Impact of Blood Transfusions After Kidney Transplantation on Clinical Outcomes and Broadness of Sensitisation
Stella L. Gerber, Matthias Diebold, Gideon Hönger, Caroline Wehmeier, Thomas Wolff, Edin Mujagic, Corinne Widmer, Andreas Buser, Stefan SchaubABSTRACT
Whether erythrocyte transfusion (ET) after kidney transplantation triggers formation of de novo donor‐specific HLA‐antibodies (HLA‐DSA) and rejection remains debated. If this were true, ET should broaden HLA sensitisation, reflected by increased calculated panel reactive antibodies (cPRA) and de novo HLA‐antibody specificities beyond HLA‐DSA. This has not been investigated in detail yet. In this retrospective study we included 519 kidney transplant recipients having single antigen bead analyses pretransplant and at one‐year posttransplant. ET was assessed both as a binary variable (with/without ET) and in quantity‐based groups (without ET, 1–2 ET, 3–5 ET, > 5 ET). No significant differences were found between patients with/without ET in the one‐year incidence of clinical rejection (19.7% vs. 15.3%, p = 0.43), clinical/subclinical rejection (30.0% vs. 28.6%, p = 0.86), TCMR (15.6% vs. 19.4%; p = 0.30) and AMR (15.6% vs. 10.1%; p = 0.19). Quantity‐based analysis also showed no significant differences, except for higher AMR incidence in patients receiving > 5 ET ( p = 0.03). This association lost significance after multivariable adjustment in a time‐dependent Cox model (HR: 0.91 [95%‐CI: 0.52–1.59]; p = 0.74). De novo HLA‐DSA incidence was similar in patients with/without ET (3.5% vs. 3.1%, p = 0.80) and across quantity‐based groups ( p = 0.17). cPRA change did not differ between patients with/without ET or across quantity‐based groups. No preferential sensitisation against highly prevalent HLA‐antigens Class I was observed (e.g., HLA‐A1 [0.4%], HLA‐A2 [0.8%], HLA‐B51 [0.8%] and HLA‐Cw7 [1.3%]). In conclusion, ET after kidney transplantation under tacrolimus/mycophenolate/prednisone‐based immunosuppression was not associated with rejection, de novo HLA‐DSA formation, and broadened HLA sensitisation arguing against the clinical need for HLA‐matched/selected ET in this setting.