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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Antibody-mediated rejection (AMR) encompasses a spectrum of injury with different phenotypes, including early acute AMR (eaAMR), smoldering AMR (sAMR), and chronic AMR (cAMR) with transplant glomerulopathy. Understanding these phenotypes is critical to refine diagnostic criteria and assess activity and chronicity. Spatial transcriptomic technology can be used to evaluate gene expression within cells in spatial compartments. Gene expression profiles can be used to inform immunohistochemical (IHC) staining, including for cyclin D1, a cell cycle regulator, and EHD3, a glomerular specific endothelial protein. We hypothesized that endothelial cells would show differential gene expression between AMR phenotypes and that differences could be seen by IHC.
NanoString CosMx Spatial Molecular Imaging with cellular resolution was performed on kidney transplant biopsies from 4 groups (n=3 per group): 1) eaAMR,C4d+; 2) sAMR,C4d-; 3) cAMR,C4d-; 4) normal 1 year protocol biopsies. Expression of 1000 targeted RNAs was analyzed within spatially defined glomerular endothelial cells (GEC) and peritubular capillary endothelial cells (PTC). Differential gene expression was performed using a negative binomial model. Resulting transcripts were categorized by function. IHC was performed for cyclin D1 and EHD3 in selected cases (n=24 for cyclin D1, n=14 for EHD3) and evaluated for stain distribution and intensity.
Compared to normal transplant biopsies, eaAMR showed increased GEC transcripts related to proliferation/cell cycle regulation (including CCND1), hemostasis, complement regulation, basement membrane, and inflammation; PTC showed increased transcripts in endothelial injury/repair, MHC class II, and cell cycle regulation. Compared to normal, cAMR showed increased GEC transcripts in proliferation/cell cycle regulation (including CCND1), basement membrane, inflammation, and decreased expression EHD3; PTC showed transcripts in proliferation, basement membrane, MHC class II, and inflammation. GEC transcripts did not differ between normal and sAMR, and in PTC slightly significant differences in 2 genes related to MHC class II and proliferation.
Cyclin D1 (CCND1) IHC showed increased cytoplasmic and nuclear staining in GEC and focally in PTC for eaAMR and cAMR, and lesser staining in sAMR and normal. EHD3 IHC showed decreased cytoplasmic staining within GEC in eaAMR and cAMR compared to sAMR and normal protocol biopsies, correlating with the reduced gene expression in the transcriptomic analysis. sAMR demonstrated the greatest variability in intensity for EHD3.
GEC and PTC transcript profiles can distinguish normal, eaAMR, and cAMR, while sAMR shows endothelial gene expression similar to normal transplants. Although both eaAMR and sAMR qualify for the Banff category of “active AMR”, they can be distinguished based on transcripts associated with inflammation and endothelial activation. sAMR can persist without graft dysfunction, implying less injury to the endothelium than active AMR phenotypes. Cytoplasmic localization of cyclin may be a marker of activity in AMR. Loss of EHD3, correlates with chronicity in GEC, reflecting loss of normal endothelial phenotype in cAMR. Cyclin D1 and EHD3 IHC shows how spatial transcriptomic analysis has potential for discovery of useful markers, which may enable categorization of AMR along an activity/chronicity spectrum and guide treatment.
