S5869 Incidental Discovery of Amyloidosis in Donor Livers: A Case Series and Implications for Liver Transplant Outcomes

Introduction: Amyloidosis is a rare condition, with an estimated prevalence of 7 cases per million persons per year, characterized by extracellular deposition of misfolded protein fibrils that can affect multiple organs, including the liver. While hepatic involvement can lead to hepatomegaly, cholestasis, and liver dysfunction, incidental amyloid deposition in donor livers used for orthotopic liver transplantation (OLT) is exceedingly rare, and its clinical significance remains uncertain. We present 2 cases of donor liver amyloidosis identified during OLT, including one confirmed as AA-type amyloid by mass spectrometry, and discuss implications for graft outcomes. Case Description/Methods: Case 1: A 64-year-old woman with metabolic dysfunction-associated steatohepatitis (MASH) and hepatitis B cirrhosis complicated by hepatic encephalopathy, ascites, and hepatic hydrothorax underwent OLT. Postop course was complicated by hepatic artery thrombosis, requiring retransplantation 1 week later. Biopsy of the second donor liver revealed globular, periportal, and perivascular amyloid deposition, confirmed by Congo red staining. Mild portal fibrosis was present without significant inflammation or steatosis. Follow-up biopsy 1 month later showed persistent amyloid deposition without acute rejection. Case 2: A 51-year-old man with alcohol-associated liver disease cirrhosis complicated by ascites and HE underwent OLT. Donor liver biopsy demonstrated sinusoidal amyloid deposition with hepatocyte atrophy. Congo red stain confirmed amyloid, and liquid chromatography tandem mass spectrometry identified AA (serum amyloid A)-type amyloid. Follow-up biopsy 3 months post-transplant showed persistent sinusoidal amyloid without evidence of acute cellular rejection or significant fibrosis. Discussion: These cases highlight the rare incidental finding of amyloidosis in donor livers. Amyloid types include AL (light chain), AA (serum amyloid A), and ATTR (transthyretin), among others, with diagnosis confirmed by Congo red staining and mass spectrometry for subtype identification. Notably, in Case 2, AA-type amyloid suggests unrecognized systemic inflammation in the donor. Neither recipient exhibited early graft dysfunction despite persistent amyloid on follow-up. While natural history studies suggest hepatic amyloidosis can progress to portal hypertension and liver dysfunction over time, such progression was not observed here. Currently, no specific guidelines exist for managing donor grafts with incidental amyloidosis; recognizing this rare finding may warrant closer post-transplant surveillance.