The Role of Adrenocorticoids in the Inappropriate Antidiuretic Hormone Syndrome

Abstract

The effects of dexamethasone, 9a-fluorohydrocortisone, and spironolactone on serum and urinary Na were determined in 20 patients with the inappropriate ADH syndrome due to chest lesions (8), central nervous system lesions (8), or idiopathic etiology (3). By bioassay, 6/10 had increased ADH in serum and 1/3 in tumor extracts. Impaired excretion of 4 - 38% of a 20 ml/kg water load in 4 hrs. with a minimum urine osmolality of 308 - 889 mOsm/kg was seen in 8/10 and corrected in 4/5 with intravenous diphenylhydantoin. In contrast to 6 patients with hypopituitarism and hyponatremia, these patients failed to correct their hyponatremia with glucocorticoids (dexamethasone, 8 [mu]g/day x 3 - 5 days). Creatinine clearance and aldosterone excretion (4 - 24 [mu]g/day) were usually normal and showed no correlation with urine Na excretion. Spironolactone (200 mg/day) caused a rise in urine Na and osmolality, and a fall in serum Na and osmolality. Fluorohydrocortisone (2 mg/day x 7-10 days) reduced urine Na and osmolality, and increased weight, serum Na and osmolality. Glucocorticoids neither improve water clearance (as in hypopituitarism) nor suppress the activity of increased ADH in this syndrome; also the appropriate response to aldosterone antagonists and mineralo-corticoids with generally normal creatinine suggests that the continued urine Na loss in this disorder is due to some factor other than increased GFR [glomerular filtration rate] or aldosterone inhibition.