Impact of circulating cathepsin K on the coronary calcification and the clinical outcome in chronic kidney disease patients

Chronic kidney disease (CKD) is a cause of coronary artery calcification (CAC) and an independent predictor of major adverse cardiac and cerebrovascular events (MACCE). Cathepsin K (CatK) is a lysosomal cysteine protease which affects vascular calcification and glucose metabolism disorder. We invest...

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Bibliographic Details
Published in:Heart and vessels 2016-01, Vol.31 (1), p.6-14
Main Authors: Izumi, Yusuke, Hayashi, Mutsuharu, Morimoto, Ryota, Cheng, Xian Wu, Wu, Hongxian, Ishii, Hideki, Yasuda, Yoshinari, Yoshikawa, Daiji, Izawa, Hideo, Matsuo, Seiichi, Oiso, Yutaka, Murohara, Toyoaki
Format: Article
Language:English
Subjects:
Aged
Aged, 80 and over
Biomedical Engineering and Bioengineering
Calcification
Cardiac Surgery
Cardiology
Cardiovascular disease
Cathepsin K - blood
Clinical outcomes
Coronary Artery Disease - blood
Diabetes Mellitus - blood
Female
Humans
Japan
Kaplan-Meier Estimate
Kidney diseases
Lipids
Logistic Models
Male
Medicine
Medicine & Public Health
Middle Aged
Multivariate Analysis
Natriuretic Peptide, Brain - blood
Original Article
Peptides
Proportional Hazards Models
Renal Insufficiency, Chronic - complications
Risk Factors
Tomography, X-Ray Computed
Vascular Calcification - blood
Vascular Surgery
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Summary:Chronic kidney disease (CKD) is a cause of coronary artery calcification (CAC) and an independent predictor of major adverse cardiac and cerebrovascular events (MACCE). Cathepsin K (CatK) is a lysosomal cysteine protease which affects vascular calcification and glucose metabolism disorder. We investigated the relationships among CatK, CAC, diabetes mellitus (DM) and MACCE in CKD patients. 113 consecutive CKD patients were enrolled. Their CAC was evaluated by computed tomography. Their plasma CatK level was measured by ELISA. They were divided into two groups by CatK levels and followed up for up to 3 years. The impact of CatK was analyzed in all participants, diabetic patients and non-diabetic patients. Kaplan–Meier analysis demonstrated a significant higher incidence of MACCE in the high CatK group ( P  = 0.028). The CatK level was significantly higher in patients with MACCE compared to that in patients without MACCE ( P  = 0.034). Cox’s model revealed the higher plasma CatK and BNP level as independent predictors of MACCE ( P  = 0.043 and P  
ISSN:0910-8327
1615-2573
DOI:10.1007/s00380-014-0570-z