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NDT Advance Access originally published online on February 5, 2009
Nephrology Dialysis Transplantation 2009 24(7):2244-2251; doi:10.1093/ndt/gfp017
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© The Author [2009].
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org


Citrate pharmacokinetics and calcium levels during high-flux dialysis with regional citrate anticoagulation

Justyna Kozik-Jaromin1, Volker Nier1, Uwe Heemann2, Bernhard Kreymann2 and Joachim Böhler3

1 Fresenius Medical Care, Bad Homburg 2 Technical University Munich, Klinikum Rechts der Isar, Department of Nephrology, Munich 3 Deutsche Klinik für Diagnostik, Department of Nephrology, Wiesbaden, Germany

Correspondence and offprint requests to: Justyna Kozik-Jaromin; E-mail: justyna.kozik-jaromin{at}fmc-ag.com



  Abstract

Background. Regional citrate anticoagulation is a very effective anticoagulation method for haemodialysis. However, it is not widely used, primarily due to the risk of hypocalcaemia. We studied citrate and calcium kinetics to better understand safety aspects of this anticoagulation method.

Methods. During 15 haemodialysis treatments with a calcium-free dialysis solution, citrate was infused pre-dialyser and calcium was substituted post-dialyser. Systemic and extracorporeal citrate and calcium concentrations were repeatedly measured to calculate citrate and calcium pharmacokinetics.

Results. Removal by dialysis constituted the major elimination pathway of citrate (83 ± 5%). Systemic citrate load and concentrations were low (17 ± 7 mmol/4 h, 0.3 ± 0.15 mmol/l). Combined use of calcium-free dialysate and citrate infusion increased diffusible calcium to 80% of total calcium and induced substantial dialytic loss of calcium (43 ± 4 mmol/4 h). Since calcium was substituted, systemic calcium balances were positive (~+5 mmol) and concentrations stable. Calcium supplementation correlated with calcium dialytic losses, which in turn were dependent on total calcium and haematocrit.

Conclusions. When using calcium-free dialysate during citrate anticoagulation, hypocalcaemia is very likely unless calcium is re-infused, because large amounts of calcium are lost in the dialysate. However, an accumulation of citrate in the patient's systemic circulation is an unlikely cause of hypocalcaemia since most of the citrate is removed by dialysis. Calcium substitution and monitoring are the most important safety measures. We propose a rational approach based on haematocrit and total calcium for the choice of the starting calcium supplementation rate.

Keywords: calcium; citrate; dialysis; pharmacokinetics; regional anticoagulation

Received for publication: 21.10.07
Accepted in revised form: 8. 1.09


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