title: Plasma tissue factor and tissue factor pathway inhibitor in patients with primary glomerulonephritis.
abstract: OBJECTIVE
  Nephrotic syndrome (NS) is associated with numerous blood coagulation abnormalities and a marked predisposition to thromboembolism. Fibrin formation within the glomeruli occurs in various forms of human and experimental glomerulonephritis and may play an important role in progressive glomerular injury. The aim of this study was to measure the plasma concentrations of tissue factor (TF) and tissue factor pathway inhibitor (TFPI) and intravascular thrombin generation markers and to analyze their relationships in patients with primary glomerulonephritis.
  
  
  METHODS
  The study population comprised 57 patients (mean age 35.2 years; range 18-63 years) with primary glomerulonephritis: 36 with NS (NS group) and 21 without (non-NS group). The control group consisted of 24 sex- and age-matched healthy volunteers. TF and TFPI antigen, prothrombin fragment F 1+2 (PF 1+2) and thrombin-antithrombin III complex (TAT) concentrations in plasma were estimated using commercially available kits.
  
  
  RESULTS
  Serum TF and TFPI concentrations in both the NS and non-NS groups were higher than those observed in the control group. Moreover, there were significant differences in TF and TFPI concentrations between the NS and non-NS groups. TF:TFPI ratios in both the examined groups were constant and significantly higher than those in the control group. Positive correlations between TF and both PF 1+2 and TAT concentrations in the total cohort of patients were shown. Furthermore, a positive correlation between TF and TFPI concentrations was observed.
  
  
  CONCLUSIONS
  Our data support the hypothesis concerning activation of coagulation pathways in patients with primary glomerulonephritis. An inadequate TFPI concentration as a result of an elevated TF:TFPI ratio characterizes not only patients with clinical manifestations of NS but also patients with mild proteinuria.
authors.affiliation: Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, Gdansk, Poland. slizak@amg.gda.pl
authors.forename: Slawomir
authors.initials: S
authors.lastname: Lizakowski
authors.forename: Zbigniew
authors.initials: Z
authors.lastname: Zdrojewski
authors.forename: Piotr
authors.initials: P
authors.lastname: Jagodzinski
authors.forename: Boleslaw
authors.initials: B
authors.lastname: Rutkowski
mesh_terms: D000293:Adolescent; D000328:Adult; D000990:Antithrombin III; D001777:Blood Coagulation / Q000502:physiology; D016022:Case-Control Studies; D018450:Disease Progression; D005260:Female; D005921:Glomerulonephritis / Q000097:blood* / Q000378:metabolism; D006801:Humans; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009404:Nephrotic Syndrome / Q000097:blood / Q000503:physiopathology; D010446:Peptide Fragments / Q000097:blood; D010447:Peptide Hydrolases / Q000097:blood; D011498:Protein Precursors / Q000097:blood; D011507:Proteinuria; D011516:Prothrombin; D013925:Thromboplastin / Q000378:metabolism*
chemical_list: D008074:Lipoproteins; D010446:Peptide Fragments; D011498:Protein Precursors; C046193:antithrombin III-protease complex; C051928:lipoprotein-associated coagulation inhibitor; C029733:prothrombin fragment 1; C044183:prothrombin fragment 2; D000990:Antithrombin III; D011516:Prothrombin; D013925:Thromboplastin; D010447:Peptide Hydrolases