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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.
The use of allogeneic vascular grafts (allografts) is an option for long-term vascular access in hemodialysis patients who have exhausted the possibilities for native arteriovenous fistula (AVF) creation. However, the long-term patency of these grafts is challenged by complications, primarily thrombosis. This study aims to describe the specific morphological alterations in the wall of a failed allogeneic vascular graft to elucidate the pathophysiological mechanisms of its dysfunction.
A morphological analysis was performed on explanted fragments of an allogeneic vascular graft harvested from a patient in a cohort where an arteriovenous fistula was formed using an allograft and had functioned for 9 months before explantation. The tissue samples were processed and examined using standard histological techniques to assess the structural integrity and pathological changes in the three vascular layers: intima, media, and adventitia. Immunohistochemical staining (CD3, CD20, CD68) was used to characterize the cellular composition of inflammatory infiltrates.
The morphological analysis revealed significant pathological remodeling of the allograft wall, consistent with allograft vasculopathy. The key findings were pronounced intimal hyperplasia, characterized by a marked and heterogeneous thickening due to smooth muscle cell proliferation, growth of loose connective tissue with abundant extracellular matrix, and uneven fibroblast proliferation, resulting in an intima-to-media thickness ratio of 4:1. Furthermore, the graft wall exhibited several areas of dissection, with some zones showing fibrinoid necrosis and others displaying replacement sclerohyalinosis.
The media showed signs of degeneration with focal deficits and fragmentation of elastic fibers.
A small focus of a mixed inflammatory infiltrate composed of CD3+ T-cells, CD20+ B-cells, and CD68+ macrophages was also detected at the border between the intima and media in a sclerotic dissection area.
The morphological changes in the allogeneic vascular graft are characterized by aggressive vasculopathy, multifocal recurrent wall dissection, significant intimal hyperplasia, and medial degeneration. These processes are driven by active cellular proliferation, extracellular matrix deposition, and a localized inflammatory response. The structural weakening and luminal narrowing caused by these changes are the likely morphological substrates for allograft thrombosis and failure. This underscores that allograft failure is not merely a thrombotic event but a complex process of pathological vascular remodeling. Prevention strategies should target the pathways of intimal hyperplasia and inflammation to improve the long-term patency of allogeneic vascular grafts for hemodialysis access.
