What is the role of the dialysis membrane in the etiology of beta-2-microglobulin (beta-2m) amyloidosis?

Updated: Nov 14, 2019
  • Author: Anita Basu, MD, FACP; Chief Editor: Vecihi Batuman, MD, FASN  more...
  • Print

The healthy kidney can eliminate endogenous end products of metabolism, as well as exogenous toxins that are both large- and small-molecular-weight substances. Cuprophan and cellulose acetate membranes previously used in conventional HD have small pores and cannot clear substances with molecular weights higher than 200 daltons. This makes them impermeable to beta-2m, elevating the protein’s serum levels. The newer cellulose triacetate dialyzers and the high-flux synthetic dialyzers remove molecules with a higher molecular weight and do a better job of removing beta-2m.

High cut-off, high-flux dialysis and online hemodiafiltration have been shown to be superior to previously used HD membranes in the removal of beta-2m, possibly decreasing beta-2 amyloidosis.

Beta-2m amyloidosis has also been described in patients receiving long-term CAPD, despite the permeability characteristics of the peritoneal membrane. Clearance of middle molecules is better, however, making CAPD a more biocompatible mode of treatment.

Nonetheless, data are conflicting. Some report the prevalence of beta-2m amyloidosis in patients on long-term CAPD as comparable to the prevalence in patients on HD. Other data show that plasma levels of beta-2m are lower in patients on CAPD, suggesting that amyloid may accumulate more slowly. Some of this may also be related to residual renal function. Results of long-term studies are needed.

Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!