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Effect of immunoadsorption alone or combined with membrane filtration on hemostasis parameters
Author(s) -
Marlu Raphaël,
Bennani Hamza Naciri,
Seyve Landry,
Malvezzi Paolo,
Janbon Bénédicte,
Noble Johan,
Christophe Maryvonne,
Motte Lionel,
Imerzoukene Farida,
Chevallier Eloi,
Rostaing Lionel,
Jouve Thomas
Publication year - 2020
Publication title -
journal of clinical apheresis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.697
H-Index - 46
eISSN - 1098-1101
pISSN - 0733-2459
DOI - 10.1002/jca.21825
Subject(s) - immunoadsorption , medicine , hemostasis , fibrinogen , abo blood group system , factor xiii , von willebrand factor , clotting factor , transplantation , immunology , platelet , endocrinology , antibody
Abstract Introduction ABO‐ or HLA‐incompatible kidney transplantation is possible thanks to pretransplant antibody‐depletion achieved by extracorporeal‐treatment modalities. These methods induce depletion of some plasma proteins and may also impact on proteins involved in hemostasis. Methods To determine the impact of one session of immunoadsorption (IA) alone or combined with membrane filtration (MF) on clotting factors and natural anticoagulants, we performed a prospective, observational study on 13 patients waiting for HLA‐/ABO‐incompatible kidney transplants. Plasma hemostasis parameters were measured before and immediately after a first session of IA alone in six patients and of IA + MF in seven patients. Results IA alone induced depletion of fibrinogen and factor XIII (FXIII) whereas IA + MF caused greater depletion of all high‐molecular‐weight hemostatic proteins (fibrinogen, FV, FVIII, FXI, FXIII, von‐Willebrand factor [VWF]). After an IA session, median reductions were 30% for fibrinogen and 43% for FXIII compared to baseline values. After a session of IA + MF, median decreases were 70% for fibrinogen, 54% for FV, 56% for FVIII, 37% for FXI, 78% for FXIII, and 62% for VWF. Noticeably, levels of low‐molecular‐weight factors (<100 kDa) were far less decreased than high‐molecular‐weight proteins with IA + MF, except for protein S and the tissue factor pathway inhibitor, which are known to be partially physiologically bound to high‐molecular‐weight molecules. Conclusions IA and IA + MF induced significant depletion of some proteins implicated in the hemostatic process; however, IA + MF resulted in stronger modifications to hemostasis parameters than IA alone. This may have potential clinical implications regarding bleeding risk, and particularly depletion of fibrinogen and FXIII.