Background Obstructive sleep apnea may be associated with development of CKD through hypoxia, inflammation, and oxidative stress. Individuals with this sleep disorder are also at increased risk for established CKD risk factors, including obesity, hypertension, and type 2 diabetes. Methods We examined the association between obstructive sleep apnea, other sleep characteristics, and risk of incident CKD (stage 3 or higher) in 1525 participants (mean age, 62.5 years; 52.4% women) in the Atherosclerosis Risk in Communities (ARIC) study who completed in-home polysomnography assessments. We used the apnea-hypopnea index (events per hour) to define obstructive sleep apnea severity (normal,,5.0; mild, 5.0–14.9; moderate, 15.0–29.9; and severe, $30.0) and defined incident CKD (stage 3 or higher) as eGFR,60 ml/min per 1.73 m2 and $25% decline from baseline, CKD-related hospitalization or death, or ESKD. Cox proportional hazards regression was used to estimate obstructive sleep apnea severity with risk of incident CKD, adjusting for demographics, lifestyle behaviors, and cardiometabolic conditions. Results During 19 years (median) of follow-up, 461 CKD events occurred. After adjustment for demographics and lifestyle behaviors, severe obstructive sleep apnea associated with increased risk of CKD (hazard ratio [HR], 1.51; 95% confidence interval [95% CI], 1.08 to 2.10), which was attenuated after adjustment for body mass index (HR, 1.07; 95% CI, 0.75 to 1.52). No other sleep characteristics associated with incident CKD. Conclusions We found a link between obstructive sleep apnea and an elevated risk of stage 3 CKD or higher, but this association was no longer significant after adjusting for obesity, a risk factor for both conditions. Given the high prevalence of obstructive sleep apnea and CKD among adults, further investigation is warranted.
Bibliographical noteFunding Information:
The ARIC study has been funded in whole or in part with federal funds from National Heart, Lung, and Blood Institute contracts HHSN268201700001I, HHSN268201700002I, HHSN268201700003I, HHSN268201700004I, and HHSN268201700005I. This work was funded, in part, by National Institute of Environmental Health Sciences Intramural Program grant Z1AES103325-01 (to C. Jackson). K. Full is supported by National Heart, Lung, and Blood Institute training grant T32 HL007779. C. Rebholz is supported by National Institute of Diabetes and Digestive and Kidney Diseases mentored research scientist development award K01 DK107782 and National Heart, Lung, and Blood Institute grant R21 HL143089.