Association of aortic valve calcification with carotid artery lesions and peripheral artery disease in patients with chronic kidney disease: a cross-sectional study.


Journal

BMC nephrology
ISSN: 1471-2369
Titre abrégé: BMC Nephrol
Pays: England
ID NLM: 100967793

Informations de publication

Date de publication:
29 05 2020
Historique:
received: 19 12 2019
accepted: 21 05 2020
entrez: 31 5 2020
pubmed: 31 5 2020
medline: 2 9 2021
Statut: epublish

Résumé

Patients with chronic kidney disease (CKD) reportedly have a high prevalence of aortic valve calcification (AVC). In population-based studies, AVC is considered a manifestation of systemic atherosclerosis. The association of AVC with atherosclerotic lesions has not been fully investigated in predialysis patients. The present study was performed to determine whether carotid artery lesions and peripheral artery disease (PAD) are associated with AVC in patients with CKD not on dialysis. In total, 749 patients were included in this cross-sectional study. AVC was evaluated using echocardiography. Carotid artery lesions including carotid artery plaque (CAP) and PAD were simultaneously examined in each patient. A logistic regression analysis was applied to determine the factors associated with AVC. AVC, CAP, and PAD were found in 201, 583, and 123 patients, respectively. In the multivariable analyses adjusted for covariates including the estimated glomerular filtration rate and makers of mineral metabolism (serum calcium, serum phosphorus, parathyroid hormone, 1,25-dihydroxyvitamin D, and fibroblast growth factor 23), AVC was significantly associated with the presence of CAP [odds ratio (OR), 3.37; 95% confidence interval (CI), 1.43-7.95], the presence of PAD (OR, 1.76; 95% CI, 1.10-2.81), the CAP score (per 1.0-point increase) (OR, 1.06; 95% CI, 1.02-1.11), and the ankle-brachial blood pressure index (per 0.1-point increase) (OR, 0.83; 95% CI, 0.72-0.95). AVC was associated with atherosclerotic lesions independent of kidney function and mineral metabolism. We consider that this association between AVC and atherosclerosis might reflect the burden of shared atherosclerotic risk factors.

Sections du résumé

BACKGROUND
Patients with chronic kidney disease (CKD) reportedly have a high prevalence of aortic valve calcification (AVC). In population-based studies, AVC is considered a manifestation of systemic atherosclerosis. The association of AVC with atherosclerotic lesions has not been fully investigated in predialysis patients. The present study was performed to determine whether carotid artery lesions and peripheral artery disease (PAD) are associated with AVC in patients with CKD not on dialysis.
METHODS
In total, 749 patients were included in this cross-sectional study. AVC was evaluated using echocardiography. Carotid artery lesions including carotid artery plaque (CAP) and PAD were simultaneously examined in each patient. A logistic regression analysis was applied to determine the factors associated with AVC.
RESULTS
AVC, CAP, and PAD were found in 201, 583, and 123 patients, respectively. In the multivariable analyses adjusted for covariates including the estimated glomerular filtration rate and makers of mineral metabolism (serum calcium, serum phosphorus, parathyroid hormone, 1,25-dihydroxyvitamin D, and fibroblast growth factor 23), AVC was significantly associated with the presence of CAP [odds ratio (OR), 3.37; 95% confidence interval (CI), 1.43-7.95], the presence of PAD (OR, 1.76; 95% CI, 1.10-2.81), the CAP score (per 1.0-point increase) (OR, 1.06; 95% CI, 1.02-1.11), and the ankle-brachial blood pressure index (per 0.1-point increase) (OR, 0.83; 95% CI, 0.72-0.95).
CONCLUSIONS
AVC was associated with atherosclerotic lesions independent of kidney function and mineral metabolism. We consider that this association between AVC and atherosclerosis might reflect the burden of shared atherosclerotic risk factors.

Identifiants

pubmed: 32471374
doi: 10.1186/s12882-020-01864-z
pii: 10.1186/s12882-020-01864-z
pmc: PMC7260754
doi:

Substances chimiques

Parathyroid Hormone 0
Lansoprazole 0K5C5T2QPG
Vitamin D 1406-16-2
Phosphorus 27YLU75U4W
Fibroblast Growth Factors 62031-54-3
1,25-dihydroxyvitamin D 66772-14-3
Fibroblast Growth Factor-23 7Q7P4S7RRE
Calcium SY7Q814VUP

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

203

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Auteurs

Yui Arita (Y)

Division of Nephrology, Department of Internal Medicine, Yamaguchi Red Cross Hospital, 53-1 Yawatanobaba, Yamaguchi, 753-0092, Japan.
Department of Internal Medicine, National Hospital Organization Kyushu Medical Center, Division of Nephrology and Clinical Research Institute, 1-8-1 Jigyohama, Chuo-ku, Fukuoka, 810-8563, Japan.

Masaru Nakayama (M)

Department of Internal Medicine, National Hospital Organization Kyushu Medical Center, Division of Nephrology and Clinical Research Institute, 1-8-1 Jigyohama, Chuo-ku, Fukuoka, 810-8563, Japan. nakayama51224@gmail.com.

Yuta Matsukuma (Y)

Department of Internal Medicine, National Hospital Organization Kyushu Medical Center, Division of Nephrology and Clinical Research Institute, 1-8-1 Jigyohama, Chuo-ku, Fukuoka, 810-8563, Japan.

Ryota Yoshitomi (R)

Department of Internal Medicine, National Hospital Organization Kyushu Medical Center, Division of Nephrology and Clinical Research Institute, 1-8-1 Jigyohama, Chuo-ku, Fukuoka, 810-8563, Japan.

Makiko Seki (M)

Department of Internal Medicine, National Hospital Organization Kyushu Medical Center, Division of Nephrology and Clinical Research Institute, 1-8-1 Jigyohama, Chuo-ku, Fukuoka, 810-8563, Japan.

Akiko Fukui (A)

Department of Internal Medicine, National Hospital Organization Kyushu Medical Center, Division of Nephrology and Clinical Research Institute, 1-8-1 Jigyohama, Chuo-ku, Fukuoka, 810-8563, Japan.

Susumu Tsuda (S)

Department of Internal Medicine, National Hospital Organization Kyushu Medical Center, Division of Nephrology and Clinical Research Institute, 1-8-1 Jigyohama, Chuo-ku, Fukuoka, 810-8563, Japan.

Yuri Sonoda (Y)

Department of Internal Medicine, National Hospital Organization Kyushu Medical Center, Division of Nephrology and Clinical Research Institute, 1-8-1 Jigyohama, Chuo-ku, Fukuoka, 810-8563, Japan.

Rina Imazu (R)

Department of Internal Medicine, National Hospital Organization Kyushu Medical Center, Division of Hypertension and Clinical Research Institute, 1-8-1 Jigyohama, Chuo-ku, Fukuoka, 810-8563, Japan.

Kimika Arakawa (K)

Department of Internal Medicine, National Hospital Organization Kyushu Medical Center, Division of Hypertension and Clinical Research Institute, 1-8-1 Jigyohama, Chuo-ku, Fukuoka, 810-8563, Japan.

Mitsuhiro Tominaga (M)

Department of Internal Medicine, National Hospital Organization Kyushu Medical Center, Division of Hypertension and Clinical Research Institute, 1-8-1 Jigyohama, Chuo-ku, Fukuoka, 810-8563, Japan.

Toshiaki Nakano (T)

Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.

Kazuhiko Tsuruya (K)

Department of Nephrology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara, 634-8521, Japan.

Takanari Kitazono (T)

Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.

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