Abstract 1493: Albumin Excretion in Hypertensives with Sleep Apnea: Cross-Sectional Results in the Context of the Cross-Talk between Kidneys and Upper Airway
Microalbuminuria reflects a state of widespread vascular dysfunction, whereas obstructive sleep apnea (OSA) further promotes atherosclerotic damage in hypertension. In a cross-sectional study, we investigated whether urinary albumin excretion, as expressed by urinary albumin to creatinine ratio (ACR) is increased in hypertensives with OSA compared to hypertensives without OSA. We studied 62 untreated hypertensives [aged 48±7 years, 49 men, 31 smokers, body mass index (BMI) 32±4Kgr/m2], with OSA documented by positive polysomnography [Apnea Hypopnea Index (AHI)>5] and 70 hypertensives without OSA (negative polysomnography), matched for age, sex, smoking status, BMI and 24h pulse pressure (PP). All subjects underwent polysomnography, 24h ambulatory blood pressure monitoring, echocardiography, routine biochemical assessment while the mean ACR of two non-consecutive morning spot urine samples was estimated. Hypertensives with OSA compared to those without OSA did not differ regarding 24h systolic BP (140±9 vs. 138±7 p=NS), while 24h diastolic BP and nighttime PP were higher in the former group (87±7 vs. 85±7 mmHg, p=0.03 and 50±10 vs. 45±10mmHg, p=0.008). Albuminuria as expressed by log10(ACR) was greater by 57% in patients with OSA compared to those without OSA (1.1±0.2 vs. 0.7±0.4mg/g, p<0.001). Metabolic profile and estimated glomerular filatration rate did not differ between the two groups (p=NS for all cases). 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), 24h PP (r=0.38, p<0.001) and nighttime PP (r=0.21, p=0.01). In a multivarible linear regression model including age, sex, BMI, smoking, GFR, glucose, LDL, 24h pulse pressure, and log10(AHI), independent predictors of ACR were AHI (β=0.36, p<0.001) and 24h PP (β=0.25, p<0.001). Albuminuria is increased within the normal range in hypertensives with OSA compared to those without OSA proportionally to OSA severity independently of confounders. The association of upper airway dysfunction with albuminuria and pultatile haemodynamic load may provide an explanatory mechanism for the OSA related risk in hypertension.