Association between chronic kidney disease and carotid intima-media thickness in relation to circulating CD34-positive cell count among community-dwelling elderly Japanese men.


Journal

Atherosclerosis
ISSN: 1879-1484
Titre abrégé: Atherosclerosis
Pays: Ireland
ID NLM: 0242543

Informations de publication

Date de publication:
04 2019
Historique:
received: 30 10 2018
revised: 30 01 2019
accepted: 01 02 2019
pubmed: 1 3 2019
medline: 19 5 2020
entrez: 1 3 2019
Statut: ppublish

Résumé

Endothelial injury is well-known as a process that can lead to chronic kidney disease (CKD) and atherosclerosis. Hematopoietic activity is known to be associated inversely with CKD and positively with atherosclerosis. Since bone-derived progenitor cells (CD34-positive cells) contribute to endothelial repair (including the progression of atherosclerosis), understanding the association between CKD and carotid intima-media thickness (CIMT), in relation to circulating CD34-positive cell count, may be an efficient means of clarifying the mechanisms underlying endothelial activity. We conducted a cross-sectional study of 570 elderly Japanese men aged 60-69 years, who underwent a general health check-up. Participants were stratified as per a median circulating CD34-positive cell count (1.01 cells/μL). Independent of the known cardiovascular risk factors, CIMT was found to be positively associated with CKD in the participants with high circulating CD34-positive cell counts but not in participants with low counts. Odds ratios were 1.40 (1.04, 1.89) for participants with high and 1.01 (0.72, 1.43) for participants with low circulating CD34-positive cell counts after adjustment for known cardiovascular risk factors at 95% confidence intervals for CKD with one standard deviation increment of CIMT. A positive association between CIMT and CKD was observed among participants with high circulating CD34-positive cell counts but not among participants with low counts. Endothelial repair activity might determine the association between CKD and CIMT.

Sections du résumé

BACKGROUND AND AIMS
Endothelial injury is well-known as a process that can lead to chronic kidney disease (CKD) and atherosclerosis. Hematopoietic activity is known to be associated inversely with CKD and positively with atherosclerosis. Since bone-derived progenitor cells (CD34-positive cells) contribute to endothelial repair (including the progression of atherosclerosis), understanding the association between CKD and carotid intima-media thickness (CIMT), in relation to circulating CD34-positive cell count, may be an efficient means of clarifying the mechanisms underlying endothelial activity.
METHODS
We conducted a cross-sectional study of 570 elderly Japanese men aged 60-69 years, who underwent a general health check-up. Participants were stratified as per a median circulating CD34-positive cell count (1.01 cells/μL).
RESULTS
Independent of the known cardiovascular risk factors, CIMT was found to be positively associated with CKD in the participants with high circulating CD34-positive cell counts but not in participants with low counts. Odds ratios were 1.40 (1.04, 1.89) for participants with high and 1.01 (0.72, 1.43) for participants with low circulating CD34-positive cell counts after adjustment for known cardiovascular risk factors at 95% confidence intervals for CKD with one standard deviation increment of CIMT.
CONCLUSIONS
A positive association between CIMT and CKD was observed among participants with high circulating CD34-positive cell counts but not among participants with low counts. Endothelial repair activity might determine the association between CKD and CIMT.

Identifiants

pubmed: 30818167
pii: S0021-9150(19)30082-6
doi: 10.1016/j.atherosclerosis.2019.02.004
pii:
doi:

Substances chimiques

Antigens, CD34 0
Biomarkers 0

Types de publication

Journal Article Multicenter Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

85-91

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Yuji Shimizu (Y)

Department of Community Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan; Department of Cardiovascular Disease Prevention, Osaka Center for Cancer and Cardiovascular Disease Prevention, Osaka, Japan. Electronic address: shimizu@osaka-ganjun.jp.

Hirotomo Yamanashi (H)

Department of General Medicine, Nagasaki University Hospital, Nagasaki, Japan.

Yuko Noguchi (Y)

Department of Community Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Jun Koyamatsu (J)

Department of Island and Community Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Mako Nagayoshi (M)

Department of Community Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Kairi Kiyoura (K)

Department of Community Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Shoichi Fukui (S)

Department of Community Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Mami Tamai (M)

Department of Immunology and Rheumatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Shin-Ya Kawashiri (SY)

Department of Community Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Hideaki Kondo (H)

Department of General Medicine, Nagasaki University Hospital, Nagasaki, Japan.

Takahiro Maeda (T)

Department of Community Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan; Department of General Medicine, Nagasaki University Hospital, Nagasaki, Japan; Department of Island and Community Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

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