Case Presentation: A 69-year-old man with prior right adrenalectomy for primary hyperaldosteronism presents with lightheadedness, resistant hypertension, and hypokalemia.He had been diagnosed with primary hyperaldosteronism several years prior following workup for resistant hypertension, chronic hypokalemia, and orthostasis. At that time, he was found to have an elevated aldosterone level associated with suppressed renin and normal serum metanephrines and normetanephrines. A CT abdomen demonstrated left sided adrenal nodule and a normal right adrenal gland. Adrenal vein sampling found aldosterone levels elevated to 211 ng/dL from the right adrenal and reduced to <1 ng/dL from the left adrenal. Total right adrenalectomy was performed, and histopathology confirmed focal hyperplastic changes in the zona glomerulosa consistent with hyperaldosteronism.The patient recovered after surgery without complications but was found to have persistent hypertension (SBP’s to the 140s-160s) and hypokalemia (potassium of 2.6) requiring substantial potassium replacement. Plasma aldosterone and renin concentration were remeasured and remained elevated at 110 ng/dL and decreased at <0.167 ng/ml/hr respectively.The patient was restarted on eplerenone in addition to other antihypertensives with plan to reduce potassium replacement. He currently has no symptoms related to his hyperaldosteronism and is awaiting further workup for continued hyperaldosteronism.
Discussion: In this case, the patient had a convincing picture for adrenal hyperplasia leading to hyperaldosteronism. Adrenal vein sampling, considered the gold standard test to distinguish unilateral versus bilateral disease, localized the excess production of aldosterone to the right adrenal. This is discordant with CT imaging that found a left adrenal nodule but no abnormality of the right adrenal. However, previous studies have also found poor correlation between imaging findings and adrenal vein sampling results. After the right adrenal was identified as the source of excess aldosterone production, surgical management was pursued, which failed to correct the hyperaldosteronism. While adrenalectomy has been found to clinically improve hypertension and hypokalemia in only 30-60% of cases, it almost always reduces aldosterone levels. The question arises as to why this patient continued to have elevated aldosterone after adrenalectomy. The patient most likely had underlying bilateral disease that was masked by more dominant aldosterone secretion from the right adrenal gland. In this case, resection of the right adrenal released inhibition of the left. If the left adrenal was also hyperplastic, as suggested by the nodule found on imaging, it would also secrete aldosterone in excess when disinhibited. The effect of the surgery essentially was to interchange one hyperactive adrenal for another.
Conclusions: Unilateral and bilateral disease in hyperaldosteronism may be difficult to distinguish even in the setting of unequivocal adrenal vein sampling, due to the possibility of suppression of one adrenal gland by the other.