IAD seems to be a rare cause of hyponatremia. In one of the larger clinical studies, in a group of 185 patients with severe hyponatremia (< 130 mmol/L) only 28 had secondary adrenal insufficiency, but most of them had also deficiencies of other pituitary hormones [4]. The mechanism of hyponatremia in IAD includes a reduced glomerular filtration rate and ineffective inhibition of vasopressin secretion caused by hypocortisolaemia [2, 5]. Because IAD is not associated with deficiency of aldosterone, the mechanism of salt-wasting is less important [2].
Diagnosis of IADDiagnostic procedures for IAD should start from assessment of morning cortisol concentrations. Results lower than 3.0 µg/dL, accompanied by low ACTH level, are indicative for IAD [2]. When cortisol is in the range 3.0-10.0 µg/dL, dynamic stimulatory tests [with insulin, glucagon, corticotropin-releasing hormone (CRH), or tetracosactide] are recommended [2,3]. It should be stressed that there is also no cortisol response to Synacthen in the secondary adrenal insufficiency if the standard (not extended) test duration is used. In Poland