Furness P N, Turner D R
Department of Pathology, University Hospital, Nottingham, U.K.
J Pathol. 1987 Oct;153(2):189-93. doi: 10.1002/path.1711530213.
There have been conflicting reports over whether or not glomerular immune complex deposits cause proteinuria by neutralizing the glomerular basement membrane anionic charge. We investigated whether the reported discrepancies could arise as a result of repair of the charge layer, in the face of continuing antigen deposition, and how rapidly this repair could be effected. We used a chronic serum sickness model of glomerulonephritis which consistently produces a nephrotic syndrome stable over 8 weeks. Charge distribution was demonstrated by the polyethyleneimine (PEI) method. Subepithelial electron dense deposits were associated with defects in the charge layer of the lamina rara externa at 2 and 4 weeks, but at 8 weeks many of the deposits had become surrounded by a new charge layer. This finding is of relevance to the interpretation of similar studies on human material.
关于肾小球免疫复合物沉积是否通过中和肾小球基底膜阴离子电荷而导致蛋白尿,一直存在相互矛盾的报道。我们研究了在持续抗原沉积的情况下,电荷层的修复是否会导致报道的差异,以及这种修复的速度有多快。我们使用了一种慢性血清病肾小球肾炎模型,该模型始终会产生持续8周稳定的肾病综合征。通过聚乙烯亚胺(PEI)方法证明电荷分布。在2周和4周时,上皮下电子致密沉积物与外疏松层电荷层的缺陷有关,但在8周时,许多沉积物已被新的电荷层包围。这一发现与对人体材料的类似研究的解释有关。