**4. Primary hyperaldosteronism**

Primary hyperaldosteronism rarely has been reported in pregnancy and is most often caused by an adrenal adenoma (Okawa et al., 2002). There are reports of glucocorticoid remediable hyperaldosteronism in pregnancy (Wyckoff et al., 2000). The elevated aldosterone levels found in patients are similar to those in normal pregnant women, but the plasma rennin activity is suppressed. Moderate to severe hypertension is seen in 85%, proteinuria in 52% and hypokalemia in 55%, and symptoms may include headache, malaise, and muscle cramps. Placental abruption and preterm delivery are risks. Progesterone has an antimineralocorticoid effect at the renal tubules, and the hypertension and hypokalemia may ameliorate during pregnancy (Matsumoto et al., 2000).

The physiologic rise in aldosterone during pregnancy overlaps the levels seen in primary aldosteronism, making diagnosis difficult. Suppressed rennin in the setting of hyperaldosteronism, is diagnostic. Salt loading test may be used to diagnose hyperaldosteronism, but there are potential fetal risks and no normative data. If baseline and suppression testing are equivocal, or radiological scanning does not suggest unilateral disease, patients may be treated medically until delivery to allow more definitive investigations. Spironolactone, the usual nonpregnant therapy, is contraindicated in pregnancy as it cross the placenta and is a potent antiandrogenic which can cause ambiguous genitalia in a male fetus. There is no published experienced with the use during pregnancy of eplerenone, the new aldosterone receptor antagonist. Surgical therapy may be delayed until postpartum if hypertension can be controlled with agents safe in pregnancy, such as amiloride, methyldopa, labetolol, and calcium channel blockers. Potassium supplementation may be required, but as noted above, the hypokalemia may ameliorate in pregnancy because of the antikaliuretic effect of progesterone. Both hypertension and hypokalemia may exacerbate postpartum due to removal of the progesterone effect ( Nursan et al., 2009).
