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VOLUME 30, ISSUE 07


Obstructive Sleep Apnea Is Associated With Increased Urinary Albumin Excretion

Michael D. Faulx, MD1; Amy Storfer-Isser, MS2; H Lester Kirchner, PhD2; Nancy S. Jenny, PhD3; Russell P. Tracy, PhD3,4; Susan Redline, MD, MPH2

1Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland Clinic Lerner College of Medicine, Cleveland, OH; 2Department of Pediatrics, Case Western Reserve University, Rainbow Babies and Children’s Hospital, Case School of Medicine, Cleveland, OH; 3Department of Pathology, 4Department of Biochemistry, University of Vermont, Burlington, VT



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Background:

Obstructive sleep apnea (OSA) is associated with cardiovascular disease through incompletely understood mechanisms. Urinary albumin excretion is a surrogate for endothelial dysfunction and a potent cardiovascular disease risk predictor. We sought to determine whether urinary albumin excretion is increased in subjects with OSA.

Methods:

Four hundred ninety-six adults, representing a spectrum of OSA severity, underwent overnight polysomnography and urine collection. OSA severity was assessed using the apnea-hypopnea index (AHI). The primary outcome measure was the adjusted albumin-to-creatinine ratio (aACR). Linear mixed models were used to assess the association between AHI category and aACR, adjusted for confounders and renal dysfunction.

Results:

Subjects had a mean age of 44 ± 17 (SD) years and approximately half were men (44%) and African American (56%). The percentages of subjects with mild (AHI 5-14), moderate (AHI 15-29), and severe (AHI ≥ 30) OSA were 23%, 15%, and 15%, respectively. The median aACR for the entire sample was 4.3 mg/g (interquartile range: 2.9, 7.5). Adjusted linear mixed-model analyses showed a significant association between AHI category and aACR, with the AHI ≥ 30 group having the highest aACR levels (7.87 ± 1.02 mg/g vs 5.08 ± 0.41 mg/g for those with AHI < 5; P < 0.006). Similar findings were observed after excluding subjects with renal dysfunction.

Conclusion:

OSA is significantly associated with increased urine albumin excretion, especially among those with more severe disease. These data provide further evidence supporting endothelial dysfunction as a mediating pathway between cardiovascular disease and OSA.
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