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The Pathogenesis of β 2 ‐Microglobulin–Induced Bone Lesions in Dialysis‐Related Amyloidosis
Author(s) -
Tran Martin,
Rutecki Gregory W.,
Sprague Stuart M.
Publication year - 2001
Publication title -
seminars in dialysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 78
eISSN - 1525-139X
pISSN - 0894-0959
DOI - 10.1046/j.1525-139x.2001.00033.x
Subject(s) - medicine , amyloidosis , beta 2 microglobulin , pathogenesis , amyloid (mycology) , dialysis , glycation , aa amyloidosis , mediator , bone resorption , pathology , resorption , disease , endocrinology , diabetes mellitus , familial mediterranean fever
Dialysis‐related amyloidosis (DRA), also referred to as β 2 ‐microglobulin amyloidosis (Aβ 2 M), is an important cause of morbidity in patients with chronic renal failure and in those who are on dialysis. Although DRA deposits from affected joints have been characterized as a unique amyloid fibril protein, β 2 M, less is known about the pathologic role of β 2 M as a mediator of bone and joint disease. Potential mechanisms for β 2 M pathologic interaction in bone include bone growth factors, cytokines, and advanced glycation end products (AGEs). It appears that DRA is the result of a complex interaction between bone resorption and surrounding tissue destruction culminating in β 2 M deposition and amyloid formation. More work is required to elucidate the relationship between β 2 M accumulation and progressive tissue destruction.