Acute infectious pneumonia is accompanied by a latent vasopressin-dependent impairment of renal water excretion.

The mechanism of hyponatremia associated with pneumonia has not been definitely established. Moreover, renal water excretion was never systematically investigated in cases of pneumonia without hyponatremia. We therefore studied nine consecutive patients breathing spontaneously (nasal oxygen in five), with acute infectious pneumonia and normal plasma sodium concentration. All the patients were previously healthy. Water loads were administered during illness and after recovery. Extracellular fluid volume, arterial blood pressure, PaO2, and PaCO2 were identical during and after pneumonia. By contrast, renal water excretion was markedly impaired during pneumonia and returned to normal values after recovery. This was attested to by a significant decrease in minimum urine osmolality together with significant increases in the percentage of the excreted water load and the maximum free water clearance, after resolution of the pneumonia. Plasma arginine vasopressin values were significantly higher during pneumonia than after recovery despite similar plasma sodium concentrations, both before and after water load. A positive correlation between plasma arginine vasopressin and minimum urine osmolality was found during pneumonia. Thus, impairment in renal water excretion appeared to be due to resetting of the vasopressin osmostat and could not be attributed to any recognized nonosmotic stimulus for vasopressin secretion. On the other hand, these defects varied in severity depending on the extent of the pneumonia and persisted until clearing of alveolar opacities, accounting for their protracted course in some patients. We conclude that water excretion is impaired in most if not in all patients with acute infectious pneumonia (especially if extended), and that the administration of hypotonic solutions should be avoided in these patients.