NDT Advance Access originally published online on September 6, 2005
Nephrology Dialysis Transplantation 2006 21(1):153-159; doi:10.1093/ndt/gfi069
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Original Articles: Dialysis and Transplantation
Citrate anticoagulation abolishes degranulation of polymorphonuclear cells and platelets and reduces oxidative stress during haemodialysis
1 Department of Nephrology and 2 Department of Clinical Chemistry, Medical Center Alkmaar, Alkmaar, 3 Department of Nephrology, 4 Department of Clinical Chemistry and 5 Department of Clinical Epidemiology and Biostatistics, VU University Medical Center, Amsterdam, The Netherlands
Correspondence and offprint requests to: M. Gritters, Department of Internal Medicine (Nephrology), 130, Wilhelminalaan 12, 1815 JD Alkmaar, The Netherlands. Email: mareillegritters{at}hotmail.com
Background. During haemodialysis (HD), polymorphonuclear cells (PMNs) and platelets are activated and release various granule products, including myeloperoxidase (MPO) and platelet factor 4 (PF4). MPO triggers the generation of reactive oxygen species, leading to irreversible protein, carbohydrate and lipid modification. PF4 probably also contributes to oxidative stress. As previously shown, HD-induced PMN degranulation is almost completely abolished during citrate anticoagulation, most probably due to its calcium chelation ability.
Methods. In the present study, apart from HD-induced PMN and platelet degranulation, oxidative stress was analysed during three modes of anticoagulation. Heparin, dalteparin and citrate (HDhep, HDdal and HDcit) were compared in a randomized, crossover fashion in eight chronic HD patients. Multiple blood samples were taken during the third HD session of each modality, from both the afferent and efferent line. Besides the degranulation markers MPO and PF4, various markers of oxidative stress were measured, including oxidized low-density lipoprotein (ox-LDL), malondialdehyde (MDA) and carboxymethyllysine (CML).
Results. During HDhep and HDdal, marked degranulation was observed shortly after the start of HD. In contrast, during HDcit, PF4 and MPO levels remained unaltered, suggesting no release at all. After 1 week of HDcit, ox-LDL levels were markedly reduced [median 26% (3–65%), P = 0.01], if compared with HDhep and HDdal. As regards MDA and CML, no differences were found.
Conclusions. This study shows first, that HD-induced PMN and platelet degranulation are early, most probably calcium-dependent processes and, secondly, that the formation of ox-LDL is clearly dependent on the type of anticoagulant applied.
Keywords: anticoagulation; haemodialysis; oxidative stress; polymorphonuclear cells; thrombocytes
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