Thromb Haemost 1999; 82(04): 1334-1341
DOI: 10.1055/s-0037-1614386
Review Article
Schattauer GmbH

Protease Dependent Activation of Endothelial Cells by Peritoneal Dialysis Effluents

Michael Krebs
1   From the Department of Vascular Biology and Thrombosis Research and University of Vienna, Vienna, Austria
,
Christoph Kaun
1   From the Department of Vascular Biology and Thrombosis Research and University of Vienna, Vienna, Austria
,
Matthias Lorenz
2   Department of Medicine III, Division of Nephrology, University of Vienna, Vienna, Austria
,
Marianne Haag-Weber
2   Department of Medicine III, Division of Nephrology, University of Vienna, Vienna, Austria
,
Margarethe Geiger
1   From the Department of Vascular Biology and Thrombosis Research and University of Vienna, Vienna, Austria
,
Bernd R. Binder
1   From the Department of Vascular Biology and Thrombosis Research and University of Vienna, Vienna, Austria
› Author Affiliations
Further Information

Publication History

Received 03 February 1999

Accepted after revision 08 March 1999

Publication Date:
08 December 2017 (online)

Summary

Incubation of cultured human umbilical vein endothelial cells (HUVECs) with dilutions of peritoneal dialysis effluents (PDEs) from 11 individual patients undergoing continuous ambulatory peritoneal dialysis (CAPD) induced cellular procoagulant activity in a dose and time dependent manner. This procoagulant activity could be attributed to tissue factor (TF) expression since it was blocked by rabbit anti-TF IgG. These data was confirmed by FACS analysis yielding surface TF expression; In addition PDEs induced the expression of E-selectin in HUVECs. This TF and selectin inducing activity was heat labile and could be inhibited by protease inhibitors. Partial purification could be achieved using a benzamidine-Sepharose column. The TF inducing activity could not be attributed to LPS, IL-1, TNF-α, mast cell tryptase, active thrombin, or complement factor D. We therefore conclude that the peritoneal cavity contains a protease activity that induces a procoagulatory and proinflammatory phenotype in HUVECs.

 
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