Dialysis‐related amyloidosis: Pathogenetic aspects and therapeutic considerations

Summary: Beyond renal transplantation and the provision of symptomatic relief, approaches to treat dialysis‐related amyloidosis (DRA), an important long‐term complication in patients on regular dialysis, must be based on the knowledge of the underlying pathogenetic process. Retention of beta 2 ‐microglobulin (β 2 m) is the prerequisite; biochemical alterations of β 32 m increasing its amyloidogenicity, and local predisposing tissue factors together with age appear to be relevant. A growing body of evidence points toward the importance of pro‐inflammatory effects of dialysis (blood‐membrane interactions, pyrogen‐related priming of cytokine producing mononuclear cells) in the development of DRA. Advanced glycation endproduct formation (AGE‐β 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 β 2 m removal (high‐flux haemodialysis, haemofiltration, especially pre‐dilution haemofiltration) and reduction of pro‐inflammatory effects of dialysis (use of non‐complement activating biocompatible membranes, pyrogen free dialysate). At least patients at high risk for DRA should be treated according to these guidelines.