Effect of hemodialysis membranes on beta 2-microglobulin amyloidosis

Early after the identification of beta(2)-microglobulin amyloidosis (A beta(2)M) as the cause of carpal tunnel syndrome, it was thought that hemodialysis was a major cause in the development of the disease. It was subsequently shown that hemodialysis was not necessary for the development of dialysis-related amyloidosis; however, it was believed that the different dialysis membranes did modulate the progression of the disease. Current data demonstrate that hemodialysis fails to prevent or reverse the disease, but there is substantial evidence that high-flux, high-efficiency dialyzers slow its progression. Many factors related to hemodialysis have been evaluated in relation to A beta(2)M, including the effect of the bioincompatibility of the membrane, the capacity of the different membranes to remove beta(2)M, and the effect of reuse on beta(2)M levels. Moreover, there have been intensive efforts to evaluate, explore, and improve the different mechanisms in beta(2)M removal, with adsorption as a promising prospect. With the available evidence, it seems that the removal of beta(2)M by the membrane plays the most important role in modulating the disease outcome and rate of progression, although a large, long-term, multicentered and randomized study is still lacking to prove this relationship. However, it is possible that with the continuing advances in optimizing the beta(2)M removal efficiency of the different membranes, the frequency and severity of the disease can be substantially decreased.