Abstract

Aim In a RTR with rising SCr, autoantibody was identified to HLA DR52 (MFI = 2382). As the patient received an HLA chromosome-identical transplant, HLA autoantibody was thought to be highly unlikely. Anti-vimentin autoantibodies have been associated with inflammation and rejection. Our hypothesis was that the RTR was synthesizing anti-vimentin antibody, detected as HLA DR52. We postulated that vimentin could be co-purified and coupled to Luminex beads, or that a shared epitope might be present on the HLA proteins. Therefore, if anti-vimentin antibody was tested against single antigen Luminex beads, certain beads would be positive, corresponding to HLA DR52 and any specificities where vimentin was co-purified or with a shared epitope. Methods Anti-vimentin murine monoclonal antibody PE-conjugate was reacted to One Lambda single antigen Luminex beads. The reaction pattern and MFIs were compared to those of the RTR serum. The anti-vimentin monoclonal was used in the standard protocol for HLA specificity analysis in the place of the anti-IgG antibody (omitting the serum incubation). A duplicate test was done using a 1 hour incubation of the anti-vimentin antibody with the beads to enhance the PE signal. Results The RTR serum had multiple non-auto-HLA Class I antibodies, which corresponded to the pretransplant sera specificities. The RTR serum showed antibodies to DR52 (MFI = 2382) and DP11 (MFI = 535) as the only HLA Class II specificities. The donor/recipient DP typing was unknown. The anti-vimentin monoclonal had no reactivity to HLA Class I but had HLA Class II reactivity to DR52 (MFI = 1073) and DP11 (MFI = 772). The RTR has been plasmapheresed X6, with a reduction in SCr from 2.2 to 1.5 mg/dL and the disappearance of the DR52 and DP11 specificities. Conclusions We conclude that our RTR had vimentin autoantibody associated with ongoing rejection. This caused the false identification by Luminex of HLA DR52 and DP11 specificities, either through the presence of vimentin or a shared epitope on the beads.

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