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Related Experiment Videos

Tissue factor pathway inhibitor expression in human crescentic glomerulonephritis.

M A Cunningham1, T Ono, T D Hewitson

  • 1Department of Medicine, Monash University, Monash Medical Center, Clayton, Australia. malcolmc@its-mmcc1.cc.monash.edu.au

Kidney International
|April 14, 1999
PubMed
Summary

Tissue factor pathway inhibitor (TFPI) is expressed late in crescent formation in human kidney disease. This late TFPI expression correlates with reduced fibrin deposition, suggesting a role in chronic crescentic glomerulonephritis.

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Area of Science:

  • Nephrology
  • Pathology
  • Immunology

Background:

  • Tissue factor (TF) pathway inhibitor (TFPI) is a key regulator of coagulation.
  • TFPI protects renal function in experimental crescentic glomerulonephritis (GN).
  • Glomerular TFPI expression in human crescentic GN remains uncharacterized.

Purpose of the Study:

  • To investigate glomerular TFPI, TF, and fibrin-related antigen (FRA) expression in human crescentic GN.
  • To correlate TFPI expression with disease chronicity and markers of coagulation.

Main Methods:

  • Analysis of renal biopsies from 11 patients with crescentic GN.
  • Comparison with control biopsies from 11 patients with thin basement membrane disease and 2 normal kidneys.
  • Immunohistochemical assessment of TFPI, TF, and FRA expression.

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Main Results:

  • TFPI was undetectable in control glomeruli but present in interstitial microvessels.
  • TFPI expression increased with crescent chronicity, being prominent in fibrous/fibrocellular crescents.
  • TF and FRA were highly expressed in early lesions, while TFPI was maximal in late lesions with less FRA.

Conclusions:

  • TFPI is upregulated in later stages of human crescent formation.
  • TFPI expression is inversely correlated with fibrin deposition in chronic crescentic GN.
  • Late TFPI induction may limit TF activity and fibrin deposition in chronic disease.