Impact of Blood Transfusions After Kidney Transplantation on Clinical Outcomes and Broadness of Sensitisation
5 affiliations
- 1Clinic for Transplantation Immunology and Nephrology University Hospital Basel Basel Switzerland
- 2HLA‐Diagnostics and Immunogenetics, Department of Laboratory Medicine University Hospital Basel Basel Switzerland
- 3Department of Vascular and Renal Transplant Surgery University Hospital Basel Basel Switzerland
- 4Department of Hematology and Laboratory Medicine University Hospital Basel Basel Switzerland
- 5Regional Blood Transfusion Service Swiss Red Cross, Northwestern Switzerland Basel Switzerland
Abstract
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.
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BibTeX
@article{gerber2026impact,
title = {{Impact of Blood Transfusions After Kidney Transplantation on Clinical Outcomes and Broadness of Sensitisation}},
author = {Stella L. Gerber and Matthias Diebold and Gideon Hönger and Caroline Wehmeier and Thomas Wolff and Edin Mujagic and Corinne Widmer and Andreas Buser and Stefan Schaub},
journal = {Hla},
year = {2026},
month = nov,
doi = {10.1111/tan.71068},
url = {https://doi.org/10.1111/tan.71068},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Impact of Blood Transfusions After Kidney Transplantation on Clinical Outcomes and Broadness of Sensitisation
AU - Stella L. Gerber
AU - Matthias Diebold
AU - Gideon Hönger
AU - Caroline Wehmeier
AU - Thomas Wolff
AU - Edin Mujagic
AU - Corinne Widmer
AU - Andreas Buser
AU - Stefan Schaub
PY - 2026
DA - 2026/11/05
JO - Hla
DO - 10.1111/tan.71068
UR - https://doi.org/10.1111/tan.71068
AB - 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.
SN - 2059-2302
SN - 2059-2310
ER -