Abstract

Background

Patients with end-stage renal disease (ESRD) exhibit a premature aging phenotype of the immune system. Nevertheless, the etiology and impact of these changes in ESRD patients remain unknown.

Results

Compared to healthy individuals, ESRD patients exhibit accelerated immunosenescence in both T cell and monocyte compartments, characterized by a dramatic reduction in naïve CD4+ and CD8+ T cell numbers but increase in CD8+ TEMRA cell and proinflammatory monocyte numbers. Notably, within ESRD patients, aging-related immune changes positively correlated not only with increasing age but also with longer dialysis vintage. In multivariable-adjusted logistic regression models, the combination of high terminally differentiated CD8+ T cell level and high intermediate monocyte level, as a composite predictive immunophenotype, was independently associated with prevalent coronary artery disease as well as cardiovascular disease, after adjustment for age, sex, systemic inflammation and presence of diabetes. Levels of terminally differentiated CD8+ T cells also positively correlated with the level of uremic toxin p-cresyl sulfate.

Conclusions

Aging-associated adaptive and innate immune changes are aggravated in ESRD and are associated with cardiovascular diseases. For the first time, our study demonstrates the potential link between immunosenescence in ESRD and duration of exposure to the uremic milieu.

Details

Title
A comprehensive characterization of aggravated aging-related changes in T lymphocytes and monocytes in end-stage renal disease: the iESRD study
Author
Yen-Ling, Chiu; Kai-Hsiang Shu; Feng-Jung, Yang; Chou, Tzu-Ying; Ping-Min, Chen; Fang-Yun, Lay; Szu-Yu Pan; Cheng-Jui, Lin; Litjens, Nicolle H R; Betjes, Michiel G H; Bermudez, Selma; Kung-Chi Kao; Jean-San Chia; Wang, George; Yu-Sen, Peng; Yi-Fang, Chuang
Publication year
2018
Publication date
2018
Publisher
BioMed Central
e-ISSN
1742-4933
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2135005265
Copyright
Copyright © 2018. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.