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Abstract: FR-PO129

Evaluation of Allostatic Load as a Mediator of Sleep and Kidney Outcomes in Blacks

Session Information

Category: CKD (Non-Dialysis)

  • 1903 CKD (Non-Dialysis): Mechanisms


  • Lunyera, Joseph, Duke University School of Medicine, Durham, North Carolina, United States
  • Davenport, Clemontina A., Duke University Medical Center, Durham, North Carolina, United States
  • Jackson, Chandra L., National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States
  • Johnson, Dayna A., Harvard Medical School, Boston, Massachusetts, United States
  • Bhavsar, Nrupen Anjan, Duke University School of Medicine, Durham, North Carolina, United States
  • Sims, Mario, University of Mississippi Medical Center, Jackson, Mississippi, United States
  • Scialla, Julia J., Duke University, Durham, North Carolina, United States
  • Stanifer, John W., Duke University, Durham, North Carolina, United States
  • Pendergast, Jane F., Duke University, Durham, North Carolina, United States
  • McMullan, Ciaran Joseph, Merck, Rahway, New Jersey, United States
  • Ricardo, Ana C., University of Illinois at Chicago, Chicago, Illinois, United States
  • Boulware, L. Ebony, Duke University School of Medicine, Durham, North Carolina, United States
  • Diamantidis, Clarissa Jonas, Duke University School of Medicine, Durham, North Carolina, United States

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 (AL) – a cumulative biologic measure of stress. Using data from the Jackson Heart Study (JHS), we examined the potential mediating effect of AL on the relation between sleep patterns and kidney outcomes


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 self-reported sleep quality: high (excellent/very good) vs. good vs. low (poor/fair) with prevalent baseline CKD (Exam 1), estimated glomerular filtration rate (eGFR) decline, and incident CKD at follow-up (Exam 3). CKD was defined as eGFR <60ml/min/1.73m2 or urine albumin-to-creatinine ratio ≥30mg/g. Models were adjusted for demographics, comorbidities and kidney function. We further evaluated AL (quantified at baseline using 11 biomarkers from neuroendocrine, metabolic, autonomic, and immune domains) as a mediator of these relations.


Among 5177 JHS participants, 40% slept the recommended 7-8 hours; 25%, 29% and 6% reported very short, short and long sleep duration, respectively. 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) after adjustment. Very short, short or long sleep duration (vs. 7-8 hours) were not associated with any other 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/1.73m2 (95% CI 0.00 to 0.36) faster eGFR decline per year over follow-up. AL did not mediate the associations of sleep duration or sleep quality with kidney outcomes.


Very short sleep duration and low sleep quality were associated with adverse kidney outcomes in this all black cohort, but AL did not appear to mediate these associations. Future work should investigate the role of other biologic mediators in the relation between sleep and CKD outcomes in blacks.


  • Other NIH Support