Endocrine Abstracts

Clinical Case: A hypertensive 60-year-old woman with nephroangiosclerotic stage IV chronic renal failure (eGFR 23.44 ml/min/1.73 m²) was referred to our hypertension clinic after the CT finding of a 26-mm left adrenal mass with adenoma density during hypertension workup, with normal right adrenal. Physical exam was unremarkable except for BP 167/98 mmHg. Plasma aldosterone was 353 ng/ml, PRA 1.3 ng/ml/h, ratio 90.2, K⁺3.1 mEq/l, and metanephrines were normal. Primary aldosteronism was confirmed by standard captopril test. Adrenal vein sampling showed full left lateralization of aldosterone secretion. The patient underwent laparoscopic adrenectomy, and a 21-g left adrenal -including a 4-cm adenoma with clean margins- was removed. One month after surgery, K⁺, aldosterone and ARP were normal, and BP was controlled with manidipine 20 mg.

One year later, BP and plasma K⁺ were still controlled but the patient showed again a pattern of primary aldosteronism with aldosterone 747 ng/ml, PRA 0.9 ng/ml/h, ratio 83.0. A new CT showed absent left adrenal, and a 17×11 mm mass in the right adrenal, with adenoma density. Low-dose (12.5 mg) spironolactone was added to the treatment, but surgery was deferred.

Diagnosis: Primary aldosteronism caused by aldosterone-producing adenoma (Litynski–Conn syndrome), with contralateral recurrence after one year. Secondary hypertension with nephroangiosclerotic stage IV chronic renal failure.

Commentary: Contralateral recurrence of an aldosterone-producing adenoma in a previously normal adrenal after a complete surgical removal is exceedingly rare, particularly after such a short follow-up. The differential diagnosis would include familial type II aldosteronism (as types I and III usually cause severe hypertension in the pediatric age and associate normal or bilaterally hyperplastic adrenals but not adenomas, while type II may associate adenomas in adult patients) but as there is no known genetic marker for this condition, confirmation is not possible at this point.