Kim Byoung Kwon, Hong Hye Kyoung, Kim Ji Hoon, Lee Hyun Soon
Department of Pathology, Seoul National University College of Medicine, Seoul, Korea.
Am J Kidney Dis. 2002 Nov;40(5):964-73. doi: 10.1053/ajkd.2002.36328.
The slit-diaphragm protein nephrin is an essential component of the glomerular filtration barrier. It is not clear whether renal injury in patients with acquired proteinuric diseases is associated with altered regulation of the nephrin gene or protein.
We examined expression patterns of nephrin protein and messenger RNA (mRNA) in renal biopsy specimens from patients with minimal lesion (n = 7), focal segmental glomerulosclerosis (FSGS; n = 14), or membranous nephropathy (MN; n = 7) and controls (n = 8) by immunohistochemistry, immunoelectron microscopy, in situ hybridization, and polymerase chain reaction (PCR) amplification of nephrin complementary DNA.
In normal kidney, nephrin staining showed a diffuse interrupted linear pattern along the glomerular basement membrane (GBM). Nephrin staining in minimal lesion specimens showed a finely granular pattern along the GBM and was positive in cell bodies of visceral glomerular epithelial cells. Nephrin staining was most disrupted in FSGS specimens. Immunoelectron microscopy showed that nephrin-specific gold particles were almost absent in effaced foot processes in proteinuric patients. An in situ hybridization study showed significantly decreased nephrin mRNA-expressing cells in cases of FSGS and MN compared with controls. Reverse-transcription PCR showed significantly lower levels of nephrin mRNA in cases of FSGS and MN than controls, but no significant difference between minimal lesion cases and controls. Relative levels of glomerular nephrin mRNA correlated inversely with percentage of glomeruli with sclerosis in proteinuric diseases.
These results suggest that nephrin-expression patterns in proteinuric diseases are different according to the specific glomerular disease or severity of glomerular damage.
裂孔隔膜蛋白nephrin是肾小球滤过屏障的重要组成部分。目前尚不清楚获得性蛋白尿疾病患者的肾损伤是否与nephrin基因或蛋白调控的改变有关。
我们通过免疫组织化学、免疫电子显微镜、原位杂交以及nephrin互补DNA的聚合酶链反应(PCR)扩增,检测了微小病变(n = 7)、局灶节段性肾小球硬化(FSGS;n = 14)或膜性肾病(MN;n = 7)患者及对照者(n = 8)肾活检标本中nephrin蛋白和信使核糖核酸(mRNA)的表达模式。
在正常肾脏中,nephrin染色沿肾小球基底膜(GBM)呈弥漫性间断线性模式。微小病变标本中的nephrin染色沿GBM呈细颗粒状模式,且在肾小球脏层上皮细胞的胞体中呈阳性。FSGS标本中的nephrin染色破坏最为严重。免疫电子显微镜显示,蛋白尿患者足突消失处几乎没有nephrin特异性金颗粒。原位杂交研究显示,与对照组相比,FSGS和MN病例中表达nephrin mRNA的细胞显著减少。逆转录PCR显示,FSGS和MN病例中nephrin mRNA水平显著低于对照组,但微小病变病例与对照组之间无显著差异。蛋白尿疾病中肾小球nephrin mRNA的相对水平与肾小球硬化百分比呈负相关。
这些结果表明,蛋白尿疾病中nephrin的表达模式因特定的肾小球疾病或肾小球损伤严重程度而异。