摘要: Summary: β2-microglobulin amyloidosis is a new type of mainly observed in dialysis patients, whose frequency increases with the elapsed time treatment. Its high incidence and its disabling characteristics bring it to front among complications chronic renal failure patients. pathophysiology not known. However, great progress has been achieved recent work identifying variety substances that are contained amyloid deposits which have known metabolic activities likely participate fibril formation. Among them, three deserve special mention: (i) advanced glycation end products (particularly AGEP-β2-microglobulin), result from non-enzymatic proteins, be altered failure; (ii) reactive oxygen species (ROS) released by cells related (macrophages endothelial cells) may tissue damage precipitation; (iii) α2-macroglobulin, P component other anti-proteases modify processing fibrils also interact macrophages enhance Unfortunately, there no treatment curing or preventing we can presently offer use flux membranes seems delay appearance agreement transplantation clearly stops progression this amyloidosis.
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