Water and sodium imbalance in COPD patients.

Water retention and hyponatraemia are typically observed in the final stages of Chronic Obstructive Pulmonary Disease (COPD) and the onset of edema is a poor prognostic factor. For several years the pathogenesis of edema in COPD patients was attributed to heart impairment because of pulmonary hypertension, but the evidence that cardiac output is often adequate for the metabolic demands has suggested, since 1960, that the pathogenesis of edema in these patients would be correlated with gas exchange impairment and in particular with carbon dioxide (CO2) retention. The gas exchange impairment induces, in these patients several hormonal abnormalities: renin (Rn), angiotensin II (AnII), aldosterone (Ald), atrial natriuretic peptide (ANP), vasopressin (ADH) and endothelial factors are some of the factors involved. The systemic response to hypercapnia has the effect of reducing the renal blood flow and, as a result, increasing water and sodium retention with the final effect of edema and hyponatraemia. The aim of this brief review is to highlight the current knowledge on renal/hormonal abnormalities in COPD and their therapeutic implications.