Impaired renal tubular reabsorption of sodium in hypothyroid man.

The renal response to acute salt loading and to stimuli for rapid sodium conservation was studied in 14 patients with untreated myxedema and in 13 euthyroid control subjects in balance on a 155 mEq. sodium intake. The salt-loading studies reveal urinary excretion of sodium in the myxedema patients within the range of controls despite reductions of 34 per cent in glomerular filtration (p less than 0.001) and 37 per cent in filtered load of sodium (p less than 0.001) in the former group. The capacity to conserve sodium in response to stimuli for rapid sodium conservation [postural change and administration of a supramaximal dose of 9alpha-fluorohydrocortisone (9alpha-F)] was impaired in patients with myxedema. The per cent decrease in sodium excretion during the upright posture in the hypothyroid patients was 28 per cent, less than half that observed in the control subjects, 62 per cent (p less than 0.005). Following administration of 2 mg. of 9 alpha-F the per cent decrease in sodium excretion was less (p less than 0.05) in the hypothyroid patients (50 per cent) than in control subjects (72 per cent). In all studies, baseline sodium excretion was comparable in both groups. Fractional excretion of sodium was significantly increased in the hypothyroid patients prior to (p less than 0.005) and during saline loading (p less than 0.05) and at the time of the subnormal responses to stimuli for acute sodium conservation (p less than 0.05 less than 0.005). Potassium excretion was reduced in the hypothyroid patients, even after 9alpha-F. These observations indicate decreased tubular reabsorption of sodium in myxedema under the experimental conditions described. The findings are most consistent with a role for thyroid hormone in normal sodium reabsorption. That this is not related to mineralocorticoid deficiency is suggested by the impaired sodium reabsorptive response to 9alpha-F.