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.
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.
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.
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.