Based on two patients, we discuss the difficulties in. diagnosing and managing primary aldosteronism in pregnancy which derive from changes of the angiotensin-aldosterone axis, from the uncertainty regarding blood pressure control along gestation and postpartum, and from the contraindication to the use of spironolactone. 717efirst case is a 27 years old woman with a long standing refractory hypertension, a hemorrhagic stroke with left bachial hemiplegia and crural beiniparesia, two miscarriages, one stillbirth and one offspring with intrauterine growth retardation. Due to hypokalemia, a plasma aldosterone/renin activity ratio of 91, and a negative genetic screening for glucocorticoid remediable aldosteronism (GRA), a primary hyperaldosteronism with, normal adrenals in CT scan was diagnosed, and good blood pressure control was attained with spironolactone. After two and a half years of normotension, a fifth pregnancy, managed with methyldopa evolved with satisfactory blood pressures, plasma potassium, fetal growth, uterine and umbilical arterial resistance indexes, and maternal endothelial function. At 37 112 weeks of pregnancy the patient delivered a healthy newborn weighing 2,960 g. Blood pressure rose during the 48 hours of postpartum in the absence of proteinuria and required iv hydralazine. The second patient is a 3 7 years old woman, with known refractory hypertension for 7 years, hypoalemia, plasma aldosterone/renin activity ratio greater than 40, normal adrenals in the CAT scan, mid a negative genetic screening for GRA. She bad normotensive Pregnancies 5 and 3 years prior to the detection of hypertension, with hypertensive crisis in both postpartum periods, retrospectively considered as expressions of primary hyperaldosteronism.