Agrawal Vinita, Prasad Narayan, Jain Manoj, Pandey Rakesh
Department of Pathology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, 226014, India,
Clin Exp Nephrol. 2013 Dec;17(6):811-8. doi: 10.1007/s10157-013-0775-y. Epub 2013 Feb 2.
Glomerular podocyte molecules are involved in the pathogenesis of congenital nephrotic syndrome. However, their role in primary nephrotic syndrome is not clear. This study investigated the expression of nephrin, podocin and synaptopodin in primary nephrotic syndrome.
Eighty-seven patients with primary nephrotic syndrome including minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous nephropathy (MN) and membranoproliferative glomerulonephritis Type I (MPGN) were included in the study. Glomerular expression of nephrin, podocin and synaptopodin was studied in renal biopsies by immunofluorescence and immunohistochemistry. Correlation of expression with clinical and biochemical parameters was performed.
The pattern of expression for all podocyte proteins in controls was uniform fine granular along the capillary walls towards the visceral epithelial cell aspect. Glomerular expression of nephrin was present in all renal biopsies and was similar to that in controls. Glomerular synaptopodin expression was seen in all MN and MPGN patients, while it was seen in 74 % (17/23) MCD and 93.5 % (29/31) FSGS. Reduced synaptopodin expression showed no correlation with clinical and biochemical factors. Podocin expression was present in 5/23 MCD (22 %), 3/31 FSGS (9.6 %), 13/17 MN (76.4 %) and 13/16 MPGN (81 %) patients. The reduced expression of podocin significantly correlated with the degree of proteinuria (p = 0.032). No correlation with age, gender and serum creatinine level was observed.
Reduction of glomerular podocin expression found in MCD and FSGS is related to the amount of proteinuria. Our findings suggest that alteration in podocyte phenotype may not be a primary event and may reflect the degree of podocyte injury in primary nephrotic syndrome.
肾小球足细胞分子参与先天性肾病综合征的发病机制。然而,它们在原发性肾病综合征中的作用尚不清楚。本研究调查了nephrin、podocin和synaptopodin在原发性肾病综合征中的表达情况。
本研究纳入了87例原发性肾病综合征患者,包括微小病变病(MCD)、局灶节段性肾小球硬化(FSGS)、膜性肾病(MN)和Ⅰ型膜增生性肾小球肾炎(MPGN)。通过免疫荧光和免疫组织化学方法研究肾活检组织中nephrin、podocin和synaptopodin的肾小球表达情况。分析其表达与临床和生化参数的相关性。
对照组中所有足细胞蛋白的表达模式均为沿毛细血管壁朝向脏层上皮细胞一侧呈均匀的细颗粒状。所有肾活检组织中均存在nephrin的肾小球表达,且与对照组相似。所有MN和MPGN患者均可见肾小球synaptopodin表达,而在74%(17/23)的MCD和93.5%(29/31)的FSGS患者中也可见到。synaptopodin表达降低与临床和生化因素无关。5/23例MCD(22%)、3/31例FSGS(9.6%)、13/17例MN(76.4%)和13/16例MPGN(81%)患者存在podocin表达。podocin表达降低与蛋白尿程度显著相关(p = 0.032)。未观察到与年龄、性别和血清肌酐水平的相关性。
在MCD和FSGS中发现的肾小球podocin表达降低与蛋白尿的量有关。我们的研究结果表明,足细胞表型的改变可能不是原发性事件,可能反映了原发性肾病综合征中足细胞损伤的程度。