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Sodium homeostasis in patients with autonomic failure.

1. The renal excretion of sodium by five patients with autonomic failure (Shy—Drager syndrome) was compared with a matched control group who had normal autonomic reflexes (Parkinson9s disease). For 8 or 9 days the daily sodium intake was reduced to 17 mmol, and for 5 subsequent days it was increased to 189 mmol. 2. The sodium excretion of the patients with autonomic failure was not significantly reduced during 7 days of restricted intake whereas that of the control group fell rapidly to values comparable with their sodium intake. Patients with autonomic failure had a larger fall in body body weight than the control subjects. 3. Both lying and standing values of mean blood pressure fell during salt restriction in the patients with autonomic failure, but not in the control subjects. 4. Values of plasma renin activity (PRA) were significantly depressed in patients with autonomic failure. However, PRA rose to values similar to those of control subjects while standing during the period of restricted sodium intake. At this time the patients with autonomic failure had a large orthostatic fall in blood pressure and creatinine clearance. 5. Aldosterone secretion rates were measured in three patients with autonomic failure at both levels of sodium intake and were considerably lower than the rates found in the control group. 6. A mineralocorticoid drug (9α-fludrocortisone; 2 mg/day), given on the last 2 days of restricted sodium intake, failed to correct fully the negative sodium balance of the patients with autonomic failure, since an excessive sodium excretion persisted during the period of recumbency at night. 7. These results demonstrate a severe defect in renal salt conservation in certain patients with autonomic failure. They suggest that the defect may not be entirely due to deficient secretion of mineralocorticoid hormones.