with MCNS (4 patients) and the other glomerulonephritides were decreased in number. Moreover, smaller and irregularly distributed anionic sites or the greater loss of them from the paramesangial region were observed in the nephrotic patients. The loss of glomerular anionic sites may induce structural alteration of the glomerular basement membrane and mesangial matrix. The loss and structural abnormalities of glomerular anionic sites in nephrotic patients may be one of the mechanisms responsible for massive proteinuria.
在人类肾病综合征中，通过超微结构研究了肾小球阴离子位点与蛋白尿的关系。采用高铁二胺-硫代碳酰肼-蛋白银法，对11例微小病变型肾病综合征（MCNS）患者及4例合并肾病综合征的其他肾小球肾炎患者的阴离子位点进行形态计量分析。MCNS缓解期患者（7例）的阴离子位点正常。相比之下，MCNS肾病患者（4例）及其他肾小球肾炎患者的阴离子位点数量减少。此外，在肾病患者中观察到阴离子位点更小且分布不规则，或系膜旁区阴离子位点大量丢失。肾小球阴离子位点的丢失可能导致肾小球基底膜和系膜基质的结构改变。肾病患者肾小球阴离子位点的丢失及结构异常可能是导致大量蛋白尿的机制之一。
