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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.
AA amyloidosis is a systemic disorder resulting from chronic inflammatory states, where misfolded serum amyloid A protein deposits in vital organs including the kidneys and heart. Lepromatous leprosy, an infrequent but persistent infection in endemic regions, provides a unique cause of secondary amyloidosis with multisystem repercussions. Although kidney transplantation is recognized as the optimal therapy for end-stage renal disease, recipients with significant extra-renal amyloid involvement, especially cardiac dysfunction, have historically faced guarded prognoses and limited eligibility. This case exemplifies the successful reversal of severe renal and cardiac dysfunction after living donor renal transplantation in AA amyloidosis secondary to lepromatous leprosy, challenging existing paradigms and suggesting new treatment possibilities for multi-organ amyloidosis.
We present a 38-year-old male with end-stage renal disease (ESRD) due to biopsy-proven AA amyloidosis secondary to treated lepromatous leprosy. Pre-transplant clinical profile: serum creatinine 6.34 mg/dL, UPCR 7.46 mg/dL, hemoglobin 6.6 g/dL (pancytopenia), elevated ESR 58 mm/hr. Comprehensive pre-transplant cardiac evaluation included cardiac MRI demonstrating restrictive cardiomyopathy with reduced systolic function (LVEF 45%), impaired GLS (−8.8%), pericardial effusion, and elevated cardiac biomarkers (hs-Troponin T 0.214 ng/mL). Following confirmed control of the underlying infection with normalized Serum Amyloid A (SAA) levels, the patient underwent living donor renal transplantation. Serial post-transplant assessments at 4 months documented functional recovery in both renal and cardiac parameters using serum creatinine, echocardiography, and cardiac biomarkers.
Four months after transplantation, the patient demonstrated dramatic dual-organ improvement. Renal function recovered substantially: serum creatinine declined to 1.52 mg/dL and proteinuria resolved (UPCR <0.5). Hemoglobin rose to normal levels, indicating resolution of the pre-transplant pancytopenia. Cardiac function also markedly improved: LVEF increased to 65%, GLS improved to –15.4%, and hs-troponin T normalized (<0.05 ng/mL). Follow-up echocardiography showed complete resolution of the pericardial effusion and normalization of cardiac chamber dimensions. These findings reflect significant reversal of amyloid-related organ dysfunction after transplant.
This case illustrates that systemic AA amyloidosis with cardiac involvement need not preclude kidney transplantation if the underlying inflammatory disease is effectively controlled. Remarkable reversibility of both renal and cardiac dysfunction was achieved post-transplant, challenging the notion that amyloid-induced organ damage is irreversible. Careful patient selection, thorough pre-transplant preparation (including SAA normalization), and vigilant post-transplant management were crucial to success. To our knowledge, this represents the first such dual renal–cardiac recovery after transplantation, highlighting the potential to expand transplant eligibility for patients with multi-organ AA amyloidosis previously deemed poor candidates.
