Sharkey R A, Mulloy E M, Kilgallen I A, O'Neill S J
Department of Respiratory Medicine, Beaumont Hospital, Dublin, Ireland.
Thorax. 1997 May;52(5):411-5. doi: 10.1136/thx.52.5.411.
Renal functional reserve is the normal increase in renal blood flow after a protein load, and reduced or absent renal functional reserve is an early index of renal impairment. Renal blood flow is frequently reduced during acute oedematous exacerbations of chronic obstructive pulmonary disease (COPD). It is possible that patients with severe COPD in the stable state may have a reduced or absent renal functional reserve which could be a factor in oedema formation.
Sixteen stable patients with severe COPD and five normal controls were studied. The mean (SD) arterial oxygen and carbon dioxide tensions (PaO2, PaCO2) and forced expiratory volume in one second (FEV1) of patients with COPD were 8.1 (1.04) kPa, 6.3 (0.69) kPa, and 0.74 (0.27) 1, respectively. The pulsatility index (PI), an index of renovascular resistance, was measured non-invasively by Doppler ultrasonography at baseline and at intervals after a protein load of 250 g steak.
The PI fell after the protein load in the normal subjects from 1.04 (0.19) to 0.84 (0.17), mean difference 0.20, 95% confidence interval of difference (CI) 0.14 to 0.27, p < 0.001. In the COPD group there was no change; baseline PI = 1.04 (0.16), PI after protein load = 1.08 (0.19), mean difference = -0.04, 95% CI-0.11 to 0.04, p = NS. Six of the patients with COPD were normocapnic and 10 were hypercapnic (PaCO2 > or = 6.0 kPa). The normocapnic patients had no significant change in PI (baseline PI = 1.07 (0.15), PI after protein load = 1.01 (0.16), mean difference = 0.06, 95% CI -0.03 to 0.15) while in the hypercapnic patients the PI tended to rise (baseline PI = 1.03 (0.17), PI after protein load = 1.12 (0.21), mean difference = -0.09, 95% CI 0.18 to 0.007, p = 0.06).
Renal haemodynamics were unchanged after a protein load in patients with severe COPD, suggesting that they had no renal functional reserve. This may be a factor in the development of oedema frequently seen in patients with severe COPD, particularly in hypercapnic patients.
肾功储备是蛋白质负荷后肾血流量的正常增加，肾功储备降低或缺乏是肾功能损害的早期指标。在慢性阻塞性肺疾病（COPD）急性水肿加重期，肾血流量常减少。重度稳定期COPD患者可能存在肾功储备降低或缺乏，这可能是水肿形成的一个因素。
研究了16例重度稳定期COPD患者和5名正常对照者。COPD患者的平均（标准差）动脉血氧和二氧化碳分压（PaO2、PaCO2）及一秒用力呼气量（FEV1）分别为8.1（1.04）kPa、6.3（0.69）kPa和0.74（0.27）L。用多普勒超声在基线时和给予250g牛排蛋白质负荷后的不同时间无创测量反映肾血管阻力的搏动指数（PI）。
正常受试者蛋白质负荷后PI从1.04（0.19）降至0.84（0.17），平均差值0.20，差值的95%置信区间（CI）为0.14至0.27，p<0.001。COPD组无变化；基线PI = 1.04（0.16），蛋白质负荷后PI = 1.08（0.19），平均差值=-0.04，95%CI -0.11至0.04，p =无显著性差异。16例COPD患者中6例为正常碳酸血症，10例为高碳酸血症（PaCO2≥6.0kPa）。正常碳酸血症患者PI无显著变化（基线PI = 1.07（0.15），蛋白质负荷后PI = 1.01（0.16），平均差值 = 0.06，95%CI -0.03至0.15），而高碳酸血症患者PI有升高趋势（基线PI = 1.03（0.17），蛋白质负荷后PI = 1.12（0.21），平均差值 = -0.09，95%CI 0.18至0.007，p = 0.06）。
重度COPD患者蛋白质负荷后肾血流动力学无变化，提示他们没有肾功储备。这可能是重度COPD患者尤其是高碳酸血症患者常见水肿发生的一个因素。
