Functional Fc gamma receptor gene polymorphisms and long-term kidney allograft survival
The functional Fc gamma receptor (FcγR) IIIA polymorphism FCGR3A-V/F158 was earlier suggested to determine the potential of donor-specific HLA antibodies to trigger microcirculation inflammation, a key lesion of antibody-mediated renal allograft rejection. Associations with long-term transplant outc...
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| Hauptverfasser: | , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
23 August 2021
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| In: |
Frontiers in immunology
Year: 2021, Jahrgang: 12, Pages: 1-8 |
| ISSN: | 1664-3224 |
| DOI: | 10.3389/fimmu.2021.724331 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.3389/fimmu.2021.724331 Verlag, lizenzpflichtig, Volltext: https://www.frontiersin.org/article/10.3389/fimmu.2021.724331 
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| Verfasserangaben: | Markus Wahrmann, Bernd Döhler, Marie-Luise Arnold, Sabine Scherer, Katharina A. Mayer, Susanne Haindl, Helmuth Haslacher, Georg A. Böhmig and Caner Süsal |
MARC
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| 520 | |a The functional Fc gamma receptor (FcγR) IIIA polymorphism FCGR3A-V/F158 was earlier suggested to determine the potential of donor-specific HLA antibodies to trigger microcirculation inflammation, a key lesion of antibody-mediated renal allograft rejection. Associations with long-term transplant outcomes, however, have not been evaluated to date. To clarify the impact of FCGR3A-V/F158 polymorphism on kidney transplant survival, we genotyped a cohort of 1,940 recipient/donor pairs. Analyzing 10-year death-censored allograft survival, we found no significant differences in relation to FCGR3A-V/F158. There was also no independent survival effect in a multivariable Cox model. Similarly, functional polymorphisms in two other activating FcγR, FCGR2A-H/R131 (FcγRIIA) and FCGR3B-NA1/NA2 (FcγRIIIB), were not associated with outcome. There were also no significant survival differences among patient subgroups at increased risk of rejection-related injury, such as pre-sensitized recipients (> 0% panel reactivity; n = 438) or recipients treated for rejection within the first year after transplantation (n = 229). Our study results suggest that the earlier shown association of FcγR polymorphism with microcirculation inflammation may not be strong enough to exert a meaningful effect on graft survival. | ||
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