Oxygen therapy improves renal function in patients with chronic obstructive pulmonary disease
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 +/-...
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Veröffentlicht in: | Renal failure 2005-01, Vol.27 (4), p.373-379 |
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Zusammenfassung: | 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. |
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ISSN: | 0886-022X 1525-6049 |
DOI: | 10.1081/JDI-200065279 |