Lima Marisa Richard Pontes de Costa, Burdmann Emmanuel A, Cipullo José Paulo
Division of Pneumology, Hospital de Base, São José do Rio Preto Medical School, São José do Rio Preto, São Paulo, Brazil.
Ren Fail. 2005;27(4):373-9.
Chronic obstructive pulmonary disease (COPD) may cause edema independently of cardiac function. This study assessed the effects of oxygen therapy in renal hemodynamics and excretion of sodium and water in COPD patients. Twelve COPD patients without cor pulmonale (PaO2 < or = 60 mmHg), aged 66 +/- 9 years, were studied before and after 72 h of O2 therapy. Oxygen increased PaO2 from 56 +/- 4 to 85 +/- 22 mmHg (p < 0.0001), whereas PaCO2 did not change significantly. Oxygen induced significant increments in glomerular filtration rate (90 +/- 21 to 111 +/- 36 mL/min/1.73 m2, p = 0.03), sodium filtered load (10 +/- 3 to 12 +/- 5 mEq/min, p = 0.004), sodium excreted load (79 +/- 67 to 194 +/- 106 mEq/day, p = 0.0006), fractional excretion of sodium (0.51 +/- 0.49 to 1.30 +/- 1.32%, p = 0.015) diuresis (1048 +/- 548 to 1893 +/- 440 mL/day, p = 0.002), osmolar clearance (1.43 +/- 0.7 to 2.08 +/- 0.6 mOsm/min, p = 0.008) and decreased hematocrit (48 +/- 4 to 44 +/- 3%, p = 0.0038). Renal plasma flow and filtration fraction did not change after oxygen. In summary, use of oxygen caused increases of 36% in GFR, 35% in filtered load of sodium, 118% in diuresis, 258% in excreted load of sodium, and 178% in fractional excretion of sodium. These data suggest that oxygen-induced natriuresis and diuresis were likely more dependent of changes in the tubular manipulation of sodium than in glomerular hemodynamics. These changes occurred with a mild increase in PCO2, showing that oxygen therapy caused renal improvement independently of amelioration of hypercapnia.
慢性阻塞性肺疾病(COPD)可独立于心脏功能导致水肿。本研究评估了氧疗对COPD患者肾脏血流动力学及钠和水排泄的影响。对12例无肺心病(动脉血氧分压[PaO₂]≤60 mmHg)、年龄为66±9岁的COPD患者在氧疗72小时前后进行了研究。吸氧使PaO₂从56±4 mmHg升至85±22 mmHg(p<0.0001),而PaCO₂无显著变化。吸氧使肾小球滤过率显著增加(从90±21增至111±36 mL/min/1.73 m²,p = 0.03)、钠滤过负荷(从10±3增至12±5 mEq/min,p = 0.004)、钠排泄负荷(从79±67增至194±106 mEq/天,p = 0.0006)、钠分数排泄(从0.51±0.49增至1.30±1.32%,p = 0.015)、利尿(从1048±548增至1893±440 mL/天,p = 0.002)、渗透清除率(从1.43±0.7增至2.08±0.6 mOsm/min,p = 0.008),并使血细胞比容降低(从48±4降至44±3%,p = 0.0038)。吸氧后肾血浆流量和滤过分数未改变。总之,吸氧使肾小球滤过率增加36%、钠滤过负荷增加35%、利尿增加118%、钠排泄负荷增加258%、钠分数排泄增加178%。这些数据表明,氧诱导的利钠和利尿可能更多地依赖于肾小管对钠处理方式的改变而非肾小球血流动力学的改变。这些变化发生在二氧化碳分压轻度升高的情况下,表明氧疗可独立于高碳酸血症的改善而使肾脏功能得到改善。