Hypoaldosteronism is a clinical condition resulting from inadequate stimulation of aIdosterone secretion (hyporeninemic hypoaIdosteronism), defects in adrenal synthesis of
aldosterone (hyperreninemic
hypoaldosteronism), or resistance to the peripheral action of this
hormone (
pseudohypoaldosteronism). The disease is characterized by a wide spectrum of clinical manifestations, ranging from asymptomatic
hyperkalemia to life-threatening volume depletion, and, if unrecognized and untreated, it increases morbidity and mortality rates. In this paper, we report a case of a woman diagnosed with autoimmune polyglandular syndrome type 2. As a consequence of adrenal cortex destruction, the patient developed subclinical
hypoaldosteronism which was effectively treated with small doses of
fludrocortisone. Two and fours years later, she required
ibuprofen and
atenolol treatment and each of these treatments was accompanied by a transient deterioration in
mineralocorticoid activity which resolved after
drug withdrawal. This case shows for the first time that drugs reducing plasma
renin activity may unmask subclinical
hypoaldosteronism in subjects with autoimmune polyglandular syndromes, and that they should be avoided in patients with even small disturbances in the hormonal function of the zona glomerulosa.