Studies on the Mechanism of Hyponatremia and Impaired Water Excretion in Myxedema

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Abstract
An inability to normally excrete a water load in primary myxedema has been previously described, but the underlying mechanism has not been clearly delineated. The authors have studied a patient with myxedema, following treatment with radioactive iodine, in whom severe hyponatremia and marked impairment in the excretion of both acute and chronic water loads existed. The patient was studied for 33 days under modified metabolic conditions. Early in the study, while severe hyponatremia and serum hypotonicity were present, significant quantities of sodium were excreted in a hyper-tonic urine. The blood urea nitrogen and serum creatinine concentrations were normal, although creatinine clearance was moderately depressed. Following the institution of a regimen of fluid restriction on a constant sodium intake serum tonicity and sodium concentration rose to normal while urinary sodium excretion fell. Three acute studies were performed. In response to the administration of 20 ml/kg of water by mouth there was a slight increase in urine flow and transient urinary dilution. The administration of ethyl alcohol resulted in a prompt fall in urine osmolality from levels which were hypertonic to serum while hyponatremia was present. During the administration of an acute sustained water load the urine osmolality fell initially to hypotonic levels during which some free water clearance occurred; however, this was followed by an abrupt rise in urine osmolality to hypertonic levels despite persistent serum hypotonicity. There were no consistent alterations in creatinine clearance, total solute excretion, and sodium excretion which could explain the alterations in urine tonicity in the above studies. Following the administration of tri-iodothyronine there was a decrease in serum cholesterol level, and hyponatremia could not be reproduced following the administration of 24-hour water loads which previously had resulted in severe hyponatremia. The data are compatible with the hypothesis that an inability to adequately inhibit the secretion of anti-diuretic hormone in response to plasma hypotonicity may be contributory to the patient''s abnormality in water metabolism.