Dialysis-associated amyloidosis

Dialysis-related arthropathy represents a major complication of uremic patients treated by hemodialysis or other renal replacement therapies. Nearly 10 years ago, this syndrome was shown to be associated with a new type of amyloid, mainly composed of beta-2 microglobulin (beta 2-M). Retention of the beta 2-M protein due to chronic renal failure, although unquestionably a prerequisite for the occurrence of beta 2-M amyloidosis, appears not to be the unique pathogenetic factor involved in this complication. A role has also been attributed to an enhanced local or systemic generation of inflammatory mediators, an increased production of beta 2-M, and an altered metabolism of the molecule including partial proteolysis and glycation. It is possible that factors related to renal replacement therapy such as dialysis membrane biocompatibility also play a role. However, the clarification of the precise underlying mechanism(s) awaits further study. Because dialysis technology has progressed considerably during the last decade, a significant beta 2-M removal can be achieved at present using high-flux dialyzers. Moreover, a marked reduction in bioincompatibility during the dialysis procedure as manifested by activation of complement and stimulation of mononuclear blood cells can now be attained. Future studies will tell whether technical progress in dialysis technique results in a decrease in the incidence of symptomatic dialysis-associated amyloidosis.