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Lipoprotein lipase responds similarly to tinzaparin as to conventional heparin during hemodialysis

DOI: 10.1186/1471-2369-11-33

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Abstract:

Twenty patients on chronic hemodialysis were switched from a primed infusion of UF-heparin to a single bolus of tinzaparin. There were long term follow up of variables for the estimation of dialysis efficacy as well as of the LPL release during dialysis and the subsequent impact on the triglycerides.The LPL activity in blood was higher on tinzaparin at 40 but lower at 180 minutes during HD. These values did not change during the 6 month study period. There were significant correlations between the LPL activities in individual patients at the beginning and end of the 6 month study period and between the activities on UF-heparin and on tinzaparin, indicating that tissue LPL was not being exhausted. Triglycerides were higher during the HD-session with tinzaparin than UF-heparin. The plasma lipid/lipoprotein levels did not change during the 6 month study period, nor during a 2-year follow up after the switch from UF-heparin to tinzaparin. Urea reduction rate and Kt/V were reduced by 4 and 7% after 6 months with tinzaparin.Our data demonstrate that repeated HD with UF-heparin or tinzaparin does not exhaust the LPL-system.During hemodialysis (HD) the patient must receive anticoagulation. According to the traditional protocol this is given as a primed infusion of UF-heparin. A newer approach, that has practical advantages, is to give a single bolus of LMW-heparin [1,2]. This is possible since the LMW preparations are cleared more slowly from blood; half-lives of 2 - 6 hours have been reported compared to only about 1 h for UF-heparin. Furthermore, whereas the pharmacodynamics of UF-heparins shows large differences between patients, the elimination kinetics for LMW-heparins is more predictable and therefore safe in most situations. One consideration when comparing the two preparations is that heparin releases the enzyme lipoprotein lipase (LPL) from its binding sites at the vascular endothelium into the circulating blood [3]. This leads to accelerated degradation of the enz

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