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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.
Dense deposit disease (DDD) is caused by the dysregulation of the alternative complement pathway. DDD exhibits histological findings of intense C3 deposition greater than other immunoreactants on immunofluorescence microscopy and electron-dense deposits of the glomerular basement membrane lamina densa forming a sausage-like appearance on electron microscopy. The progression to end-stage kidney disease (ESRD) is within several years for a large portion of the patient population. Not only so, the rate of recurrence in kidney transplant recipients are high, ranging 80 to 100% in various studies, with cases noting recurrence within days to weeks post transplantation.
32-year-old female with history of ESRD due to biopsy proven dense deposit disease (DDD), s/p living related donor kidney transplant (mother) on 6/29/2016. Post transplant course was complicated by early recurrent DDD at 1-month post-transplant. Factor H autoantibody was elevated to 53 units/ml and C3 nephritic factor was high. The patient underwent apheresis and was started on eculizumab q2wk infusions, in addition to immunosuppression. Unfortunately missed a few infusion doses, developed AKI, continued on eculizumab.
Repeat kidney biopsy was performed to rule out rejection, showed recurrent dense deposit disease as shown below with modest C3 staining, no active crescents, evidence of acute tubular injury with 24% glomerular obsolescence and no evidence of rejection.
Patient reported mental exhaustion due to repeated and long term eculizumab infusions affecting compliance; and it was switched to oral Iptacopan.
Kidney function and proteinuria improved and has been stable for 6 months. No adverse effects occurred. Iptacopan has been FDA approved in March 2025 to treat C3 glomerular GN in the native kidneys after the APPEAR-C3 trial, which largely excluded transplant patients.The phase 2 trial included transplant patients and showed reduction in proteinuria, C3 level and histologic C3 deposit scores. Eculizumab has been historically used off label to treat post-transplant C3 GN with limited efficacy in DDD. Mechanistically, eculizumab blocks the terminal complement pathway leaving upstream unchecked, whereas Iptacopan blocks complement pathway upstream and prevents formation of C3 convertase, which is a pathologic driver making it more disease specific. The oral route of Iptacopan offers another advantage. To our knowledge, no prior case reports have mentioned successful use of Iptacopan therapy after eculizumab therapy in post-transplant C3GN or DDD.
Iptacopan could potentially be a well tolerated option in transplant patients with DDD or C3GN, in cases with intolerance or failure to eculizumab. Further studies are needed to define its exact role.
