Literature DB >> 29940557

Thrombomodulin and Endothelial Dysfunction: A Disease-Modifier Shared between Malignant Hypertension and Atypical Hemolytic Uremic Syndrome.

Marieke Demeulenaere1, Katrien Devreese2, Hilde Vanbelleghem3, Julie De Zaeytijd4, Johan Vande Walle5, Wim Van Biesen1, Steven Van Laecke1.   

Abstract

Thrombomodulin (TM) is an endothelial glycoprotein that is present in all blood vessels. Five percent of all patients with atypical hemolytic uremic syndrome (aHUS) have mutations in the gene coding for TM, with a peak presentation in young children. Mutations often translate into quantitative and qualitative abnormalities of this endothelial glycoprotein. Outcome of the TM-associated aHUS is relatively poor with frequent relapses after transplantation despite its membrane-bound character. We observed a woman presenting with malignant hypertension (MHT) and associated kidney, brain, cardiac, and hematological involvement with thrombotic microangiopathy on kidney biopsy. She had a documented mutation of the gene coding for TM, which was associated with both aHUS and an increased risk for venous and arterial thrombosis. As TM has anti-coagulant, anti-inflammatory, and cytoprotective properties and also attenuates alternative complement activation, this glycoprotein could play an active role in other diseases with endothelial involvement apart from aHUS. We discuss the potential role of TM in the pathophysiology of various endotheliopathies including MHT. We also provide a framework for future therapeutic options.
© 2018 S. Karger AG, Basel.

Entities:  

Keywords:  Endothelial; Malignant hypertension; Thrombomodulin; Thrombotic microangiopathy

Mesh:

Substances:

Year:  2018        PMID: 29940557     DOI: 10.1159/000490201

Source DB:  PubMed          Journal:  Nephron        ISSN: 1660-8151            Impact factor:   2.847


  4 in total

1.  A novel homozygous variant of the thrombomodulin gene causes a hereditary bleeding disorder.

Authors:  Makoto Osada; Keiko Maruyama; Koichi Kokame; Ryunosuke Denda; Kohei Yamazaki; Hisako Kunieda; Maki Hirao; Seiji Madoiwa; Nobuo Okumura; Mitsuru Murata; Yasuo Ikeda; Kentaro Watanabe; Yuiko Tsukada; Takahide Kikuchi
Journal:  Blood Adv       Date:  2021-10-12

2.  Deterioration in Clinical Status Is Not Enough to Suspend Eculizumab: A Genetic Complement-Mediated Atypical Hemolytic Uremic Syndrome Case Report.

Authors:  Luca Calvaruso; Alessandro Naticchia; Pietro Manuel Ferraro; Gisella Vischini; Stefano Costanzi
Journal:  Case Rep Nephrol       Date:  2019-07-09

Review 3.  Complement Factor D as a Strategic Target for Regulating the Alternative Complement Pathway.

Authors:  Jonathan Barratt; Ilene Weitz
Journal:  Front Immunol       Date:  2021-09-09       Impact factor: 7.561

4.  RNA sequencing reveals induction of specific renal inflammatory pathways in a rat model of malignant hypertension.

Authors:  Carlos Menendez-Castro; Nada Cordasic; Fabian B Fahlbusch; Arif B Ekici; Philipp Kirchner; Christoph Daniel; Kerstin Amann; Roland Velkeen; Joachim Wölfle; Mario Schiffer; Andrea Hartner; Karl F Hilgers
Journal:  J Mol Med (Berl)       Date:  2021-09-15       Impact factor: 4.599

  4 in total

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