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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.
Post-transplant thrombotic microangiopathy (TMA) is an uncommon but clinically significant histologic finding associated with severe endothelial injury and high rates of graft loss. Its pathophysiology involves complement activation, endothelial dysfunction, and immune-mediated vascular injury, frequently in the context of antibody-mediated rejection (ABMR). The coexistence of TMA and ABMR reflects advanced microvascular and immunologic damage. This study evaluates the time of presentation of TMA and associated factors to kidney allograft survival.
We conducted a single-center retrospective study of kidney transplant recipients diagnosed with histologic evidence of thrombotic microangiopathy (TMA) between 2010 and 2024. Clinical, laboratory, and histopathologic features were recorded at the time of diagnosis. Patients were classified according to the timing of presentation as early (<3 months) or late (>3 months) post-transplant. Graft survival was analyzed in relation to presentation timing, as well as clinical, histologic, and prognostic factors associated with kidney allograft loss.
Fifty kidney transplant recipients with biopsy-proven TMA were included. Median age at transplantation was 29 years (IQR 25–38), and 58% received kidneys from living donors. The main cause of end-stage kidney disease was undetermined etiology 27(54%), followed by lupus nephritis 13(26%). Overall graft survival after TMA diagnosis was 48% at 10 years [Figure1A]. Early TMA (<3 months post-transplant) occurred in 17 (34%) patients and late TMA (>3 months) in 33 (66%). Among early cases, 11 (64%) responded to therapy, whereas 6 (36%) were non-responsive. Biopsies from early cases showed predominantly acute lesions (77%); only responders lacked microvascular inflammation (MVI) and C4d deposition. Late TMA was further classified as active ABMR-associated (n = 13) or chronic TMA (n = 20). The ABMR-associated phenotype exhibited more active lesions, higher MVI scores, C4d positivity, greater interstitial fibrosis, and higher dialysis requirements at presentation compared with chronic TMA. Active ABMR-associated TMA showed the highest rate of graft loss (92%), while early presentation tended to have better outcomes than late (log-rank p = 0.08). When stratified by phenotype, early responsive TMA had the best graft survival (100% at 10 years), followed by chronic TMA (64.5%), whereas early non-responsive and ABMR-associated TMA had markedly poorer outcomes [Figure 1C].
Kidney-limited thrombotic microangiopathy indicates severe endothelial and immune injury with variable outcomes. Early responsive forms show better graft survival, whereas non-responsive, antibody-mediated, and chronic phenotypes predict graft loss. Intermittent detection of TMA across AMR biopsies suggests sampling variability or progressive injury, underscoring its prognostic value in transplant management.
