DIALYSIS-RELATED AMYLOIDOSIS - PATHOGENETIC ASPECTS AND THERAPEUTIC CONSIDERATIONS

Beyond renal transplantation and the provision of symptomatic relief, approaches to treat dialysis-related amyloidosis (DRA), an important l ong-term complication in patients on regular dialysis, must be based o n the knowledge of the underlying pathogenetic process. Retention of b eta(2)-microglobulin (beta(2)m) is the prerequisite; biochemical alter ations of beta(2)m increasing its amyloidogenicity, and local predispo sing tissue factors together with age appear to be relevant. A growing body of evidence points toward the importance of pro-inflammatory eff ects of dialysis (blood-membrane interactions, pyrogen-related priming of cytokine-producing mononuclear cells) in the development of DRA. A dvanced glycation endproduct formation (AGE-beta(2)m) may represent a central element in the pathogenesis of DRA. For non-transplant therapy of DRA, the main goals must be the optimization of beta(2)m removal ( high-flux haemodialysis, haemofiltration, especially pre-dilution haem ofiltration) and reduction of pro-inflammatory effects of dialysis (us e of noncomplement activating biocompatible membranes, pyrogen free di alysate). At least patients at high risk for DRA should be treated acc ording to these guidelines.