Abstract
Abeta-2M-amyloidosis is a type of systemic amyloidosis that is specifically seen in patients with chronic kidney diseases. The precursor protein of Abeta-2M-amyloid fibril is beta2-microglobulin, and its elevated serum level is the main cause of Abeta-2M-amyloidosis in patients with kidney failure. However, the precise mechanism of Abeta-2M-amyloidogenesis remains unclear. In vitro analyses of Abeta-2M amyloidogenesis are still being actively conducted. Osteolytic lesions are often found around synovial membrane with Abeta-2M-amyloid deposition. Both evident osteoclastogenesis and active osteoclastic bone resorption are found, while osteoblastic bone formation is absent in the lesion most likely associated with the inflammation caused by infiltrating macrophages/monocytes into Abeta-2M-amyloid deposition. The precise cell biological mechanism of this inflammatory change is unknown. Further studies are needed to establish specific treatments against this as yet unsolved problem with long-term dialysis therapy.
Published Version
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