Habitual sleep and kidney function in chronic kidney disease: the Chronic Renal Insufficiency Cohort study

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Over 20 million adults (approximately 10% of the adult US population) have chronic kidney disease (CKD; Coresh et al., 2007; Eckardt et al., 2013). Impaired kidney function is associated with increased risk of cardiovascular disease and age‐adjusted mortality and, as kidney function worsens, these risks increase (Eckardt et al., 2013; Gansevoort et al., 2013). Thus, identification of novel, modifiable risk factors associated with the progression of CKD would increase our understanding of the pathophysiology of CKD, and potentially lead to new therapies to prevent or delay end‐stage renal disease (ESRD) and reduce the health burden associated with CKD.
One novel risk factor may be inadequate sleep, including insufficient sleep, poor sleep quality and later sleep timing. Under normal conditions, sleep profoundly modulates the key hormones involved in the control of kidney function, particularly those of the rennin–angiotensin–aldosterone system, which exhibit large diurnal variations that are dependent on sleep (Brandenberger et al., 1994; Charloux et al., 1999; Hurwitz et al., 2004; Turek et al., 2012). Normal sleep suppresses urinary sodium excretion (Rubin et al., 1978), and acute total sleep deprivation reduces the normal nocturnal increases in plasma renin activity (PRA) and aldosterone (Charloux et al., 2001). Sleep quality, independently of sleep duration, may also play an important role in kidney function because during normal sleep, the rapid eye movement (REM)–non(N)REM cycle drives a robust ultradian oscillation of PRA and aldosterone (Brandenberger et al., 1988, 1994). Experimental studies that manipulated sleep or the circadian system have observed significant changes in several physiological systems that could affect kidney function, including increased sympathetic nervous system activity (Buxton et al., 2010; Spiegel et al., 1999, 2004; Stamatakis and Punjabi, 2010; Tasali et al., 2008), alterations in the 24‐h profiles of growth hormone and cortisol (Buxton et al., 2010; Spiegel et al., 1999, 2000), increased blood pressure (Sayk et al., 2010; Scheer et al., 2009; Tochikubo et al., 1996), and impaired glucose tolerance (Buxton et al., 2010; Leproult et al., 2014; Nedeltcheva et al., 2009; Scheer et al., 2009; Spiegel et al., 1999; Stamatakis and Punjabi, 2010; Tasali et al., 2008). Given these established associations between sleep, circadian alignment and several physiological systems that affect kidney function, it is possible that habitual sleep patterns could influence the risk and severity of CKD.
Previous research has found that self‐reported habitual sleep duration is associated with prevalent and incident CKD (Turek et al., 2012). Studies have found that the prevalence of kidney disease or renal hyperfiltration was higher in those reporting short sleep durations as well as in those reporting long sleep durations compared with those sleeping 7–8 h per night (Cheungpasitporn et al., 2016; Kim et al., 2017; Lin et al., 2017; Salifu et al., 2014), although one study only observed this association in women (Choi et al., 2017). Further, the incidence of proteinuria was greater among people reporting shorter sleep duration (≤5 h per night) in a sample of employees of Osaka University in Japan (Yamamoto et al., 2012). Finally, a study of Japanese type 2 diabetic patients without CKD found that both self‐reported short and long sleep durations were significantly associated with higher urinary albumin–creatinine ratios (Ohkuma et al., 2013). Whether or not sleep characteristics are associated with kidney function among people who already have kidney disease remains to be determined.
The aim of the present study was to examine the association between sleep and kidney function, as assessed by both the estimated glomerular filtration rate (eGFR) and the urine protein to creatinine ratio (PCR) in patients with mild to moderate CKD.
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