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Renal and hormonal abnormalities, usually manifested as oedema or hyponatraemia, are encountered frequently in patients with chronic obstructive pulmonary disease (COPD). The exact incidence of clinically significant oedema and hyponatraemia has not been documented. In advanced disease some degree of oedema is observed in a large proportion of patients; the pattern of hyponatraemia parallels that of oedema, but with a lower frequency. In the past, oedema in patients with COPD has been attributed to “cor pulmonale with backward heart failure”—that is, pulmonary hypertension induced by hypoxia and by structural changes in pulmonary arteries, increased systemic venous pressure, and reduced cardiac output. The onset of oedema is a poor prognostic factor; Renzetti and coworkers1 reported a four year mortality rate of 73% in patients with cor pulmonale compared with 53% for the whole group. Whether this reflects the advanced stage of the disease, the indirect effect of chronic diuretic therapy, or some undetermined insult on the function of critical organs is unclear. What is clear is that oedema formation in COPD is not cardiac in origin: in most patients, even when they are frankly oedematous, cardiac output is adequate for the body’s metabolic demands2 3 unless there is significant co-existent cardiac disease.
In 1960 Campbell and Short4 pointed out that, in patients with COPD, oedema is almost invariably associated with carbon dioxide (CO2) retention. They concluded that, in hypoxaemic normocapnic patients with chronic diffuse lung disease such as pulmonary fibrosis, oedema is uncommon and, in this setting, transient worsening in blood gas tensions during exercise or sleep, for example, should be suspected and ruled out. Since then sodium (Na+) retention in COPD has been considered to be the result of electrochemical imbalance (enhanced renal tubular H+/Na+ exchange with attendant increase in Na+ …
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