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Updated: Apr 5, 2026

In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
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Thrombosis, Microangiopathies, and Inflammation

Karen Matevosyan1, Ravi Sarode1

  • 1Division of Transfusion Medicine and Hemostasis, Department of Pathology, UT Southwestern Medical Center, Dallas, Texas.

Seminars in Thrombosis and Hemostasis
|August 16, 2015
PubMed

Insights

Thrombotic microangiopathy (TMA) involves microangiopathic hemolytic anemia and thrombocytopenia. This review covers key developments in understanding the causes, diagnosis, and treatment of common TMAs like TTP and aHUS.

Area of Science:

  • Hematology
  • Pathology
  • Immunology

Background:

  • Thrombotic microangiopathy (TMA) is a condition characterized by microangiopathic hemolytic anemia and thrombocytopenia.
  • Neutrophils and their extracellular traps (NETs) play a role in TMA pathogenesis.
  • Key TMAs include thrombotic thrombocytopenic purpura (TTP) due to ADAMTS-13 deficiency and atypical hemolytic uremic syndrome (aHUS) linked to complement dysregulation.

Purpose of the Study:

  • To review recent advancements in the etiopathogenesis, diagnosis, and treatment of commonly encountered TMAs.
  • To highlight the importance of differentiating various TMA causes for appropriate management.
  • To discuss the role of neutrophil extracellular traps in TMA.

Main Methods:

  • Literature review of recent studies on TMA.
  • Analysis of current understanding of TTP and aHUS pathogenesis.
  • Discussion of diagnostic approaches and evolving treatment strategies for TMAs.

Main Results:

  • Significant progress has been made in understanding the molecular mechanisms underlying TTP and aHUS.
  • Improved diagnostic tools allow for more precise identification of TMA subtypes.
  • Treatment strategies for TMAs have evolved, with better outcomes reported.

Conclusions:

  • TMAs encompass diverse disorders with genetic and acquired causes, requiring thorough investigation.
  • Understanding the specific etiology of TMA is crucial for selecting effective therapies.
  • Continued research into TMA pathogenesis, including the role of NETs, is essential for further therapeutic advancements.

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