Literature DB >> 19515805

Plasma markers of coagulation and endothelial activation in Fabry disease: impact of renal impairment.

Anouk C Vedder1, Eva Biró, Johannes M F G Aerts, Rienk Nieuwland, Guus Sturk, Carla E M Hollak.   

Abstract

BACKGROUND: In Fabry disease, storage of globotriaosylceramide (Gb3) in arterial walls is one of the main pathogenetic factors that are thought to underlie the clinical manifestations of the disease. Abnormalities of the vessel wall, haemodynamics and pro- and anticoagulant factors may play a role, though the exact pathophysiology is incompletely understood. In this study, we try to clarify inconsistencies regarding coagulation activation, fibrinolysis, platelet activation and endothelial activation in 36 patients with Fabry disease.
METHODS: Cell-derived microparticles, markers for coagulation activation (F(1+2), TAT, sTF, sEPCR), fibrinolysis (D-dimer, tPA, alpha(2)-AP), platelet activation (beta-TG, PF4), endothelial activation (vWF) and acute phase response (IL-6, CRP) were studied in relation to renal function and severity of the disease and compared to data from 36 age- and sex-matched healthy controls (17 males).
RESULTS: Markers for endothelial activation and fibrinolysis were normal. Male patients had elevated levels of sTF and beta-TG, with an association between sTF and renal function and severity of the disease. In female patients, levels of TAT, beta-TG, PF4, CD63-positive platelet-derived microparticles and IL-6 were somewhat increased, with no correlation with renal function or disease severity.
CONCLUSIONS: Only minimal abnormalities in markers for platelet, endothelial activation and coagulation activation and fibrinolysis could be established in a large cohort of Fabry disease patients. The existing laboratory abnormalities are more likely related to renal insufficiency rather than to Fabry disease itself.

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Year:  2009        PMID: 19515805     DOI: 10.1093/ndt/gfp263

Source DB:  PubMed          Journal:  Nephrol Dial Transplant        ISSN: 0931-0509            Impact factor:   5.992


  8 in total

1.  Homocysteine and erythrocyte sedimentation rate correlate with cerebrovascular disease in fabry disease.

Authors:  R Cheung; D O Sillence; M C Tchan
Journal:  JIMD Rep       Date:  2012-02-01

2.  α-galactosidase A deficiency promotes von Willebrand factor secretion in models of Fabry disease.

Authors:  Justin J Kang; Nayiri M Kaissarian; Karl C Desch; Robert J Kelly; Liming Shu; Peter F Bodary; James A Shayman
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Journal:  Curr Treat Options Neurol       Date:  2016-07       Impact factor: 3.598

Review 4.  Biomarkers in the diagnosis of lysosomal storage disorders: proteins, lipids, and inhibodies.

Authors:  Johannes M F G Aerts; Wouter W Kallemeijn; Wouter Wegdam; Maria Joao Ferraz; Marielle J van Breemen; Nick Dekker; Gertjan Kramer; Ben J Poorthuis; Johanna E M Groener; Josanne Cox-Brinkman; Saskia M Rombach; Carla E M Hollak; Gabor E Linthorst; Martin D Witte; Henrik Gold; Gijs A van der Marel; Herman S Overkleeft; Rolf G Boot
Journal:  J Inherit Metab Dis       Date:  2011-03-29       Impact factor: 4.982

5.  Cerebral hemodynamics and endothelial function in patients with Fabry disease.

Authors:  Tomás Segura; Oscar Ayo-Martín; Isabel Gómez-Fernandez; Carolina Andrés; Miguel A Barba; José Vivancos
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6.  Integrative Systems Biology Investigation of Fabry Disease.

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Journal:  Diseases       Date:  2016-11-15

7.  Urine bikunin as a marker of renal impairment in Fabry's disease.

Authors:  Antonio Junior Lepedda; Laura Fancellu; Elisabetta Zinellu; Pierina De Muro; Gabriele Nieddu; Giovanni Andrea Deiana; Piera Canu; Daniela Concolino; Simona Sestito; Marilena Formato; Gianpietro Sechi
Journal:  Biomed Res Int       Date:  2013-06-12       Impact factor: 3.411

8.  Platelet and myeloid cell phenotypes in a rat model of Fabry disease.

Authors:  Adam J Kanack; Kazuhiro Aoki; Michael Tiemeyer; Nancy M Dahms
Journal:  FASEB J       Date:  2021-08       Impact factor: 5.834

  8 in total

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