Sleep Duration and Chronic Kidney Disease: Analysis of the National Health Interview Survey

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Abstract

Background: Patients with chronic kidney disease (CKD) have a high prevalence of sleep disorders. The association between sleep duration and self-reported CKD was examined in a population of Americans who participated in a national survey over a 3-year period. Study Design: A cross-sectional study using survey data from theNational Health Interview Survey (NHIS) from the year 2004-2006 was carried out. A retrospective examination of data from acommunity-based survey of 128,486 noninstitutionalized US civilian residents over the age of 18 years was conducted. Self-reportedCKD was defined as having ‘weak or failing kidneys'. The sleep duration was defined by a self-reported estimate of habitual sleep duration. Results: The prevalence of participants self-reporting kidney disease was higher in those with short (≤6 h per night) and long (≥8 h per night) sleep durations when compared to those sleeping 7 h per night. Self-reported information about sleep, demographic information, and information on comorbidities were assessed using standardized validated questionnaires which reported no kidney disease. A multivariate logistic regression analysis showed increased odds of self-reported kidney disease in study participants with both short and long sleep durations compared to healthy sleepers (sleeping >7-8 h per night). Observational data do not permit examination of causality, although possible confounders in observations of interest can be adjusted. Conclusion: AmongAmericans surveyed in the NHIS (2004-2006), those with short or long sleep duration had higher odds of reporting that they had CKD. i 2014 S. Karger AG, Basel

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Most cited references 26

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Mortality associated with sleep duration and insomnia.

Daniel F. Kripke, Lawrence Garfinkel, Deborah L. Wingard … (2002)

Patients often complain about insufficient sleep or chronic insomnia in the belief that they need 8 hours of sleep. Treatment strategies may be guided by what sleep durations predict optimal survival and whether insomnia might signal mortality risks. In 1982, the Cancer Prevention Study II of the American Cancer Society asked participants about their sleep duration and frequency of insomnia. Cox proportional hazards survival models were computed to determine whether sleep duration or frequency of insomnia was associated with excess mortality up to 1988, controlling simultaneously for demographics, habits, health factors, and use of various medications. Participants were more than 1.1 million men and women from 30 to 102 years of age. The best survival was found among those who slept 7 hours per night. Participants who reported sleeping 8 hours or more experienced significantly increased mortality hazard, as did those who slept 6 hours or less. The increased risk exceeded 15% for those reporting more than 8.5 hours sleep or less than 3.5 or 4.5 hours. In contrast, reports of "insomnia" were not associated with excess mortality hazard. As previously described, prescription sleeping pill use was associated with significantly increased mortality after control for reported sleep durations and insomnia. Patients can be reassured that short sleep and insomnia seem associated with little risk distinct from comorbidities. Slight risks associated with 8 or more hours of sleep and sleeping pill use need further study. Causality is unproven.

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Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk.

Hans Meier-Ewert, Paul Ridker, Nader Rifai … (2004)

We sought to investigate the effects of sleep loss on high-sensitivity C-reactive protein (CRP) levels. Concentrations of high-sensitivity CRP are predictive of future cardiovascular morbidity. In epidemiologic studies, short sleep duration and sleep complaints have also been associated with increased cardiovascular morbidity. Two studies were undertaken to examine the effect of acute total and short-term partial sleep deprivation on concentrations of high-sensitivity CRP in healthy human subjects. In Experiment 1, 10 healthy adult subjects stayed awake for 88 continuous hours. Samples of high-sensitivity CRP were collected every 90 min for 5 consecutive days, encompassing the vigil. In Experiment 2, 10 subjects were randomly assigned to either 8.2 h (control) or 4.2 h (partial sleep deprivation) of nighttime sleep for 10 consecutive days. Hourly samples of high-sensitivity CRP were taken during a baseline night and on day 10 of the study protocol. The CRP concentrations increased during both total and partial sleep deprivation conditions, but remained stable in the control condition. Systolic blood pressure increased across deprivation in Experiment 1, and heart rate increased in Experiment 2. Both acute total and short-term partial sleep deprivation resulted in elevated high-sensitivity CRP concentrations, a stable marker of inflammation that has been shown to be predictive of cardiovascular morbidity. We propose that sleep loss may be one of the ways that inflammatory processes are activated and contribute to the association of sleep complaints, short sleep duration, and cardiovascular morbidity observed in epidemiologic surveys.

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Association of sleep time with diabetes mellitus and impaired glucose tolerance.

H Resnick, F Nieto, H. B. Newman … (2005)

Experimental sleep restriction causes impaired glucose tolerance (IGT); however, little is known about the metabolic effects of habitual sleep restriction. We assessed the cross-sectional relation of usual sleep time to diabetes mellitus (DM) and IGT among participants in the Sleep Heart Health Study, a community-based prospective study of the cardiovascular consequences of sleep-disordered breathing. Participants were 722 men and 764 women, aged 53 to 93 years. Usual sleep time was obtained by standardized questionnaire. Diabetes mellitus was defined as a serum glucose level of 126 mg/dL or more (> or =7.0 mmol/L) fasting or 200 mg/dL or more (> or =11.1 mmol/L) 2 hours following standard oral glucose challenge or medication use for DM. Impaired glucose tolerance was defined as a 2-hour postchallenge glucose level of 140 mg/dL or more (> or =7.8 mmol/L) and less than 200 mg/dL. The relation of sleep time to DM and IGT was examined using categorical logistic regression with adjustment for age, sex, race, body habitus, and apnea-hypopnea index. The median sleep time was 7 hours per night, with 27.1% of subjects sleeping 6 hours or less per night. Compared with those sleeping 7 to 8 hours per night, subjects sleeping 5 hours or less and 6 hours per night had adjusted odds ratios for DM of 2.51 (95% confidence interval, 1.57-4.02) and 1.66 (95% confidence interval, 1.15-2.39), respectively. Adjusted odds ratios for IGT were 1.33 (95% confidence interval, 0.83-2.15) and 1.58 (95% confidence interval, 1.15-2.18), respectively. Subjects sleeping 9 hours or more per night also had increased odds ratios for DM and IGT. These associations persisted when subjects with insomnia symptoms were excluded. A sleep duration of 6 hours or less or 9 hours or more is associated with increased prevalence of DM and IGT. Because this effect was present in subjects without insomnia, voluntary sleep restriction may contribute to the large public health burden of DM.

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Author and article information

Journal

Journal ID (publisher-id): CRM

Journal ID (nlm-ta): Cardiorenal Med

Journal ID (doi): 10.1159/issn.1664-5502

Title: Cardiorenal Medicine

Publisher: S. Karger AG

ISSN (Print): 1664-3828

ISSN (Electronic): 1664-5502

Publication date Subscription-year: 2014

Publication date (Print): December 2014

Publication date (Electronic): 17 October 2014

Volume: 4

Issue: 3-4

Pages: 210-216

Affiliations

^aCenter for Healthful Behavior Change, NYU School of Medicine, New York, N.Y., ^bDepartment of Obstetrics and Gynecology, Lutheran Medical Center, and Departments of ^cMedicine and ^dEndocrinology, SUNY Downstate Medical Center, Brooklyn, N.Y., USA

Author notes

*Girardin Jean-Louis, PhD, Professor of Population Health and Psychiatry, Center for Healthful Behavior Change, Department of Population Health, New York University School of Medicine, 227 East 30th St., 6th Floor, New York, NY 10016 (USA), E-Mail Girardin.Jean-Louis@nyumc.org

Article

Publisher ID: 368205 Pmcid ID: PMC4299261 Other ID: Cardiorenal Med 2014;4:210-216

DOI: 10.1159/000368205

PMC ID: PMC4299261

PubMed ID: 25737685

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