Department of Geriatric Medicine and Nephrology, Osaka University Graduate School of Medicine, Japan.
Clin J Am Soc Nephrol. 2013 Sep;8(9):1502-7. doi: 10.2215/CJN.11931112. Epub 2013 Jun 6.
Nocturnal hypoxemia is highly prevalent among patients with CKD. Nocturnal hypoxemia contributes to systemic inflammation, oxidative stress, endothelial cell dysfunction, and activation of the renin-angiotensin system, which are common pathologic mechanisms of CKD progression. This study investigated whether nocturnal hypoxemia is independently associated with CKD progression.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: This two-center retrospective cohort study included 161 patients with stages 3-4 CKD enrolled from January of 2009 to July of 2011 with a body mass index less than 25.0 kg/m(2). The 4% oxygen desaturation index, the number of events per hour in which oxygen saturation decreases by >4% during sleep, was measured, and the declining rate of the estimated GFR was followed over 1 year. The severity of nocturnal hypoxemia was categorized as none (oxygen desaturation index<5.0), mild (5.0≤oxygen desaturation index<15.0), or moderate to severe (15.0≤oxygen desaturation index).
The mean estimated GFR of the total cohort at baseline was 31 ml/min per 1.73 m(2). Eighty patients (49.7%) were diagnosed with nocturnal hypoxemia; 64 patients were diagnosed with mild nocturnal hypoxemia, and 16 patients were diagnosed with moderate-to-severe nocturnal hypoxemia. The estimated GFR declined three- to fourfold faster in patients with moderate-to-severe nocturnal hypoxemia than patients with no or mild nocturnal hypoxemia (the mean values [95% confidence intervals] were -2.14 [-1.06 to -3.21], -3.02 [-1.31 to -4.74], and -8.59 [-2.00 to -15.2] ml/min per 1.73 m(2) per year in the no, mild, and moderate-to-severe nocturnal hypoxemia groups, respectively; P=0.003). Nocturnal hypoxemia remained a significant predictor of decline in estimated GFR after adjustment for various baseline clinical factors.
In nonobese patients with CKD, nocturnal hypoxemia is an independent risk factor of a rapid decline in kidney function.
夜间低氧血症在 CKD 患者中非常普遍。夜间低氧血症会导致全身炎症、氧化应激、内皮细胞功能障碍和肾素-血管紧张素系统激活，这些都是 CKD 进展的常见病理机制。本研究旨在探讨夜间低氧血症是否与 CKD 进展有关。
设计、地点、参与者和测量：本项两中心回顾性队列研究纳入了 2009 年 1 月至 2011 年 7 月期间BMI 小于 25.0kg/m2的 161 例 3-4 期 CKD 患者。测量 4%氧减饱和指数（睡眠中氧饱和度下降超过 4%的事件数/小时），并在 1 年内随访估计肾小球滤过率（eGFR）的下降率。夜间低氧血症的严重程度分为无（氧减饱和指数<5.0）、轻度（5.0≤氧减饱和指数<15.0）或中重度（15.0≤氧减饱和指数）。
总队列的基线 eGFR 平均值为 31ml/min/1.73m2。80 例（49.7%）患者被诊断为夜间低氧血症；64 例为轻度夜间低氧血症，16 例为中重度夜间低氧血症。中重度夜间低氧血症患者的 eGFR 下降速度是无或轻度夜间低氧血症患者的 3-4 倍（平均（95%置信区间）分别为-2.14[-1.06 至-3.21]、-3.02[-1.31 至-4.74]和-8.59[-2.00 至-15.2]ml/min/1.73m2/年；P=0.003）。调整各种基线临床因素后，夜间低氧血症仍是 eGFR 下降的独立预测因素。
在非肥胖的 CKD 患者中，夜间低氧血症是肾功能快速下降的独立危险因素。
