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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.
Atypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy (TMA) primarily caused by dysregulated activation of the alternative complement pathway. Current diagnostic approaches rely on the detection of pathogenic variants in seven known complement-related genes or the presence of autoantibodies against complement regulatory factors. However, these tests do not directly assess complement activity, and pathogenic variants are identified in only 40–60% of patients. The classical sheep red blood cell hemolysis assay evaluates alternative pathway activity but mainly detects factor H–related aHUS and is often negative in other cases. Consequently, the diagnostic yield remains approximately 50%, which frequently delays initiation of effective treatments such as plasma exchange or C5 inhibition.
To establish a novel diagnostic assay directly assessing complement activation, we analyzed 51 patients referred to the aHUS registry between April 2020 and June 2024, including patients with aHUS, secondary TMAs, and other TMAs. Citrated plasma samples were incubated with human C3–expressing mouse endothelial cells (UV2-hC3). Complement activation on the cell surface was quantified by flow cytometry using antibodies against human C3b and C5b-9. Normal plasma treated with an anti–complement factor H antibody (O72-16) served as a positive control for calculating cut-off values. Clinical data, including lactate dehydrogenase (LDH) levels, were integrated to optimize diagnostic accuracy.
The proportion of UV2-hC3 cells positive for surface-deposited C3b and C5b-9 was significantly higher in aHUS patients than in those with other TMAs. When C3b deposition was used as a diagnostic marker, the specificity reached 96.7%, while C5b-9 formation yielded a sensitivity of 90.5%. Combining C5b-9 formation with LDH levels improved the overall diagnostic accuracy to 90.2%. Notably, two secondary TMA cases showed positive results in this assay—one corresponded to a clinically Eculizumab-responsive case, and the other to a weakly positive case in the classical hemolytic assay—indicating that complement activation could not be ruled out in these conditions.
We successfully developed a flow cytometry–based assay that directly measures complement activation on cell surfaces. Although neither C3b nor C5b-9 deposition alone provided sufficient diagnostic precision, combining C5b-9 formation with LDH levels achieved high sensitivity and specificity. This approach enables detection of complement activation that were previously difficult to assess. Incorporating this assay into the diagnostic workflow for aHUS may facilitate earlier therapeutic intervention and improve clinical outcomes by enhancing, rather than replacing, current diagnostic methods.
