Tissue factor pathway inhibitor (TFPI) activity in uremic patients during hemodialysis
| Autor: | Ernesto Rampin, Alessandra Sbarai, Ugo Vertolli, Giuseppe Cella, William Strauss, G. Boeri, Agostino Naso, Alessandro Vianello |
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| Rok vydání: | 1996 |
| Předmět: |
Male
medicine.medical_specialty Extracorporeal Circulation Endothelium medicine.drug_class medicine.medical_treatment Lipoproteins Tissue factor Thrombin Tissue factor pathway inhibitor Renal Dialysis Internal medicine medicine Humans Platelet Aged Uremia Aged 80 and over business.industry Anticoagulant Hematology Heparin Middle Aged Endocrinology medicine.anatomical_structure Case-Control Studies Kidney Failure Chronic Female Hemodialysis business medicine.drug |
| Zdroj: | Thrombosis research. 81(6) |
| ISSN: | 0049-3848 |
| Popis: | We studied tissue factor pathway inhibitor (TFPI) activity during hemodialysis in 10 uremic patients who were not receiving anticoagulant for at least 120 minutes. TFPI activity before dialysis was normal (patients 107 +/- 5.8%, controls 104 +/- 4.5%). During extracorporeal circuit it rose progressively with a statistically significant difference, reaching a plateau between 60 and 120 minutes. Since thrombin induces a marked redistribution and release of TFPI from stimulated endothelial cells and platelets contain about 10% of TFPI activity that is secreted following activation it is possible that thrombin-induced release of TFPI by endothelium and platelets could account for the increased TFPI we found during hemodialysis. To investigate this possibility we measured during dialysis beta-thromboglobulin (beta-TG), thrombin-antithrombin complex (TAT) and prothrombin fragment 1.2 (F 1.2). The increased levels of beta-TG, TAT and F1.2 we noted during extracorporeal circuit are in keeping with this concept. One hundred eighty minutes after initiation of dialysis, by which time all patients were receiving heparin there was a further increase in TFPI (to more than 200% of baseline), due to the presence of the glycosaminoglycan. This was due the previously reported displacement by heparin of the major intravascular pool of TFPI, from endothelial cell surfaces. |
| Databáze: | OpenAIRE |
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