Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · ·Added 12 Nov 2026

Effect of albumin in patients receiving hemodialysis on β2-microglobulin amyloid fibril formation.

Shoko Yamazaki, Keiichi Yamaguchi, Hirokazu Matsuda, Yuji Goto, Kichitaro Nakajima, Hirotsugu Ogi, Hirofumi Watanabe, Ryohei Kaseda, Isei Ei, Yutaka Kitazato, Hiroshi Watanabe, Toru Maruyama, Yoshitomi Kanemitsu, Sawako Goto, Ryota Kujirai, Yotaro Matsumoto, Yoshihisa Tomioka, Takaaki Abe, Suguru Yamamoto

DOI ↗

Abstract

BACKGROUND: Dialysis-related amyloidosis (DRA) involves β2-microglobulin (β2M) amyloid (Aβ2M) deposition. While albumin suppresses amyloidogenesis in vitro, the impact of its quality (oxidation/uremic toxin binding) in patients receiving hemodialysis (HD) remains unclear. We investigated how albumin quantity/quality in patients receiving HD affects Aβ2M fibrillogenesis. METHODS: Serum from patients receiving HD (n = 30) and healthy individuals (n = 30) was incubated with β2M monomers. Fibrillogenesis was monitored via Thioflavin T (ThT) fluorescence. Oxidized albumin and uremic toxins were quantified using liquid chromatography-mass spectrometry. RESULTS: Serum suppressed Aβ2M amyloid fibril formation in a concentration-dependent manner. Compared to healthy serum, HD serum showed significantly higher maximum ThT fluorescence (23.3 ± 5.2 vs. 16.2 ± 8.4 a.u., p < 0.001) and shorter half times (37.2 ± 10.3 vs. 51.6 ± 13.7 h, p < 0.001). Serum albumin levels were correlated with ThTmax (r = -0.53, p < 0.001) and half time (r = 0.59, p < 0.001). In multiple regression analyses, albumin concentration was independently associated with both parameters, whereas oxidized albumin and uremic toxins were not significantly associated. CONCLUSIONS: HD serum showed a reduced suppressive effect on Aβ2M amyloid fibril formation. Albumin quantity, rather than quality, primarily determines Aβ2M amyloidogenesis.

Abstract as supplied by the indexing source. © the authors / publisher.