阻塞性睡眠呼吸暂停低通气综合征对患者肾功能的影响
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摘要
目的观察阻塞性睡眠呼吸暂停低通气综合征(OSAHS)对患者肾功能的影响,初步探讨OSAHS对肾功能损害的机制。方法收集2017年3月至2018年3月在贵州省人民医院住院及门诊就诊的230例患者,采用多导睡眠监测(PSG)进行睡眠监测,根据呼吸暂停低通气指数(AHI)分为正常对照组、轻度组、中度组及重度组,同时测定患者血清中活性氧(ROS)、缺氧诱导因子-1α(HIF-1α)、一氧化氮(NO)、尿素氮(BUN)、肌酐(Cr)、尿酸(UA),计算肾小球滤过率(GFR)。结果中重度OSAHS组ROS、水平明显高于正常对照组,NO水平明显低于正常对照组,重度OSAHS组GFR明显低于正常对照组(P <0.05)。ROS、HIF-1α水平与最低血氧饱和度(minSaO_2)呈负相关。结论 OSAHS患者由于慢性间歇性缺氧,是导致慢性肾功能不全的潜在危险因素。
Objective To observe the influence of obstructive sleep apnea hypopnea syndrom(OSAHS on patients′ renal function and to explore the mechanism of impairment of renal function in OSAHS patients.Method Totally 230 patients in Guizhou Provincial People′s Hospital from March 2017 to March 2018 were enrolled. All patients were divided into control group,mild group,moderate group and severe group according to the apnea hypoventilation index(AHI)after sleep monitoring by polysomnography(PSG)monitor. The active oxygen(ROS),hypoxia inducing factor-1 alpha(HIF-1α),nitric oxide(NO),urea nitrogen(BUN),creatinine(Cr)and uric acid(UA)of serum were tested and glomerular filtration rate(GFR)was calculated. Results The level of ROS and HIF-1 α was significantly higher but the level of NO significantly lower in moderate and severe group than those in control group and GFR in severe OSAHS group was significantly lower than that in control group(P < 0.05). There was negative correlation between ROS,HIF-1 α and minimum oxygen saturation(minSaO_2)(P < 0.05). Conclusion OSAHS is a potential risk factor of renal insufficiency because of chronic intermittent hypoxia.
Objective To observe the influence of obstructive sleep apnea hypopnea syndrom(OSAHS on patients′ renal function and to explore the mechanism of impairment of renal function in OSAHS patients.Method Totally 230 patients in Guizhou Provincial People′s Hospital from March 2017 to March 2018 were enrolled. All patients were divided into control group,mild group,moderate group and severe group according to the apnea hypoventilation index(AHI)after sleep monitoring by polysomnography(PSG)monitor. The active oxygen(ROS),hypoxia inducing factor-1 alpha(HIF-1α),nitric oxide(NO),urea nitrogen(BUN),creatinine(Cr)and uric acid(UA)of serum were tested and glomerular filtration rate(GFR)was calculated. Results The level of ROS and HIF-1 α was significantly higher but the level of NO significantly lower in moderate and severe group than those in control group and GFR in severe OSAHS group was significantly lower than that in control group(P < 0.05). There was negative correlation between ROS,HIF-1 α and minimum oxygen saturation(minSaO_2)(P < 0.05). Conclusion OSAHS is a potential risk factor of renal insufficiency because of chronic intermittent hypoxia.
引文
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[15]SUN W,YIN X,WANG Y,et al.Intermittent hypoxia-induced renal antioxidants and oxidative damage in male mice:hormetic dose response[J].Dose Response,2013,11(3):385-400.
[16]PERRY J C,BERGAMASCHI C T,CAMPOS R R,et al.Differential sympathetic activation induced by intermittent hypoxia and sleep loss in rats:action of angiotensin(1-7)[J].Auton Neurosci,2011,160(1-2):32-36.
[2]GILDEH N,DRAKATOS P,HIGGINS S,et al.Emerging comorbidities of obstructive sleep apnea:cognition,kidney disease,and cancer[J].J Thorac Dis,2016,8(9):E901.
[3]中华医学会呼吸病学分会睡眠呼吸障碍学组,阻塞性睡眠呼吸暂停低通气综合征诊治指南[J].中华结核与呼吸杂志,2012,5(1):9-12.
[4]SFORZA E,ROCHE F.Chronic intermittent hypoxia and obstructive sleep apnea:an experimental and clinical approach[J].Hypoxia(Auckl),2016,4:99-108.
[5]BAGUET J P,BARONE-ROCHETTE G,TAMISIER R,et al.Mechanisms of cardiac dysfunction in obstructive sleep apnea[J].Nat Rev Cardiol,2012,9(12):679-688.
[6]DEWAN N A,NIETO F J,SOMERS V K.Intermittent hypoxemia and OSA:implications for comorbidities[J].Chest,2015,147(1):266-274.
[7]HANLY P J,AHMED S B.Sleep apnea and the kidney:is sleep apnea a risk factor for chronic kidney disease[J].Chest,2014,146(4):1114-1122.
[8]NIGAM G,CAMACHO M,CHANG E T,et al.Exploring sleep disorders in patients with chronic kidney disease[J].Nat Sci Sleep,2018,10:35-43.
[9]ABUYASSIN B,SHARMA K,AYAS N T,et al.Obstructive sleep apnea and kidney disease:a potential bidirectional relationship[J].J Clin Sleep Med,2015,11(8):915-924.
[10]DA SILVA B C,KASAI T,COELHO F M,et al.Fluid redistribution in sleep apnea:Therapeutic implications in edematous states[J].Front Med(Lausanne),2017,4:256.
[11]FRAMNES S N,ARBLE D M.The Bidirectional relationship between obstructive sleep apnea and metabolic disease[J].Front Endocrinol(Lausanne),2018,9:440.
[12]UYAR M,DAVUTOGLU V,GüNDOGDU N,et al.Renal functions in obstructive sleep apnea patients[J].Sleep Breath,2016,20(1):191-195.
[13]SARDO L,PALANGE P,DI MARIO F,et al.Intrarenal hemodynamic and oxidative stress in patients with obstructive sleep apnea syndrome[J].Sleep Breath,2015,19(4):1205-1212.
[14]ZALUCKY A A,NICHOLL D D,HANLY P J,et al.Nocturnal hypoxemia severity ands reninangiotensin system activity in obstructive sleep apnea[J].Am J Respir Crit Care Med,2015,192(7):873-880.
[15]SUN W,YIN X,WANG Y,et al.Intermittent hypoxia-induced renal antioxidants and oxidative damage in male mice:hormetic dose response[J].Dose Response,2013,11(3):385-400.
[16]PERRY J C,BERGAMASCHI C T,CAMPOS R R,et al.Differential sympathetic activation induced by intermittent hypoxia and sleep loss in rats:action of angiotensin(1-7)[J].Auton Neurosci,2011,160(1-2):32-36.