Μελέτη της μικρολευκωματινουρίας σε ασθενείς με σύνδρομο άπνοιας ύπνου

Σκοπός: 1) Να διερευνηθεί η υπόθεση ότι το ΣΑΑΥ-Υ αυξάνει την απέκκριση της λευκωματίνης -σε επίπεδα μικρολευκωματινουρίας- στα πρωινά ούρα, φαινόμενο αναστρέψιμο μετά την-θεραπευτική για το σύνδρομο-εφαρμογή της συσκευής CPAP. 2) Να μελετηθεί η σχέση της μικρολευκωματινουρίας στα πρωινά ούρα ασθενώ...

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Bibliographic Details
Main Author: Λιάββας, Χρήστος Κ.
Format: Text
Language:Greek
Published: Aristotle University of Thessaloniki 2009
Subjects:
Online Access:https://dx.doi.org/10.26262/heal.auth.ir.112915
https://ikee.lib.auth.gr/record/112915
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Summary:Σκοπός: 1) Να διερευνηθεί η υπόθεση ότι το ΣΑΑΥ-Υ αυξάνει την απέκκριση της λευκωματίνης -σε επίπεδα μικρολευκωματινουρίας- στα πρωινά ούρα, φαινόμενο αναστρέψιμο μετά την-θεραπευτική για το σύνδρομο-εφαρμογή της συσκευής CPAP. 2) Να μελετηθεί η σχέση της μικρολευκωματινουρίας στα πρωινά ούρα ασθενών με ΣΑΑΥ-Υ με την Αρτηριακή Πίεση (ΑΠ) 24ωρου και το nondipping φαινόμενο : Aim: To investigate the hypothesis that OSAHS induces nocturnal albumin excretion-at microalbuminuria levels-, a phenomenon reversible by the use of Continuous Positive Airway Pressure (CPAP) device. Furthermore, to investigate the relationship between microalbuminuria, 24-hour Blood Pressure (BP) and nondipping phenomenon in patients with OSAHS. Material and methods: 224 male patients, newly diagnosed with OSAHS, participated in the study. They had no other known comorbidity and they were taking no medications. Their mean±SD age was 43.72±9.37 years and their BMI (Body Mass Index) was 33.18±6.17 kg/m2. They were compared to 38 matched healthy male subjects (controls). During the first night, patients and controls underwent a sleep study, while, within 1 to 7 days after diagnosis, 121 of the 224 patients were treated with CPAP. In 133 of the 224 patients, 24-hour ambulatory BP measurements were obtained. For the respiration study during sleep, the Embletta portable device (Somnologica, Iceland) was used and more specific, positions and movements of the body (thorax, abdomen, lower limbs), cardiac pulse and rhythm, blood oxygen saturation (SaO2%), air flow detection in the upper airways, snoring and detection of air flow limitation due to increased resistance were recorded. Parameters used for further analysis were the Apnea Hypopnea Index (AHI), the Desaturation Index (DI), the lowest and mean % value of SaO2, the % percentage of sleep with SaO2 <90% (% SaO2 <90% ), <80% (% SaO2 <80%) and <70% (% SaO2 <70%). During CPAP titration, for which we used an auto-CPAP device (autoCPAP, Autoset T, ResMed, Sydney, Australia), the respiratory study was performed using the EDENTEC 3711 recording device. Ambulatory 24-hour BP measurements were performed at 30 minutes interval, with the Diasys Integra (NOVACOR SA, France) device. For further analysis we used: a) the mean value of Systolic Blood Pressures day (SBPd), Diastolic Blood Pressures day (DBPd) and the Mean Blood Pressure day (MBPd) and b) the mean value of SBP night (SBPn), of DBP night (DBPn) and the MBP night (MBPn). Determination of albumin (A), creatinine (C) and albumin/creatinine (A/C) ratio was performed using the DCA2000® Microalbumin/Creatinine reagent cartridge (Siemens Medical Solutions Diagnostics, NY), in urine samples before (A/Cnight) and immediately after sleep (A/Cmorning) in patients, for the nights of sleep study and first CPAP treatment and in controls. The same procedure was followed in 46 out of the 121 patients, who were re-evaluated after a 3-month period of constant therapeutic use of CPAP device. Results: In patients, the mean value±SD of AHI was 48.85±24.04, of DI 46.42±27.79, of the lowest SaO2% 73.14±11.49, of the average SaO2% 92.08±4.83, of % SaO2 <90% 20.37±25.06, of % SaO2 <80% 7.18±16.24 and of % SaO2 <70% 2.33±8.29. In controls, the mean value±SD of AHI was 2.55±2.08, of DI 1.93±1.50, of the lowest SaO2% 89.86±2.10, of the mean SaO2% 95.91±1.11, of % SaO2 <90%, <80% and <70% 0.0. Levels of A/Cnight ratio in controls were 11.21±15.82 and in patients 16.99±23.84 mg/g (p=0.032), while of A/Cmorning ratio was 6.54±6.53 and 17.82±31.10 mg/g respectively (p<0.0001). The % change of A/Cmorning-night in controls was -26.87±18.95 and in patients 8.82±61.06 (p<0.0001). In patients, who CPAP device was applied to, the A/Cmorning ratio before CPAP was 23.57±39.65 and after CPAP 16.78±20.93 mg/g (p<0.0001), while the % change of A/Cmorning-night was 10.73±69.93 and -21.39±24.59 mg/g respectively (p<0.0001). The levels of A/Cmorning ratio, in patients with OSAHS, were statistically significantly positively correlated with BMI, AHI, DI, the % SaO2 <90, 80 and 70% and statistically significantly negatively correlated with the mean and lowest SaO2%. Based on the degree of SBP decrease during sleep, patients were divided into dippers (≥10% decrease, n=74), and nondippers (<10% decrease, n=59). The A/Cmorning ratio in dippers was 11.71±13.26 and in nondippers 22.24±40.98 mg/g (p=0.007), while the % change of A/Cmorning-night was -5.57±40.81 and 29.33±57.67 respectively (p<0.0001). The levels of A/Cmorning ratio in dippers correlated statistically significantly positively with SBPd (r=0.280, p=0.016), DBPd (r=0.382, p=0.001), MBPd (r=0.394, p=0.001), DBPn (r=0.323, p=0.005) and MBPn (r=0.295, p=0.011). They didn’t correlate statistically significantly with SBPn (r=0.218, p=0.063). The levels of A/Cmorning ratio in nondippers correlated statistically significantly positively with SBPd (r=0.277, p=0.034), DBPd (r=0.448, p<0.0001), MBPd (r=0.407, p=0.001), SBPn (r=0.374, p=0.004), DBPn (r=0.553, p<0.0001) and MBPn (r=0.519, p<0.0001). In patients, who were re-evaluated after a 3-month period of CPAP use, the A/Cmorning ratio was 11.78±20.86 mg/g, while the night of the diagnostic sleep study it was 19.71±35.52 mg/g (p<0,001) and the night of CPAP titration 11.47±16.25 mg/g (p=0530). Conclusions: The OSAHS induces albumin excretion -at microalbuminuria levels- in morning urine, through the hemodynamic changes caused by respiratory disturbances during sleep. We might come to the conclusion that microalbuminuria, expressed by an icreased A/Cmorning ratio and the % change of A/Cmorning-night, could be considered as a detection biomarker of obstructive apneas and hypopneas during sleep. This increase of the A/Cmorning ratio is reversible after therapeutic use of CPAP device, a phenomenon preservable by the constant use of the device. Nocturnal albumin excretion was found to be statistically significantly correlated particularly with elevated night BP levels, as a result of a disturbed normal circadian rhythm of BP. Conclusively and in connection to that, we could say that microalbuminuria, expressed by an icreased A/Cmorning ratio and the % change of A/Cmorning-night, could be considered as a detection biomarker, not only of disturbed-elevated BP during night, but also of nondipping phenomenon and furthermore, as an early finding of future essential hypertension in patients with OSAHS