Dialysis Membranes Inhibit Synthesis and Release of β&lt;sub&gt;2&lt;/sub&gt;-Microglobulin in Lymphocyte Culture

Jm, Campistol; Molina, Rafael; Rodriguez, R.; Mirapeix, E; J, Muñoz-Gomez; Revert, L

doi:10.1159/000186681

Cited by 7 publications

(3 citation statements)

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“…Carpal tunnel syndrome and destructive arthropathy associated with cystic bone lesions are the major clinical manifestations of Aβ2M amyloidosis ( , ). Several biochemical and cell biological studies have revealed that intact β2-microglobulin (β2-m) ( M r = 11 731) is a major structural component of amyloid fibrils deposited in the synovia of the carpal tunnel ( − ). The mechanism of the deposition of these Aβ2M amyloid fibrils is still unknown.…”

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confidence: 99%

Apolipoprotein E Inhibits the Depolymerization of β2-Microglobulin-Related Amyloid Fibrils at a Neutral pH

et al. 2001

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beta 2-Microglobulin-related (A beta 2M) amyloidosis is a common and serious complication in patients on long-term hemodialysis, and beta 2-microglobulin (beta 2-m) is a major structural component of A beta 2M amyloid fibrils. Fluorescence spectroscopic analysis with thioflavin T and electron microscopic study revealed that A beta 2M amyloid fibrils readily depolymerize into monomeric beta 2-m at a neutral to basic pH. Circular dichroism analysis revealed that soon after the initiation of the depolymerization reaction at pH 7.5, the characteristic spectrum of beta 2-m in A beta 2M amyloid fibrils changes to resemble that of monomeric beta 2-m at pH 7.5. Apolipoprotein E (apoE), a representative amyloid-associated protein, formed a stable complex with A beta 2M amyloid fibrils and inhibited the depolymerization of A beta 2M amyloid fibrils dose-dependently in a range of 0--10 microM. These results showed that apoE could enhance the deposition of amyloid fibrils in vivo, possibly by binding directly to the surface of the fibrils and stabilizing the conformation of beta 2-m in the fibrils.

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confidence: 99%

Apolipoprotein E Inhibits the Depolymerization of β2-Microglobulin-Related Amyloid Fibrils at a Neutral pH

et al. 2001

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“…It is recognized that incubation of cuprophane or polyacrylonitrile membranes with peripheral blood monocytes in vitro will lead to an inhibition of ß 2 M synthesis by these cells. This would suggest that the ß 2 M synthesis is likely not activated by direct blood-dialysis membrane interaction [22]. However, other in vitro studies have shown an increased release of ß 2 M by direct contact of mononuclear cells with cellulosic membranes which was accentuated in the presence of products of complement activation [23,24].…”

Section: Serum ß 2 -Microglobulin and Dialysis Membranementioning

confidence: 97%

Serum β<sub>2</sub>-Microglobulin Levels in Patients Chronically Dialyzed with CA-210 versus CT-190 Dialysis Membranes

et al. 1998

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β₂-Microglobulin (B₂M) amyloidosis (dialysis-related amyloidosis), manifested primarily by carpal tunnel syndrome and destructive osteoarthropathy, is a major sequel of long-term dialysis. Previous investigators have shown that high-flux biocompatible synthetic membranes (e.g., polyacrylonitrile) lower β₂M levels when compared to cellulosic membranes (e.g., cuprophane). To date, however, no study has compared β₂M levels of patients dialyzed with the two more biocompatible cellulosic membranes CA-210 (cellulose acetate) and CT-190 (cellulose triacetate; high flux, more biocompatible). We retrospectively compared the serum β₂M levels in two chronic hemodialysis populations: 22 patients on CT-190 and 21 patients on CA-210. There was no difference between the two groups with regard to age, sex, or duration of dialysis. The patients on the CA-210 membrane had significantly higher serum β₂M levels (mean ± SE; 53.6 ± 4.7 vs. 36.8 ± 2.6 mg/l, CA-210 vs. CT-190, respectively, p = 0.003). Subsequently we switched 13 patients dialyzed with a CA-210 membrane to a CT-190 membrane and followed serum β₂M levels for 14 months. We found a significant decrease in serum β₂M levels within 1 month which was maintained over 14 months of follow-up (47.4 ± 4.4 vs. 62.8 ± 6.7 mg/l, CT-190 at 14 months vs. CA-210 at baseline, respectively, p < 0.01).

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“…Subsequent studies evaluated the possibility that mononuclear cells from patients chronically dialyzed with cuprophane membranes (bioincompatible) released more β 2 M than those from patients dialyzed with biocompatible membranes, which was further accentuated in the presence of complement activation products (11–14). However, there was also significant evidence from in vitro studies suggesting that bioincompatible cuprophane membranes had no significant role in the synthesis of β 2 M (15, 16), and that direct exposure of peripheral blood monocytes to bioincompatible and biocompatible membranes actually inhibited β 2 M synthesis (17). Moreover, interleukin (IL)‐1B and IL‐6, which were incriminated in the elevation of β 2 M synthesis in patients undergoing hemodialysis with bioincompatible membranes, were not capable of inducing β 2 M gene expression in monocytes (18).…”

Section: Relationship Between Membrane Biocompatibility and β2mmentioning

confidence: 99%

Effect of Hemodialysis Membranes on β₂‐Microglobulin Amyloidosis

Jaradat

Moe

2001

Seminars in Dialysis

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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.

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Dialysis Membranes Inhibit Synthesis and Release of β<sub>2</sub>-Microglobulin in Lymphocyte Culture

Cited by 7 publications

References 3 publications

Apolipoprotein E Inhibits the Depolymerization of β2-Microglobulin-Related Amyloid Fibrils at a Neutral pH

Apolipoprotein E Inhibits the Depolymerization of β2-Microglobulin-Related Amyloid Fibrils at a Neutral pH

Serum β<sub>2</sub>-Microglobulin Levels in Patients Chronically Dialyzed with CA-210 versus CT-190 Dialysis Membranes

Effect of Hemodialysis Membranes on β₂‐Microglobulin Amyloidosis

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Dialysis Membranes Inhibit Synthesis and Release of β<sub>2</sub>-Microglobulin in Lymphocyte Culture

Cited by 7 publications

References 3 publications

Apolipoprotein E Inhibits the Depolymerization of β2-Microglobulin-Related Amyloid Fibrils at a Neutral pH

Apolipoprotein E Inhibits the Depolymerization of β2-Microglobulin-Related Amyloid Fibrils at a Neutral pH

Serum β<sub>2</sub>-Microglobulin Levels in Patients Chronically Dialyzed with CA-210 versus CT-190 Dialysis Membranes

Effect of Hemodialysis Membranes on β2‐Microglobulin Amyloidosis

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Effect of Hemodialysis Membranes on β₂‐Microglobulin Amyloidosis