open access

Vol 49, No 3 (2011)
Original paper
Submitted: 2012-01-05
Published online: 2011-10-28
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Nephrotic syndrome unfavorable course correlates with downregulation of podocyte vascular endothelial growth factor receptor (VEGFR)-2

Danuta Ostalska-Nowicka, Agnieszka Malinska, Maciej Zabel, Wojciech Witkiewicz, Michal Nowicki
DOI: 10.5603/FHC.2011.0067
·
Folia Histochem Cytobiol 2011;49(3):472-478.

open access

Vol 49, No 3 (2011)
ORIGINAL PAPERS
Submitted: 2012-01-05
Published online: 2011-10-28

Abstract

Idiopathic nephrotic syndrome (INS) in children is most commonly caused by primary glomerulopathies. Morphological lesions observed in INS might be secondary to inflammatory factors of mainly extra-renal origin. The vascular endothelial growth factor (VEGF) family is regarded as playing a crucial role in this pathomechanism. The aim of the present work was to analyze the possible relation between VEGF-C and VEGF receptor (VEGFR)-2 expressions at electron microscopy level in different INS cases. The study group comprised 18 children with minimal change disease (MCD), 30 patients diagnosed with diffuse mesangial proliferation (DMP) and 11 subjects with focal segmental glomerulosclerosis (FSGS). An indirect immunohistochemical assay employing monoclonal anti-VEGF-C and anti-VEGFR-2 antibodies was applied in the study. The immunohistochemical expression of VEGF-C within podocyte cytoplasm was significantly increased in DMP subjects who were resistant to steroids and in all FSGS patients compared to MCD children and controls (p < 0.05). VEGF-C over-expression in these cases was followed by downregulation of VEGFR-2. Nephrotic syndrome progression correlates with the downregulation of podocyte VEGFR-2. For this reason, decreased VEGFR-2 expression in the podocyte processes of children with idiopathic nephrotic syndrome might be regarded as a potent factor of unfavorable prognosis. (Folia Histochemica et Cytobiologica 2011; Vol. 49, No. 3, pp. 472–478)

Abstract

Idiopathic nephrotic syndrome (INS) in children is most commonly caused by primary glomerulopathies. Morphological lesions observed in INS might be secondary to inflammatory factors of mainly extra-renal origin. The vascular endothelial growth factor (VEGF) family is regarded as playing a crucial role in this pathomechanism. The aim of the present work was to analyze the possible relation between VEGF-C and VEGF receptor (VEGFR)-2 expressions at electron microscopy level in different INS cases. The study group comprised 18 children with minimal change disease (MCD), 30 patients diagnosed with diffuse mesangial proliferation (DMP) and 11 subjects with focal segmental glomerulosclerosis (FSGS). An indirect immunohistochemical assay employing monoclonal anti-VEGF-C and anti-VEGFR-2 antibodies was applied in the study. The immunohistochemical expression of VEGF-C within podocyte cytoplasm was significantly increased in DMP subjects who were resistant to steroids and in all FSGS patients compared to MCD children and controls (p < 0.05). VEGF-C over-expression in these cases was followed by downregulation of VEGFR-2. Nephrotic syndrome progression correlates with the downregulation of podocyte VEGFR-2. For this reason, decreased VEGFR-2 expression in the podocyte processes of children with idiopathic nephrotic syndrome might be regarded as a potent factor of unfavorable prognosis. (Folia Histochemica et Cytobiologica 2011; Vol. 49, No. 3, pp. 472–478)
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Keywords

VEGFR-2; nephrotic syndrome; electron microscopy; children

About this article
Title

Nephrotic syndrome unfavorable course correlates with downregulation of podocyte vascular endothelial growth factor receptor (VEGFR)-2

Journal

Folia Histochemica et Cytobiologica

Issue

Vol 49, No 3 (2011)

Article type

Original paper

Pages

472-478

Published online

2011-10-28

DOI

10.5603/FHC.2011.0067

Bibliographic record

Folia Histochem Cytobiol 2011;49(3):472-478.

Keywords

VEGFR-2
nephrotic syndrome
electron microscopy
children

Authors

Danuta Ostalska-Nowicka
Agnieszka Malinska
Maciej Zabel
Wojciech Witkiewicz
Michal Nowicki

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