Literature DB >> 14551356

Does vascular endothelial growth factor (VEGF) play a role in the pathogenesis of minimal change disease?

Geoffrey Boner1, Alison J Cox, Darren J Kelly, Ana Tobar, Joëlle Bernheim, Robyn G Langham, Mark E Cooper, Richard E Gilbert.   

Abstract

BACKGROUND: Minimal change disease (MCD) is one of the major causes of nephrotic syndrome both in children and adults. The pathogenesis of this condition is not clear and it has been suggested that a plasma permeability factor may play a role. Vascular endothelial growth factor (VEGF), also known as vascular permeability factor, has been thought to be one the factors involved. The aim of this study was thus to investigate the role of VEGF in the pathogenesis of MCD.
METHODS: The expression of the gene for VEGF and VEGF receptor-2 (VEGFR-2) was estimated using in situ hybridization in renal biopsy specimens taken from patients with nephrotic syndrome and diagnosed histologically as MCD. The results were compared with those obtained in normal renal tissue. Biopsy specimens from eight patients diagnosed as having MCD were randomly selected for the study. The patients were aged 4-60 years at the time of the biopsy. There were four females and four males. All patients had presented with a nephrotic syndrome, five with recent onset of the disease, two with repeated attacks of the syndrome and one had reduced renal function.
RESULTS: The gene expression for VEGF, measured as the proportional glomerular area occupied by autoradiographic grains, was significantly less in the patients with MCD than in controls (1.9 +/- 0.4 vs 4.8 +/- 0.6%, P < 0.0025), whereas the gene expression for VEGFR-2 was no different to controls (1.9 +/- 0.4 vs 2.0 +/- 0.2%).
CONCLUSIONS: MCD is associated with a reduction in the expression of the gene for VEGF. As VEGF may play an important role in renal repair and survival, it is postulated that the deficiency, which we have shown, may lead to the dysregulation of the repair process in MCD.

Entities:  

Mesh:

Substances:

Year:  2003        PMID: 14551356     DOI: 10.1093/ndt/gfg372

Source DB:  PubMed          Journal:  Nephrol Dial Transplant        ISSN: 0931-0509            Impact factor:   5.992


  6 in total

1.  A boy with congenital analbuminemia and steroid-sensitive idiopathic nephrotic syndrome: an experiment of nature.

Authors:  Thomas J Neuhaus; Thomas Stallmach; Agnes Genewein
Journal:  Eur J Pediatr       Date:  2007-10-19       Impact factor: 3.183

2.  Familial steroid-sensitive nephrotic syndrome in Southern Israel: clinical and genetic observations.

Authors:  Daniel Landau; Tal Oved; Dan Geiger; Luba Abizov; Hanna Shalev; Ruti Parvari
Journal:  Pediatr Nephrol       Date:  2007-01-12       Impact factor: 3.714

3.  Nephrotic syndrome associated with tyrosine kinase inhibitors for pediatric malignancy: case series and review of the literature.

Authors:  Rebecca L Ruebner; Lawrence Copelovitch; Nicholas F Evageliou; Michelle R Denburg; Jean B Belasco; Bernard S Kaplan
Journal:  Pediatr Nephrol       Date:  2013-12-07       Impact factor: 3.714

4.  Induction of podocyte-derived VEGF ameliorates podocyte injury and subsequent abnormal glomerular development caused by puromycin aminonucleoside.

Authors:  Ji Ma; Taiji Matsusaka; Hai-Chun Yang; Jianyong Zhong; Nobuaki Takagi; Agnes B Fogo; Valentina Kon; Iekuni Ichikawa
Journal:  Pediatr Res       Date:  2011-07       Impact factor: 3.756

5.  Inhibition of Rho-associated kinase relieves C5a-induced proteinuria in murine nephrotic syndrome.

Authors:  I-Jung Tsai; Chia-Hung Chou; Yao-Hsu Yang; Wei-Chou Lin; Yen-Hung Lin; Lu-Ping Chow; Hsiao-Hui Lee; Pei-Gang Kao; Wan-Ting Liau; Tzuu-Shuh Jou; Yong-Kwei Tsau
Journal:  Cell Mol Life Sci       Date:  2015-03-20       Impact factor: 9.261

6.  Sunitinib induced nephrotic syndrome and thrombotic microangiopathy.

Authors:  P K Jha; M Vankalakunti; V Siddini; R Bonu; G K Prakash; K Babu; H S Ballal
Journal:  Indian J Nephrol       Date:  2013-01
  6 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.