Department of Medicine, Schulich School of Medicine and Dentistry, Western University, London, ON, Canada.
Department of Medicine, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.
Sleep. 2021 May 14;44(5). doi: 10.1093/sleep/zsaa228.
Nocturnal hypoxemia (NH) in obstructive sleep apnea (OSA) is associated with renal renin-angiotensin-aldosterone system (RAAS) up-regulation and loss of kidney function. Continuous positive airway pressure (CPAP) therapy is associated with RAAS down-regulation, though the impact of NH severity remains unknown. We sought to determine whether NH severity alters the effect of CPAP on renal hemodynamics and RAAS activity in humans.
Thirty sodium-replete, otherwise healthy, OSA participants (oxygen desaturation index ≥ 15 h-1) with NH (SpO2 < 90% ≥ 12%/night) were studied pre- and post-CPAP (>4 h/night∙4 weeks). NH severity was characterized as moderate (mean SpO2[MSpO2] ≥ 90%; N = 15) or severe (MSpO2 < 90%; N = 15). Glomerular filtration rate (GFR), renal plasma flow (RPF), and filtration fraction (FF) were measured at baseline and in response to angiotensin-II (3 ng/kg/min∙30 min, 6 ng/kg/min∙30 min), a marker of RAAS activity.
Pre-CPAP, baseline renal hemodynamics did not differ by NH severity. Pre-CPAP, severe NH participants demonstrated blunted GFR (Δ30 min, -9 ± 4 vs 1 ± 3 mL/min, p = 0.021; Δ60 min, -5 ± 5 vs 8 ± 5 mL/min, p = 0.017) and RPF (Δ30 min, -165 ± 13 vs -93 ± 19 mL/min, p = 0.003; Δ60 min, -208 ± 18 vs -112 ± 22 mL/min, p = 0.001; moderate vs severe) responses to angiotensin-II. Post-CPAP, severe NH participants demonstrated maintained GFR (112 ± 5 vs 108 ± 3 mL/min, p = 0.9), increased RPF (664 ± 35 vs 745 ± 34 mL/min, p = 0.009), reduced FF (17.6 ± 1.4 vs 14.9 ± 0.6%, p = 0.009), and augmented RPF responses to Angiotensin-II (Δ30 min, -93 ± 19 vs -138 ± 16 mL/min, p = 0.009; Δ60 min, -112 ± 22 vs -175 ± 20 mL/min, p = 0.001; pre- vs post-CPAP), while moderate participants were unchanged.
Correction of severe, but not moderate, NH with CPAP therapy was associated with improved renal hemodynamics and decreased renal RAAS activity in humans with OSA.
阻塞性睡眠呼吸暂停（OSA）患者的夜间低氧血症（NH）与肾素-血管紧张素-醛固酮系统（RAAS）的上调和肾功能丧失有关。持续气道正压通气（CPAP）治疗与 RAAS 下调有关，但 NH 严重程度的影响尚不清楚。我们旨在确定 NH 严重程度是否会改变 CPAP 对人类肾脏血液动力学和 RAAS 活性的影响。
30 名钠充足、 otherwise healthy、OSA 参与者（脱氧饱和度指数≥15 h-1）伴有 NH（SpO2 < 90%≥12%/night），在 CPAP 治疗前（>4 h/night∙4 周）和 CPAP 治疗后进行研究。NH 严重程度的特点是中度（平均 SpO2[MSpO2]≥90%；N=15）或重度（MSpO2 < 90%；N=15）。在基线和血管紧张素-II（3 ng/kg/min∙30 min，6 ng/kg/min∙30 min）反应时测量肾小球滤过率（GFR）、肾血浆流量（RPF）和滤过分数（FF），这是 RAAS 活性的标志物。
CPAP 治疗前，基线肾脏血液动力学不受 NH 严重程度的影响。CPAP 治疗前，严重 NH 患者的 GFR 反应减弱（30 分钟时的差异，-9 ± 4 对 1 ± 3 mL/min，p = 0.021；60 分钟时的差异，-5 ± 5 对 8 ± 5 mL/min，p = 0.017）和 RPF（30 分钟时的差异，-165 ± 13 对-93 ± 19 mL/min，p = 0.003；60 分钟时的差异，-208 ± 18 对-112 ± 22 mL/min，p = 0.001；中度对重度）对血管紧张素-II 的反应。CPAP 治疗后，严重 NH 患者的 GFR 保持不变（112 ± 5 对 108 ± 3 mL/min，p = 0.9），RPF 增加（664 ± 35 对 745 ± 34 mL/min，p = 0.009），FF 降低（17.6 ± 1.4 对 14.9 ± 0.6%，p = 0.009），对血管紧张素-II 的 RPF 反应增强（30 分钟时的差异，-93 ± 19 对-138 ± 16 mL/min，p = 0.009；60 分钟时的差异，-112 ± 22 对-175 ± 20 mL/min，p = 0.001；CPAP 治疗前对 CPAP 治疗后），而中度患者则没有变化。
用 CPAP 治疗纠正严重（但不是中度）NH 与 OSA 患者的肾脏血液动力学改善和肾脏 RAAS 活性降低有关。
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