C-reactive protein levels, airflow obstruction, and chronic kidney disease
- نوع فایل : کتاب
- زبان : انگلیسی
- مؤلف : Yayoi Funakoshi Hisamitsu Omori Shuichi Mihara Ayumi Onoue Yasuhiro Ogata Hisamichi Aizawa Takahiko Katoh
- چاپ و سال / کشور: 2011
Description
Objectives There is some evidence that chronic obstructive pulmonary disease and chronic kidney disease (CKD) may be related, perhaps through systemic inflammation, which is common to both. However, this relationship has not yet been clearly demonstrated. The aim of this study was to investigate the association between airflow obstruction, CKD, and C-reactive protein (CRP) levels in Japanese men. Methods The study included 11,587 men, aged 40–88 years, who underwent a health check-up. Airflow obstruction was defined as a forced expiratory volume in 1 s/forced vital capacity of \70%, and its severity was based on the Global Initiative for Chronic Obstructive Lung Disease guidelines (GOLD). CKD was defined as an estimated glomerular filtration rate of\60 mL/min/1.73 m2. Results Airflow obstruction was present in 7.9% of the participants, and 10.6% of the participants had CKD. The average CRP levels were 0.11 ± 0.36, 0.13 ± 0.41, and 0.18 ± 0.41 mg/L for subjects with normal lung function, GOLD stage I, and GOLD stage II–IV, respectively. With regard to CKD, the average CRP levels were 0.11 ± 0.32 and 0.18 ± 0.6 mg/L for subjects without and with CKD, respectively. Analysis of covariance showed no significant differences between the CRP level and lung function status or CKD after age was adjusted for. Logistic regression analysis showed no association among subjects with the three different lung function statuses after age, body mass index, hypertension, diabetes, hyper-low-density-lipoprotein- cholesterolemia, smoking, physical activity, and alcohol intake were controlled for. Conclusions Based on the results of this study, we conclude that there is no interrelationship between CRP level, airflow obstruction, and CKD.
Environ Health Prev Med DOI 10.1007/s12199-011-0214-1 Received: 3 January 2011 / Accepted: 27 March 2011
