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Vascular endothelial growth factor (VEGF‐C1)‐dependent inflammatory response of podocytes in nephrotic syndrome glomerulopathies in children: an immunohistochemical approach
Author(s) -
OstalskaNowicka D,
Zachwieja J,
Nowicki M,
Kaczmarek E,
Siwinska A,
Witt M
Publication year - 2005
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.2005.02076.x
Subject(s) - synaptopodin , podocalyxin , podocyte , nephrotic syndrome , pathology , immunohistochemistry , vascular endothelial growth factor , focal segmental glomerulosclerosis , medicine , glomerulonephritis , biology , kidney , proteinuria , vegf receptors
Aims : To analyse expression and distribution of vascular endothelial growth factor (VEGF‐C1), podocalyxin and synaptopodin within renal tissue in nephrotic syndrome glomerulopathies in children. Methods and results : Renal biopsies performed at the time and in the manner recommended by the World Health Organization. The study group consisted of submicroscopic glomerulonephritis ( n = 10), diffuse mesangial proliferation ( n = 14) and focal segmental glomerulosclerosis ( n = 5). The control tissue consisted of macroscopically normal appearing cortex taken from kidneys resected for localized neoplasms ( n = 3). Material for immunohistochemistry was fixed in Bouin's solution and embedded in paraffin. Indirect immunohistochemistry using monoclonal anti‐human antibodies directed against VEGF‐C1, podocalyxin and synaptopodin was employed. The distribution of markers was quantified by computerized image analysis. In non‐sclerosed glomeruli (within podocyte cytoplasm), VEGF‐C1 was more expressed in podocytes of all groups ( P < 0.0002), while the distribution of synaptopodin was less expressed in all groups ( P < 0.0002). There was no statistical difference between all groups in the expression of podocalyxin. Conclusions : The increased permeability of the filtration barrier in steroid‐resistant glomerulopathies may be a consequence of subcellular changes in podocytes resulting from decreased expression of synaptopodin. Moreover, impaired permeability of endothelium could be secondary to increased expression of podocyte‐derived VEGF‐C1.