title: Does vascular endothelial growth factor (VEGF) play a role in the pathogenesis of minimal change disease?
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.
authors.affiliation: Baker Medical Research Institute, St Kilda Central, Melbourne, Australia. gboner@post.tau.ac.il
authors.forename: Geoffrey
authors.initials: G
authors.lastname: Boner
authors.forename: Alison J
authors.initials: AJ
authors.lastname: Cox
authors.forename: Darren J
authors.initials: DJ
authors.lastname: Kelly
authors.forename: Ana
authors.initials: A
authors.lastname: Tobar
authors.forename: Joëlle
authors.initials: J
authors.lastname: Bernheim
authors.forename: Robyn G
authors.initials: RG
authors.lastname: Langham
authors.forename: Mark E
authors.initials: ME
authors.lastname: Cooper
authors.forename: Richard E
authors.initials: RE
authors.lastname: Gilbert
mesh_terms: D000328:Adult; D000368:Aged; D002648:Child; D005260:Female; D005920:Glomerular Mesangium / Q000378:metabolism / Q000473:pathology; D006801:Humans; D017403:In Situ Hybridization; D008297:Male; D008875:Middle Aged; D009402:Nephrosis, Lipoid / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D009404:Nephrotic Syndrome / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism*; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000235:genetics / Q000378:metabolism*
chemical_list: D042461:Vascular Endothelial Growth Factor A; D040301:Vascular Endothelial Growth Factor Receptor-2