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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.
Renal relapse or persistence of amyloid deposition after hematologic remission remains a diagnostic and pathophysiologic challenge in systemic light chain (AL) amyloidosis. Although hematologic response correlates with improved survival and renal outcomes, the natural history of amyloid deposits within the kidney after successful therapy is incompletely understood. Histologic recurrence may reflect either newly formed fibrils, re-expansion of residual deposits, or long-term persistence of “inert” amyloid unaccompanied by ongoing precursor production. This case highlights the ambiguity in interpreting recurrent renal amyloid findings years after complete hematologic response.
We report a woman diagnosed with systemic AL amyloidosis involving the kidney. Baseline evaluation revealed 2.5 g proteinuria, biopsy-proven AL amyloid with lambda light chain restriction, and mild interstitial fibrosis. Bone marrow biopsy demonstrated 5–8 % clonal plasma cells with Congo red positivity. The patient received cyclophosphamide, bortezomib, and dexamethasone (CyBorD) followed by autologous stem cell transplantation with melphalan conditioning. Serial laboratory, clinical, and histopathologic assessments were used to monitor hematologic and organ response according to consensus criteria.
Following therapy, the patient achieved a hematologic complete response and marked renal improvement, with reduction of proteinuria and stable renal function. Eight years later, despite continued remission and treatment with angiotensin receptor blockade and an SGLT2 inhibitor, she developed recurrent proteinuria (2.3 g/g). A repeat renal biopsy again demonstrated Congo red–positive amyloid deposits consistent with AL amyloidosis, but with 44% global scerosis and 40% interstitial fibrosis.
This case underscores a major area of uncertainty in the post-treatment course of AL amyloidosis: how to distinguish between residual, biologically inert amyloid and true recurrent deposition. The presence of amyloid on biopsy years after complete hematologic remission raises several unanswered questions. Are the observed deposits remnants of the original fibrils, incompletely cleared but histologically stable? Currently, proteinuria remains the principal marker of renal response and relapse, yet it may reflect hemodynamic or structural factors unrelated to active fibril deposition (e.g., glomeruloscrosis). There are no validated pathological tools or stains to differentiate old versus newly formed amyloid within the kidney. This diagnostic ambiguity highlights the need for imaging biomarkers capable of quantifying active amyloid turnover and for histologic methods that can distinguish legacy deposits from new synthesis. Understanding these dynamics is critical to defining true organ relapse, optimizing surveillance, and guiding the use of emerging amyloid-clearing therapies.
