Dialysis-associated amyloidosis.

摘要: 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 new type amyloid, mainly composed β-2 microglobulin (β2-M). Retention the β2-M protein due chronic failure, although unquestionably prerequisite for occurrence amyloidosis, appears not unique pathogenetic factor involved in complication. A role has also been attributed an enhanced local systemic generation inflammatory mediators, increased production β2-M, and altered metabolism molecule including partial proteolysis glycation. It is possible that factors related therapy such as dialysis membrane biocompatibility play role. However, clarification precise underlying mechanism(s) awaits further study. Because technology progressed considerably during last decade, significant β-M removal can achieved at present using high-flux dialyzers. Moreover, marked reduction bioincompatibility procedure manifested activation complement stimulation mononuclear blood cells now attained. Future studies will tell whether technical progress techniques results decrease incidence symptomatic dialysis-associated amyloidosis.