Ramjee G, Coovadia H M, Adhikari M
Department of Paediatrics and Child Health, Faculty of Medicine, University of Natal., Durban, South Africa.
J Lab Clin Med. 1996 Feb;127(2):195-9. doi: 10.1016/s0022-2143(96)90078-5.
We studied direct and indirect methods of measuring membrane charge by detecting fixed anionic sites with polyethylenimine (PEI) on the glomerular basement membrane (GBM) and Alcian blue on red blood cell (RBC) membrane (ABRBC), respectively, in 40 children with nephrotic syndrome (NS). Size selectivity of the GBM was measured indirectly by fine analysis of urinary proteins with sodium dodecyl sulfate-polyacrylamide gel electrophoresis in 22 of these children. Correlation between ABRBC and PEI was strongest (r = 0.79; p = 0.0037) in 11 children with steroid-responsive NS (SRNS), moderate (r = 0.31) in 10 children with focal glomerulosclerosis (FGS), and absent in 14 children with hepatitis B antigen membranous nephropathy (MGN) and 5 with mesangioproliferative glomerulonephritis (MPGN). ABRBC and PEI were reduced in the group as a whole as compared with their controls (ABRBC: 44.53 +/- 9.81 vs 71.54 +/- 12.14, p < 0.05; PEI: 16.31 +/- 4.34 vs 33.3 +/- 1.09, p < 0.005). This reduction was greater in SRNS (26.35 +/- 7.15 p = 0.004) but was also detected in the remainder of the group taken together (52.31 +/- 26.07, p < 0.001). Excretion of glomerular proteins was restricted by size (< or = 80 kd) in SRNS but unrestricted (< or = 80 kd plus > 80 kd) in FGS, MGN, and MPGN. The main cause of proteinuria is likely to be depletion of negative charge on the GBM in SRNS, and distortion of capillary pore size in MGN and MPGN, with probable overlap of these mechanisms in each disease, especially in FGS. Basement membrane injury appears widespread in SRNS but confined to the kidney in MGN and MPGN.
我们分别通过用聚乙烯亚胺（PEI）检测肾小球基底膜（GBM）上的固定阴离子位点以及用阿尔新蓝检测红细胞（RBC）膜（ABRBC）上的固定阴离子位点，研究了测量膜电荷的直接和间接方法，共纳入40例肾病综合征（NS）患儿。其中22例患儿通过十二烷基硫酸钠 - 聚丙烯酰胺凝胶电泳对尿蛋白进行精细分析，间接测量GBM的大小选择性。在11例激素反应性肾病综合征（SRNS）患儿中，ABRBC与PEI的相关性最强（r = 0.79；p = 0.0037），在10例局灶性肾小球硬化（FGS）患儿中相关性中等（r = 0.31），在14例乙型肝炎抗原膜性肾病（MGN）患儿和5例系膜增生性肾小球肾炎（MPGN）患儿中无相关性。与对照组相比，整个研究组的ABRBC和PEI均降低（ABRBC：44.53±9.81 vs 71.54±12.14，p < 0.05；PEI：16.31±4.34 vs 33.3±1.09，p < 0.005）。这种降低在SRNS中更明显（26.35±7.15，p = 0.004），但在研究组的其余患儿中也有发现（52.31±26.07，p < 0.001）。SRNS中肾小球蛋白的排泄受大小限制（≤80kd），而FGS、MGN和MPGN中不受限制（≤80kd加> 80kd）。蛋白尿的主要原因在SRNS中可能是GBM上负电荷的减少，在MGN和MPGN中是毛细血管孔径的扭曲，每种疾病中这些机制可能存在重叠，尤其是在FGS中。基底膜损伤在SRNS中似乎广泛存在，但在MGN和MPGN中局限于肾脏。
