title: Studies of glomerular permeability factor (GPF) in focal segmental glomerular sclerosis and the relationship between GPF and vascular permeability factor (VPF).
abstract: BACKGROUND
  We previously demonstrated that the supernatants of cultured concanavalin-A (con-A) stimulated peripheral blood mononuclear cells (PBMC) from patients with minimal change nephrotic syndrome (MCNS) increased the urinary protein excretion in injected rats and suggested that PBMC released a factor, which we called glomerular permeability factor (GPF), changes in the glomerular permeability and thus resulted in proteinuria in MCNS.
  
  
  METHODS
  In this study we investigated the GPF activity in focal segmental glomerular sclerosis (FGS) and other conditions of chronic glomerulonephritis (CGN), and also the relationship between GPF and vascular permeability factor (VPF). In experiment 1 the supernatants of the cultured con-A stimulated PBMC from patients with 10 FGS, 5 other CGN and 10 controls were tested regarding their ability to produce GPE The GPF activity was defined as positive when the 8-hour urinary protein excretion after the injection of the supernatant in Sprague-Dawley rats exceeded the mean value plus 2 standard deviations (M + 2 SD) of that before injection.
  
  
  RESULTS
  Three out of 10 FGS patients and 1 membranous nephropathy patient out of the 5 other CGN patients were positive for GPF activity. In experiment 2 the relationship between GPF and VPF was analyzed using culture supernatants of PBMC from 10 nephrotic MCNS patients and 15 controls. The VPF activity was measured following the method developed by Ovary [1975]. All 7 cases that were positive for GPF activity were simultaneously positive for VPF activity. On the other hand, 16 cases that were positive for VPF activity were not always positive for GPF activity (7 cases were positive and 9 were negative for VPF activity).
  
  
  CONCLUSIONS
  Experiments 1 and 2 thus suggested that GPF was not active in MCNS alone, but also in other CGN conditions and it was therefore not considered to be the same factor/substance(s) as VPF.
authors.affiliation: Department of Public Health, National Defense Medical College, Saitama, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Kondo
authors.forename: N
authors.initials: N
authors.lastname: Yoshizawa
authors.forename: Y
authors.initials: Y
authors.lastname: Kusumi
authors.forename: A
authors.initials: A
authors.lastname: Takeuchi
authors.forename: C
authors.initials: C
authors.lastname: Torikata
mesh_terms: D000293:Adolescent; D000328:Adult; D000818:Animals; D001681:Biological Assay; D002478:Cells, Cultured; D002648:Child; D002908:Chronic Disease; D016228:Endothelial Growth Factors / Q000096:biosynthesis*; D005260:Female; D005921:Glomerulonephritis / Q000378:metabolism; D005923:Glomerulosclerosis, Focal Segmental / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000378:metabolism*; D008222:Lymphokines / Q000096:biosynthesis*; D008297:Male; D008875:Middle Aged; D011507:Proteinuria / Q000209:etiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
chemical_list: D016228:Endothelial Growth Factors; D008222:Lymphokines; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors