Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA
Intramural Program, National Institute on Minority Health and Health Disparities, Bethesda, Maryland, USA.
Thorax. 2021 Jul;76(7):704-713. doi: 10.1136/thoraxjnl-2020-214713. Epub 2020 Dec 4.
Poor sleep may contribute to chronic kidney disease (CKD) through several pathways, including hypoxia-induced systemic and intraglomerular pressure, inflammation, oxidative stress and endothelial dysfunction. However, few studies have investigated the association between multiple objectively measured sleep dimensions and CKD.
We investigated the cross-sectional association between sleep dimensions and CKD among 1895 Multi-Ethnic Study of Atherosclerosis Sleep Ancillary Study participants who completed in-home polysomnography, wrist actigraphy and a sleep questionnaire. Using Poisson regression models with robust variance, we estimated separate prevalence ratios (PR) and 95% CIs for moderate-to-severe CKD (glomerular filtration rate <60 mL/min/1.73 m or albuminuria >30 mg/g) among participants according to multiple sleep dimensions, including very short (≤5 hours) sleep, Apnoea-Hypopnoea Index and sleep apnoea-specific hypoxic burden (SASHB) (total area under the respiratory event-related desaturation curve divided by total sleep duration, %min/hour)). Regression models were adjusted for sociodemographic characteristics, health behaviours and clinical characteristics.
Of the 1895 participants, mean age was 68.2±9.1 years, 54% were women, 37% were white, 28% black, 24% Hispanic/Latino and 11% Asian. Several sleep metrics were associated with higher adjusted PR of moderate-to-severe CKD: very short versus recommended sleep duration (PR=1.40, 95% CI 1.06 to 1.83); SASHB (Box-Cox transformed SASHB: PR=1.06, 95% CI 1.02 to 1.12); and for participants in the highest quintile of SASHB plus sleep apnoea: PR=1.28, 95% CI 1.01 to 1.63.
Sleep apnoea associated hypoxia and very short sleep, likely representing independent biological mechanisms, were associated with a higher moderate-to-severe CKD prevalence, which highlights the potential role for novel interventions.
睡眠质量差可能通过多种途径导致慢性肾脏病(CKD),包括缺氧引起的全身和肾小球内压力、炎症、氧化应激和内皮功能障碍。然而,很少有研究调查过多个客观测量的睡眠维度与 CKD 之间的关系。
我们在完成家庭多导睡眠图、腕部活动记录仪和睡眠问卷的 1895 名动脉粥样硬化多民族研究睡眠辅助研究参与者中调查了睡眠维度与 CKD 之间的横断面关系。我们使用具有稳健方差的泊松回归模型,根据多个睡眠维度(包括睡眠时间极短(≤5 小时)、呼吸暂停-低通气指数和睡眠呼吸暂停特异性缺氧负担(SASHB)(呼吸事件相关脱氧曲线下总面积除以总睡眠时间,%min/hour)),为参与者估计了中度至重度 CKD(肾小球滤过率 <60mL/min/1.73m 或蛋白尿 >30mg/g)的患病率比(PR)和 95%置信区间(CI)。回归模型调整了社会人口统计学特征、健康行为和临床特征。
在 1895 名参与者中,平均年龄为 68.2±9.1 岁,54%为女性,37%为白人,28%为黑人,24%为西班牙裔/拉丁裔,11%为亚裔。几个睡眠指标与中度至重度 CKD 的调整后 PR 较高相关:睡眠时间极短与推荐睡眠时间相比(PR=1.40,95%CI 1.06 至 1.83);SASHB(Box-Cox 转换的 SASHB:PR=1.06,95%CI 1.02 至 1.12);以及 SASHB 加上睡眠呼吸暂停最高五分位的参与者:PR=1.28,95%CI 1.01 至 1.63。
睡眠呼吸暂停相关缺氧和极短睡眠时间可能代表独立的生物学机制,与更高的中度至重度 CKD 患病率相关,这凸显了新型干预措施的潜在作用。