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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.
Thrombotic microangiopathy (TMA) is a serious complication following kidney transplantation, associated with significant graft loss. Its diagnosis and management are challenging due to diverse triggers and etiologies. This study aimed to analyze the histopathological features and clinical outcomes of post-transplant TMA in a single-center cohort.
We conducted a retrospective cohort study of kidney transplant recipients between 2013-2023 with biopsy-proven TMA. Patients were categorized as having rejection-related TMA or TMA from other causes. Histopathological analysis followed Banff criteria, focusing on documenting the presence of thrombi in glomerular, arteriolar/arterial, and peritubular capillaries. Graft and patient survival were analyzed using Kaplan-Meier curves.
A total of 67 TMA cases were identified among 538 patients with a functioning graft, representing an incidence of 12.5%. Notably, most cases (54/67, 80.6%) were classified as rejection-related. This group showed significantly higher scores of microvascular inflammation (MVI), glomerulitis (g score), and C4d positivity in peritubular capillaries (p<0.05). Endothelial edema was only present in rejection-related TMA (41.5% vs. 0%, p=0.004). TMA was the main diagnosis in only 7.4% of rejection cases compared to 30.8% in the other causes group (p=0.02). Immunofluorescence positivity was more frequent in the other causes group (46.2% vs. 3.8%, p<0.001).
With a median follow-up of 58-63 months across groups, graft loss or death occurred in 45 of 64 patients (70.3%). The event rates were similarly high in both rejection-related TMA and other causes TMA groups (70.6% vs 69.2%).
The incidence of TMA in our cohort (12.5%) is higher than most international reports, emphasizing its significance as a frequent and serious complication in kidney transplant recipients. Rejection-related TMA, the most common cause, shows a distinct histopathological profile with active microvascular inflammation and complement activation, typically as a secondary finding. In contrast, TMA from other causes is more often the primary diagnosis and associated with immune complex deposition. Our results underline the need for a precise biopsy-based classification to guide targeted therapy. Furthermore, the survival analysis reveals a poor long-term prognosis once TMA is established, regardless of the underlying etiologies.
