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Related Experiment Videos

Glomerular procoagulant activity in human proliferative glomerulonephritis.

P G Tipping1, J P Dowling, S R Holdsworth

  • 1Department of Medicine, Monash University, Melbourne, Australia.

The Journal of Clinical Investigation
|January 1, 1988
PubMed
Summary

Glomerular fibrin deposition in rapidly progressive glomerulonephritis is linked to tissue factor, primarily from activated monocytes. This finding highlights the extrinsic pathway

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Area of Science:

  • Nephrology
  • Immunology
  • Hematology

Background:

  • Rapidly progressive glomerulonephritis (RPGN) is characterized by rapid loss of kidney function.
  • Fibrin deposition within glomeruli contributes to crescent formation and disease progression in RPGN.
  • The precise mechanisms initiating intraglomerular fibrin deposition in RPGN remain incompletely understood.

Purpose of the Study:

  • To investigate the mechanisms of glomerular fibrin deposition in patients with crescentic RPGN.
  • To identify the source and nature of procoagulant activity within affected glomeruli.

Main Methods:

  • Analysis of renal tissue from two patients with crescentic RPGN.
  • Assessment of procoagulant activity (PCA) in isolated glomeruli.
  • Characterization of PCA using functional assays, enzyme inhibitors, and a specific anti-tissue factor antibody.

Related Experiment Videos

  • Immunofluorescence staining for tissue factor in glomerular tissue.

    • Main Results:

    • Glomeruli from RPGN patients exhibited significantly elevated PCA compared to normal glomeruli.
    • The PCA was identified as tissue factor, dependent on Factors VII and V, and inhibited by concanavalin A, phospholipase C, and an anti-tissue factor antibody.
    • Tissue factor was localized within the glomeruli of affected patients.
    • Activated monocytes were abundant in the glomeruli.

    Conclusions:

    • Extrinsic pathway activation mediated by tissue factor plays a crucial role in initiating glomerular fibrin deposition in RPGN.
    • Activated monocytes infiltrating the glomeruli are the likely source of this tissue factor.
    • Targeting tissue factor may offer a therapeutic strategy for RPGN.