Kondo S, Yoshizawa N, Kusumi Y, Takeuchi A, Torikata C
Department of Public Health, National Defense Medical College, Saitama, Japan.
Clin Nephrol. 1999 Nov;52(5):278-84.
We previously demonstrated that the supernatants of cultured concanavalin-A (con-A) stimulated peripheral blood mononuclear cells (PBMC) from patients with minimal change nephrotic syndrome (MCNS) increased the urinary protein excretion in injected rats and suggested that PBMC released a factor, which we called glomerular permeability factor (GPF), changes in the glomerular permeability and thus resulted in proteinuria in MCNS.
In this study we investigated the GPF activity in focal segmental glomerular sclerosis (FGS) and other conditions of chronic glomerulonephritis (CGN), and also the relationship between GPF and vascular permeability factor (VPF). In experiment 1 the supernatants of the cultured con-A stimulated PBMC from patients with 10 FGS, 5 other CGN and 10 controls were tested regarding their ability to produce GPE The GPF activity was defined as positive when the 8-hour urinary protein excretion after the injection of the supernatant in Sprague-Dawley rats exceeded the mean value plus 2 standard deviations (M + 2 SD) of that before injection.
Three out of 10 FGS patients and 1 membranous nephropathy patient out of the 5 other CGN patients were positive for GPF activity. In experiment 2 the relationship between GPF and VPF was analyzed using culture supernatants of PBMC from 10 nephrotic MCNS patients and 15 controls. The VPF activity was measured following the method developed by Ovary [1975]. All 7 cases that were positive for GPF activity were simultaneously positive for VPF activity. On the other hand, 16 cases that were positive for VPF activity were not always positive for GPF activity (7 cases were positive and 9 were negative for VPF activity).
Experiments 1 and 2 thus suggested that GPF was not active in MCNS alone, but also in other CGN conditions and it was therefore not considered to be the same factor/substance(s) as VPF.
我们之前证实，用刀豆蛋白A（Con-A）刺激微小病变肾病（MCNS）患者的外周血单个核细胞（PBMC）后，其培养上清液会使注射后的大鼠尿蛋白排泄增加，并提示PBMC释放了一种我们称为肾小球通透性因子（GPF）的因子，该因子改变了肾小球通透性，从而导致MCNS患者出现蛋白尿。
在本研究中，我们调查了局灶节段性肾小球硬化（FGS）和其他慢性肾小球肾炎（CGN）情况下的GPF活性，以及GPF与血管通透性因子（VPF）之间的关系。在实验1中，检测了来自10例FGS患者、5例其他CGN患者和10例对照者的Con-A刺激的PBMC培养上清液产生GPF的能力。当将上清液注射到Sprague-Dawley大鼠体内8小时后的尿蛋白排泄量超过注射前平均值加2个标准差（M + 2 SD）时，GPF活性被定义为阳性。
10例FGS患者中有3例以及5例其他CGN患者中的1例膜性肾病患者的GPF活性呈阳性。在实验2中，使用来自10例肾病性MCNS患者和15例对照者的PBMC培养上清液分析了GPF与VPF之间的关系。按照Ovary [1975]开发的方法测量VPF活性。所有7例GPF活性呈阳性的病例同时VPF活性也呈阳性。另一方面，16例VPF活性呈阳性的病例并非总是GPF活性呈阳性（7例VPF活性呈阳性，9例VPF活性呈阴性）。
实验1和2因此提示，GPF不仅在MCNS中具有活性，在其他CGN情况下也具有活性，因此它不被认为与VPF是相同的因子/物质。
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