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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 (ABMR) in renal allografts induces microvascular inflammation and endothelial injury, processes that contribute to the release of circulating microparticles (MPs). These MPs, derived from various cell types, may serve as non-invasive biomarkers reflecting immune activation and vascular damage. This study aimed to assess plasma-derived MPs specifically monocyte-derived MPs (MMPs), platelet-derived MPs (PMPs), endothelial cell-derived MPs (EMPs), T-helper cell-derived MPs (THMPs), and T-cytotoxic cell-derived MPs (TCMPs) as potential biomarkers in ABMR.
The study included fifty renal allograft recipients diagnosed with ABMR on for-cause biopsies, twenty-five with stable graft function (SGF), and twenty-five age- and sex-matched healthy controls (HC) from January 2021 to January 2024. All biopsies were classified per Banff criteria. Plasma MPs were isolated and quantified using TruCount Tubes (BD), with flow cytometric analysis (gate limit between 0.5 µm and 1.0 µm).MPs were stained and quantified with Annexin V, CD14, CD42a , CD31, CD4, CD8.
All ABMR participants were males with a mean age of 38.2 ± 9 years. Mean serum creatinine was 3.0 ± 2.6 mg/dL in ABMR, 1.2 ± 0.2 mg/dL in SGF, and 0.7 ± 0.1 mg/dL in HC. Total circulating MPs were significantly elevated in ABMR (1.9 × 10⁴ ± 9 × 10³ counts/µL) compared to SGF (1.6 × 10⁴ ± 9.1 × 10³ counts/µL) and HC (1.3 × 10⁴ ± 2.6 × 10³ counts/µL). Among all subsets, MMPs constituted the highest proportion (26.4%). PMP (14%), EMP (11%), THMPs (17%), and TCMPs (11%) levels were significantly increased in ABMR compared with SGF and HC (p < 0.05). A negative correlation was observed between total MPs and estimated glomerular filtration rate (eGFR; p = –0.021). PMPs, THMPs, and TCMPs were positively associated with tubular atrophy on graft histology.
Renal allograft recipients with ABMR demonstrate a significant elevation of circulating cell-derived MPs, particularly monocyte-derived subtypes, indicating higher cellular activation and injury. MP phenotyping in ABMR may represent mechanistic biomarkers linked to immune-mediated vascular injury and it shows pathophysiological pathways, including endothelial dysfunction, immune activation, and pro-thrombotic states. As a non-invasive biomarker, MPs holds potential for improving ABMR diagnosis, monitoring graft injury progression, and enabling therapeutic strategies in kidney transplantation.
