Abstract

Dialysis-related amyloidosis is a serious complication in patients on long-term dialysis. Amyloid fibrils, that major component is beta(2)-microglobulin (beta(2)-m) , deposit mainly in osteoarticular joint tissues and cause various complications such as carpal tunnel syndrome, destructive spondyloarthropathy, bone cysts, and various organ dysfunction. The retention of beta(2)-m in chronic kidney disease (CKD) induces the amyloid fibril formation according to a nucleation-dependent polymerization model. Specific molecules such as glycosaminoglycans and proteoglycans that affect the conformation and stability of beta(2)-m and amyloid fibrils are considered to have significant effects on the formation and deposition of amyloid fibrils.

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