LAUSR

Accumulation of amyloid fibrils from β2‐microglobulin (β2M) was first recognized as a characteristic osteoarticular complication in long‐term hemodialysis (HD) patients and called “HD‐related amyloidosis” (HRA). However, this syndrome can also be observed in end‐stage renal diseases (ESRD) patients undergoing peritoneal dialysis, and even in patients with chronic renal failure before the initiation of dialytic therapy, suggesting that HD is not a direct cause but that accumulation of β2M or some β2M‐associated molecules in the body is a common pathogenesis. Currently the term “dialysis‐related amyloidosis” (DRA) is widely used for β2M‐amyloid (Aβ2M) amyloidosis associated with ESRD, although DRA patients consist mostly of those undergoing long‐term HD. Factors other than β2M accumulation also play a role in the formation/local deposition of Aβ2M and disruption of tissue architecture. Conformational changes of β2M by misfolding/unfolding, and promoting/inhibitory effects induced by other coexisting molecules, advanced glycation and oxidation, and direct cell toxicity have also been documented. Two technological improvements of HD have been the keys to prevent the development and progression of DRA: the efficient removal of β2M by using high‐flux membranes, high‐volume convection and adsorptive column/membrane, as well as the use of biocompatible membranes and dialysates (eg, ultrapure and acetate‐free dialysates) have minimized both inflammation and β2M production. Epidemiologically, a decrease in the incidence of DRA has recently been reported; however, longer survival of HD patients may contribute to the development of more DRA, though with a delayed onset. In this article, we describe the pathogenesis of DRA, the strategies developed for its prevention and minimization, and the favorable epidemiological data achieved by these efforts.