PMID- 17895513 OWN - NLM STAT- MEDLINE DCOM- 20090319 LR - 20090119 IS - 1076-0296 (Print) IS - 1076-0296 (Linking) VI - 15 IP - 1 DP - 2009 Feb TI - Unfractionated heparin but not enoxaparin causes delayed plasma PAI-1 depletion in hemodialysis patients: a prospective study. PG - 84-91 AB - BACKGROUND AND AIMS: Heparin modulates function of vascular endothelial cells. We studied the effects of unfractionated heparin (UFH) versus low-molecular-weight heparin (LMWH), enoxaparin, used as anticoagulants during hemodialysis (HD) on plasma levels of circulating endothelium-derived molecules: thrombomodulin (TM), von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI-1), cell surface adhesion molecules (E-selectin), intercellular adhesion molecule-1 (ICAM-1), and prothrombin fragment 1+2 (PF 1+2). METHODS: Twenty-five patients undergoing enoxaparin-anticoagulated HD were randomly assigned either to continue enoxaparin (n = 13) or receive UFH (n = 12) during HD and followed prospectively for 12 weeks. Plasma immunoreactive TM, vWF, PAI-1, ICAM-1, E-selectin, and PF 1+2 were measured before the randomization procedure and after 12 weeks, at the start, after 10 and 180 minutes of HD. RESULTS: The switch from LMWH to UFH resulted in decreased pre-HD levels of PAI-1 and TM and increased PF 1+2 concentrations. Predialysis PAI-1 negatively correlated with the total dose of UFH/kg/HD. No significant differences were observed in the other variables before and during HD after switching from LMWH to UFH. During enoxaparin-anticoagulated HD, only plasma PAI-1 levels decreased by 32% after 180 minutes compared with the baseline values. This percentage decrease positively correlated with predialysis PAI-1 levels and marginally with PF 1+2 concentrations after 180 minutes of enoxaparin-anticoagulated HD. CONCLUSION: Enoxaparin-anticoagulated HD is related to transient plasma PAI-1 decrease, whereas UFH anticoagulation may be the cause of delayed PAI-1 and TM depletion, which is an untoward consequence of enhanced coagulation activity in chronic HD patients. FAU - Naumnik, Beata AU - Naumnik B AD - Department of Nephrology and Transplantation With Dialysis Unit, Medical University, Bialystok, Poland. bnaumnik@poczta.onet.pl FAU - Pawlak, Krystyna AU - Pawlak K FAU - Mys'liwiec, Michal AU - Mys'liwiec M LA - eng PT - Comparative Study PT - Journal Article PT - Randomized Controlled Trial PT - Research Support, Non-U.S. Gov't DEP - 20070925 PL - United States TA - Clin Appl Thromb Hemost JT - Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis JID - 9508125 RN - 0 (Anticoagulants) RN - 0 (E-Selectin) RN - 0 (Enoxaparin) RN - 0 (Peptide Fragments) RN - 0 (Plasminogen Activator Inhibitor 1) RN - 0 (Protein Precursors) RN - 0 (Thrombomodulin) RN - 0 (von Willebrand Factor) RN - 126547-89-5 (Intercellular Adhesion Molecule-1) RN - 72270-84-9 (prothrombin fragment 1) RN - 78768-79-3 (prothrombin fragment 2) RN - 9001-26-7 (Prothrombin) RN - 9005-49-6 (Heparin) SB - IM MH - Aged MH - Anticoagulants/*pharmacology MH - E-Selectin/blood MH - Enoxaparin/*pharmacology MH - Female MH - Heparin/*pharmacology MH - Humans MH - Intercellular Adhesion Molecule-1/blood MH - Kidney Failure, Chronic/*blood/therapy MH - Male MH - Middle Aged MH - Peptide Fragments/blood MH - Plasminogen Activator Inhibitor 1/*blood MH - Prospective Studies MH - Protein Precursors/blood MH - Prothrombin MH - *Renal Dialysis MH - Thrombomodulin/blood MH - von Willebrand Factor/analysis EDAT- 2007/09/27 09:00 MHDA- 2009/03/20 09:00 CRDT- 2007/09/27 09:00 PHST- 2007/09/27 09:00 [pubmed] PHST- 2009/03/20 09:00 [medline] PHST- 2007/09/27 09:00 [entrez] AID - 1076029607304725 [pii] AID - 10.1177/1076029607304725 [doi] PST - ppublish SO - Clin Appl Thromb Hemost. 2009 Feb;15(1):84-91. doi: 10.1177/1076029607304725. Epub 2007 Sep 25.