Proteomics investigation of the changes in serum proteins after high- and low-flux hemodialysis

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Abstract

Purpose: This study aimed to use proteomics methods to investigate the changes in serum protein levels after high- and low-flux hemodialysis (HD).

Methods: Before and after HD, serum samples were obtained from two selected patients who were treated with a Polyflux 140 H high-flux dialyzer and a Polyflux 14 L low-flux dialyzer during two continuous therapy sessions. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was performed to identify the proteins.

Results: A total of 212 and 203 serum proteins were identified after high-flux and low-flux HD, respectively. After high-flux HD, 21 proteins increased, and 132 proteins decreased. After low-flux HD, 87 proteins increased, and 45 proteins decreased. High-flux HD led to a significantly greater reduction in protein levels than low-flux HD (0.73 ± 0.13 vs. 0.84 ± 0.18, p = .00). Among the increased and decreased proteins, the isoelectric point (pI) values mainly ranged from 5 to 7, and the molecular weights (Mws) were mostly smaller than 30 kDa. The serum proteins showed no difference in pI or Mw for high- and low-flux HD. Gene ontology (GO) analysis showed that the detected proteins were related to immune system processes and complement activation.

Conclusions: Serum protein levels differentially changed after high- and low-flux HD. Long-term effects should be observed in future studies.

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Most cited references 35

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Accelerated atherosclerosis in prolonged maintenance hemodialysis.

A Lindner, B Charra, D J Sherrard … (1974)

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Dyslipidemia of chronic renal failure: the nature, mechanisms, and potential consequences.

N. Vaziri (2006)

Chronic renal failure (CRF) results in profound lipid disorders, which stem largely from dysregulation of high-density lipoprotein (HDL) and triglyceride-rich lipoprotein metabolism. Specifically, maturation of HDL is impaired and its composition is altered in CRF. In addition, clearance of triglyceride-rich lipoproteins and their atherogenic remnants is impaired, their composition is altered, and their plasma concentrations are elevated in CRF. Impaired maturation of HDL in CRF is primarily due to downregulation of lecithin-cholesterol acyltransferase (LCAT) and, to a lesser extent, increased plasma cholesteryl ester transfer protein (CETP). Triglyceride enrichment of HDL in CRF is primarily due to hepatic lipase deficiency and elevated CETP activity. The CRF-induced hypertriglyceridemia, abnormal composition, and impaired clearance of triglyceride-rich lipoproteins and their remnants are primarily due to downregulation of lipoprotein lipase, hepatic lipase, and the very-low-density lipoprotein receptor, as well as, upregulation of hepatic acyl-CoA cholesterol acyltransferase (ACAT). In addition, impaired HDL metabolism contributes to the disturbances of triglyceride-rich lipoprotein metabolism. These abnormalities are compounded by downregulation of apolipoproteins apoA-I, apoA-II, and apoC-II in CRF. Together, these abnormalities may contribute to the risk of arteriosclerotic cardiovascular disease and may adversely affect progression of renal disease and energy metabolism in CRF.

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Apolipoprotein M is required for prebeta-HDL formation and cholesterol efflux to HDL and protects against atherosclerosis.

Christian Wolfrum, Matthew Poy, Markus Stoffel (2005)

High-density lipoproteins (HDLs) are considered antiatherogenic because they mediate reverse cholesterol transport from the periphery to the liver for excretion and degradation. Here we show that mice deficient in apolipoprotein M (apoM), a component of the HDL particle, accumulated cholesterol in large HDL particles (HDL(1)) while the conversion of HDL to prebeta-HDL was impaired. Accordingly, apoM-deficient mice lacked prebeta-HDL, a subclass of lipid-poor apolipoproteins that serves as a key acceptor of peripheral cellular cholesterol. This deficiency led to a markedly reduced cholesterol efflux from macrophages to apoM-deficient HDL compared to normal HDL in vitro. Overexpression of apoM in Ldlr(-/-) mice protected against atherosclerosis when the mice were challenged with a cholesterol-enriched diet, showing that apoM is important for the formation of prebeta-HDL and cholesterol efflux to HDL, and thereby inhibits formation of atherosclerotic lesions.

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Author and article information

Journal

Journal ID (nlm-ta): Ren Fail

Journal ID (iso-abbrev): Ren Fail

Journal ID (publisher-id): IRNF

Journal ID (publisher-id): irnf20

Title: Renal Failure

Publisher: Taylor & Francis

ISSN (Print): 0886-022X

ISSN (Electronic): 1525-6049

Publication date Collection: 2018

Publication date (Electronic): 04 October 2018

Volume: 40

Issue: 1

Pages: 506-513

Affiliations

[a ]Affiliated Zhongshan Hospital of Dalian University , Dalian, China;

[b ]Key Laboratory of Separation Science for Analytical Chemistry, Dalian Institute of Chemical Physics, Chinese Academy of Science, National Chromatographic Research and Analysis Center , Dalian, China;

[c ]Department of Nephritic Medicine, Second Affiliated Hospital of Dalian Medical University , Dalian, China

Author notes

[*]

These authors contributed equally to this study.

Supplemental data for this article can be accessed here .

CONTACT Jiuyang Zhao zhaojiuy9@ 123456163.com Department of Nephritic Medicine, Second Affiliated Hospital of Dalian Medical University , Dalian116023, China; Lihua Zhang lihuazhang@ 123456dicp.ac.cn Key Laboratory of Separation Science for Analytical Chemistry, Dalian Institute of Chemical Physics, Chinese Academy of Science, National Chromatographic Research and Analysis Center , 457 Zhongshan Road, Dalian116023, China

Article

Publisher ID: 1491406

DOI: 10.1080/0886022X.2018.1491406

PMC ID: 6179064

PubMed ID: 30284957

SO-VID: 33280503-fb11-498e-8df6-d97410c128d1

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 03 May 2018

Date revision received : 10 June 2018

Date accepted : 14 June 2018

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Pages: 8, Words: 4639

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Proteomics investigation of the changes in serum proteins after high- and low-flux hemodialysis

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Karger: Nephrology

Most cited references 35

Accelerated atherosclerosis in prolonged maintenance hemodialysis.

Dyslipidemia of chronic renal failure: the nature, mechanisms, and potential consequences.

Apolipoprotein M is required for prebeta-HDL formation and cholesterol efflux to HDL and protects against atherosclerosis.

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