The pathogenesis of beta(2)-microglobulin-induced bone lesions in dialysis-related amyloidosis.

Dialysis-related amyloidosis (DRA), also referred to as beta(2)-microglobulin amyloidosis (A beta(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, beta(2)M, less is known about the pathologic role of beta(2)M as a mediator of bone and joint disease. Potential mechanisms for beta(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 beta(2)M deposition and amyloid formation. More work is required to elucidate the relationship between beta(2)M accumulation and progressive tissue destruction.