Myeloperoxidase up-regulation during haemodialysis: is heparin the missing link?

Nephrology Dialysis Transplantation, Apr 2006

Jacek Borawski, Beata Naumnik, Alicja Rydzewska-Rosołowska, Michał Myśliwiec

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Myeloperoxidase up-regulation during haemodialysis: is heparin the missing link?

0 Department of Nephrology and Transplantology with Dialysis Unit Medical University Bialystok , Poland The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: - it could clarify their results, as well as improve or call into question their meanings. Conflict of interest statement. None declared. 1. Wu CC, Chen JS, Wu WM et al. Myeloperoxidase serves as a marker of oxidative stress during single haemodialysis session using two different biocompatible membranes. Nephrol Dial Transplant 2005; 20: 11341139 2. Gritters M, Grooteman MPC, Schoorl M et al. Citrate anticoagulation abolishes degranulation of polymorphonuclear cells and platelets and reduces oxidative stress during haemodialysis. Nephrol Dial Transplant 2006; 21: 153159 3. Krieter DH, Lemke HD, Wanner C. Myeloperoxidase serves as a marker of oxidative stress during single haemodialysis session using two different biocompatible membranes. Nephrol Dial Transplant 2006; 21: 546 4. Inose K, Ono K, Tsuchida A et al. Active inhibitory effect of nafamostat mesylate against the elevation of plasma myeloperoxidase during hemodialysis. Nephron 1997; 75: 420425 5. Wu CC, Lin SH, Lin YF. Reply. Nephrol Dial Transplant 2006; 21: 546 6. Borawski J. Myeloperoxidase as a marker of hemodialysis biocompatibility and oxidative stress: the underestimated modifying effects of heparin. Am J Kidney Dis 2006; 47: 3741 doi:10.1093/ndt/gfl002 We would like to thank the authors for their comments on our study. In their letter, they suggest that the haemodialysis (HD)-induced rise in myeloperoxidase (MPO) results from mobilization from the endothelium by exogenousadministered heparin. However, as described in our recent [1] and earlier studies [2,3], MPO reached its peak levels directly after first passage (t1 min). Moreover, substantial blood cell degranulation was observed in a closed loop recirculation model [4]. This process could be blunted by the chelation of plasmatic calcium (Ca) by sodium citrate or EDTA, and did not correlate with C3a or C5a concentrations [5]. The latter finding is in agreement with clinical studies, showing that degranulation and complement activation depend to a large extent on the type of dialyser used and are, in fact, independent of each other [6]. Based on the above mentioned data from clinical and experimental studies, it seems justified to conclude that MPO release occurs with certainty within the ECC, whereas endothelial mobilization remains to be proven. With respect to the cause of HD-induced degranulation, the mode of anticoagulation appears to be crucial. Several studies have indicated that Ca plays a critical role in the interaction between platelets and


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Jacek Borawski, Beata Naumnik, Alicja Rydzewska-Rosołowska, Michał Myśliwiec. Myeloperoxidase up-regulation during haemodialysis: is heparin the missing link?, Nephrology Dialysis Transplantation, 2006, 1128-1128, DOI: 10.1093/ndt/gfl002