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] < or = 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 (beta = 0.36; P < 0.001) and 24-hour pulse pressure (beta = 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.