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Author Spotlight: High-Sensitivity Tissue Factor Activity Assay for Plasma Diagnosis
Published on: December 29, 2023
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Tissue factor expressed by adherent cells contributes to hemodialysis-membrane thrombogenicity
Souad Lakbakbi1, Alexandre Debrumetz2, Christine Terryn3
1Equipe d'accueil 3801 Hémostase et Remodelage Vasculaire Post-Ischémie, Université de Reims, France.
Thrombosis Research
|July 17, 2016
Summary
Tissue factor (TF) drives blood clotting during hemodialysis in end-stage renal disease patients. Inhibiting TF with human recombinant factor VIIa (hrFVIIai) prevented clotting in a sheep model without systemic anticoagulation.
Area of Science:
- Nephrology
- Hematology
- Biochemistry
Background:
- End-stage renal disease patients have high risks of thrombosis and bleeding.
- Preventing clotting during hemodialysis (HD) is clinically challenging.
- Tissue factor (TF) may contribute to HD-associated thrombosis via the contact system.
Purpose of the Study:
- Investigate the role of TF in hemodialysis-associated thrombosis.
- Identify cells and mechanisms responsible for TF-driven clotting in extracorporeal circuits.
- Evaluate TF inhibition as a strategy to prevent HD thrombosis.
Main Methods:
- Collected cells adhering to AN69-ST membranes used in HD.
- Utilized microscopy, flow cytometry, and fluorogenic assays to analyze cells and thrombin generation.
- Quantified TF mRNA via Q-PCR and visualized TF and neutrophil extracellular traps (NETs) using immunofluorescence.
- Tested inactivated human recombinant factor VIIa (hrFVIIai) in a sheep HD model.
Main Results:
- Adherent cells were primarily activated polymorphonuclear neutrophils (PMNs).
- These PMNs triggered TF-dependent thrombin generation.
- TF mRNA, TF in PMNs, and TF-decorated NETs were identified.
- A single hrFVIIai bolus maintained circuit patency without systemic anticoagulation.
Conclusions:
- Activated PMNs and NETs contribute to HD-associated thrombosis through TF.
- TF is a key mediator of clotting in the extracorporeal circuit during HD.
- Targeting TF with hrFVIIai is a promising strategy for preventing HD thrombosis.
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