Department of Neurology, Northwestern University, Chicago, IL, USA.
Department of Medicine, University of Illinois, Chicago, IL, USA.
J Sleep Res. 2018 Apr;27(2):281-289. doi: 10.1111/jsr.12573. Epub 2017 Jun 23.
Physiological evidence suggests that sleep modulates kidney function. Our objective was to examine the cross-sectional association between kidney function and objectively-estimated habitual sleep duration, quality and timing in a cohort of patients with mild to moderate chronic kidney disease. This study involved two US clinical centers of the Chronic Renal Insufficiency Cohort (CRIC) study, including 432 participants in a CRIC ancillary sleep study. Habitual sleep duration, quality and timing were measured using wrist actigraphy for 5-7 days. Validated sleep questionnaires assessed subjective sleep quality, daytime sleepiness and risk of sleep apnea. Kidney function was assessed with the estimated glomerular filtration rate using the Chronic Kidney Disease Epidemiology Collaboration equation, and the urinary protein to creatinine ratio. Lower estimated glomerular filtration rate was associated with shorter sleep duration (-1.1 mL min 1.73 m per hour less sleep, P = 0.03), greater sleep fragmentation (-2.6 mL min 1.73 m per 10% higher fragmentation, P < 0.001) and later timing of sleep (-0.9 mL min 1.73 m per hour later, P = 0.05). Higher protein to creatinine ratio was also associated with greater sleep fragmentation (approximately 28% higher per 10% higher fragmentation, P < 0.001). Subjective sleep quality, sleepiness and persistent snoring were not associated with estimated glomerular filtration rate or protein to creatinine ratio. Thus, worse objective sleep quality was associated with lower estimated glomerular filtration rate and higher protein to creatinine ratio. Shorter sleep duration and later sleep timing were also associated with lower estimated glomerular filtration rate. Physicians treating patients with chronic kidney disease should consider inquiring about sleep and possibly sending for clinical sleep assessment. Longitudinal and interventional trials are needed to understand causal direction.
生理证据表明睡眠可以调节肾脏功能。我们的目的是在慢性肾脏病轻度至中度患者队列中，研究肾脏功能与客观估计的习惯性睡眠时长、睡眠质量和睡眠时相关联。这项研究涉及美国慢性肾功能不全队列（CRIC）研究的两个临床中心，包括 CRIC 辅助睡眠研究中的 432 名参与者。使用手腕活动记录仪测量了 5-7 天的习惯性睡眠时长、质量和时间。经过验证的睡眠问卷评估了主观睡眠质量、白天嗜睡和睡眠呼吸暂停风险。使用慢性肾脏病合作研究方程和尿蛋白与肌酐比值评估了肾小球滤过率。估计肾小球滤过率越低与睡眠时长越短（每小时少睡 1.1 毫升/分钟/1.73 平方米，P=0.03）、睡眠碎片化程度越高（每增加 10%的碎片化，肾小球滤过率降低 2.6 毫升/分钟/1.73 平方米，P<0.001）和睡眠时间越晚（每小时推迟 0.9 毫升/分钟/1.73 平方米，P=0.05）有关。较高的尿蛋白与肌酐比值也与睡眠碎片化程度更高有关（每增加 10%的碎片化，尿蛋白与肌酐比值增加约 28%，P<0.001）。主观睡眠质量、嗜睡和持续性打鼾与估计肾小球滤过率或尿蛋白与肌酐比值无关。因此，较差的客观睡眠质量与较低的估计肾小球滤过率和较高的尿蛋白与肌酐比值有关。睡眠时长较短和睡眠时间较晚也与较低的估计肾小球滤过率有关。治疗慢性肾脏病患者的医生应考虑询问睡眠情况，并可能进行临床睡眠评估。需要进行纵向和干预性试验以了解因果关系。
