The Release of Monocyte-Derived Tissue Factor-Positive Microparticles Contributes to a Hypercoagulable State in

Gui Hua Wang1, Jian Lu1, Kun Ling Ma1

  • 1Institute of Nephrology, Zhongda Hospital, School of Medicine, Southeast University.

Abstract

Insights

In idiopathic membranous nephropathy (IMN), increased lipopolysaccharide (LPS) may drive the release of tissue factor (TF)-positive microparticles (MPs), contributing to a hypercoagulable state and higher risk of thromboembolic complications.

Area of Science:

  • Nephrology
  • Hematology
  • Immunology

Background:

  • Idiopathic membranous nephropathy (IMN) is an immune-mediated disease associated with increased risk of thromboembolic events.
  • Microparticles (MPs), particularly those expressing tissue factor (TF), are implicated in procoagulant activity.

Purpose of the Study:

  • To investigate the role of circulating TF-positive MPs in the hypercoagulable state of IMN patients.
  • To explore the relationship between TF-positive MPs, lipopolysaccharide (LPS), and coagulation markers in IMN.

Main Methods:

  • Flow cytometry was used to quantify circulating MPs and TF expression in 20 IMN patients and 14 healthy controls.
  • TF activity of MPs, plasma LPS levels, and routine coagulation parameters were measured.
  • In vitro experiments assessed the effect of LPS on MP release and TF activity.

Main Results:

  • While total MPs were not elevated, circulating TF-positive MPs, specifically monocyte-derived (CD14+/TF+), were significantly increased in IMN patients.
  • Elevated TF-positive MPs showed a positive correlation with D-dimer levels, indicating heightened procoagulant activity.
  • Circulating LPS levels were significantly higher in IMN patients and were shown to enhance TF-positive MP release and activity in vitro.

Conclusions:

  • Increased circulating LPS may trigger the release of monocyte-derived TF-positive MPs in IMN.
  • These TF-positive MPs contribute to the hypercoagulable state observed in IMN patients.
  • This pathway offers a potential mechanism explaining the increased thromboembolic risk in IMN.

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