Association of Obstructive Sleep Apnea With Urinary Albumin Excretion in Essential Hypertension: A Cross-sectional Study
Received 21 November 2007; accepted 9 May 2008. published online 10 July 2008.
Background
Microalbuminuria reflects a state of widespread vascular dysfunction, whereas obstructive sleep apnea (OSA) further promotes atherosclerotic damage in hypertension.
Study Design
Cross-sectional.
Setting & Participants
In an outpatient hypertensive unit, 62 untreated hypertensive patients (aged 48 ± 7 years; office blood pressure [BP], 151 ± 8/97 ± 7 mm Hg) with OSA and 70 hypertensive patients without OSA (apnea hypopnea index [AHI] ≤ 5) matched for age, sex, smoking status, body mass index, and 24-hour pulse pressure were studied.
Predictor Variable
Hypertension and OSA compared with hypertension without OSA. OSA defined as AHI greater than 5, documented by polysomnography.
Outcome Variable
Albuminuria assessed by urinary albumin-creatinine ratio (ACR).
Measurements
Participants underwent polysomnography, ambulatory BP monitoring, echocardiography, routine metabolic profile assessment, and glomerular filtration rate estimation, whereas ACR was measured from 2 nonconsecutive morning spot urine samples.
Results
Hypertensive patients with OSA compared with those without OSA showed increased 24-hour diastolic BP (87 ± 7 versus 85 ± 7 mm Hg; P = 0.03) and nighttime pulse pressure (50 ± 10 versus 45 ± 10 mm Hg; P = 0.008), but did not differ regarding metabolic profile and estimated glomerular filtration rate. Albuminuria was greater by 57% in patients with OSA compared with those without OSA: log(10)ACR, 1.1 ± 0.2 versus 0.7 ± 0.4 mg/g; P < 0.001). In the entire study population, log10(ACR) correlated with log10(AHI) (r = 0.35; P < 0.001), minimum oxygen saturation during sleep (r = −0.33; P < 0.001), 24-hour pulse pressure (r = 0.38; P < 0.001), and nighttime pulse pressure (r = 0.21; P =0 .01). In a multivariable linear regression model, independent predictors of ACR were AHI (β = 0.36; P < 0.001) and 24-hour pulse pressure (β = 0.25; P = 0.01).
Limitations
Cross-sectional study.
Conclusions
Albuminuria increases within the normal range in hypertensive individuals with OSA compared with those without OSA proportionally to OSA severity independently of confounders. The association of upper-airway dysfunction with albuminuria and pulsatile hemodynamic load may provide an explanatory mechanism for the OSA-related risk in hypertension.
ABSTRACT