Abstract
INTRODUCTION: Poor sleep associates with adverse chronic kidney disease (CKD) outcomes yet the biological mechanisms underlying this relation remain unclear. One proposed mechanism is via allostatic load, a cumulative biologic measure of stress. METHODS: Using data from 5177 Jackson Heart Study participants with sleep measures available, we examined the association of self-reported sleep duration: very short, short, recommended, and long (≤5, 6, 7-8, or ≥9 hours per 24 hours, respectively) and sleep quality (high, moderate, low) with prevalent baseline CKD, and estimated glomerular filtration rate (eGFR) decline and incident CKD at follow-up. CKD was defined as eGFR <60 ml/min per 1.73 m(2) or urine albumin-to-creatinine ratio ≥30 mg/g. Models were adjusted for demographics, comorbidities, and kidney function. We further evaluated allostatic load (quantified at baseline using 11 biomarkers from neuroendocrine, metabolic, autonomic, and immune domains) as a mediator of these relations using a process analysis approach. RESULTS: Participants with very short sleep duration (vs. 7-8 hours) had greater odds of prevalent CKD (odds ratio [OR] 1.31, 95% confidence interval [CI] 1.03-1.66). Very short, short, or long sleep duration (vs. 7-8 hours) was not associated with kidney outcomes over a median follow-up of 8 years. Low sleep quality (vs. high) associated with greater odds of prevalent CKD (OR 1.26, 95% CI 1.00-1.60) and 0.18 ml/min per 1.73 m(2) (95% CI 0.00-0.36) faster eGFR decline per year. Allostatic load did not mediate the associations of sleep duration or sleep quality with kidney outcomes. CONCLUSIONS: Very short sleep duration and low sleep quality were associated with adverse kidney outcomes in this all-black cohort, but allostatic load did not appear to mediate these associations.