BILATERAL ADRENAL CORTICAL ADENOMAS IN PRIMARY HYPERALDOSTERONISM JASON D. ENGEL, PETER ANGELOS, ROBERT V. REGE, AND RAYMOND J. JOEHL ABSTRACT Bilateral adrenal cortical adenomas in the presence of primary hyperaldosteronism is an extremely rare condition. We present a case of primary hyperaldosteronism in which a unilateral hypersecreting aldoste- rone-producing adenoma coexisted with a large, contralateral adrenal mass ultimately found to be consis- tent with cortical adenoma. Management consisted of total adrenalectomy and enucleation of adenoma from the opposite adrenal. The patient is normotensive 3 years after surgery. Enucleation as a successful approach to hyperfunctioning cortical adenomas is proposed. UROLOGY 52: 711–714, 1998. © 1998, Elsevier Science Inc. All rights reserved. P rimary aldosteronism consists of hypertension, hypokalemia, increased aldosterone produc- tion, and decreased renin secretion. This syndrome accounts for approximately 1 of every 200 cases of hypertension 1 and is caused most commonly by either unilateral aldosterone-producing adenoma (APA) or bilateral adrenocortical hyperplasia/idio- pathic hyperaldosteronism (IHA). Bilateral adeno- mas in the setting of primary aldosteronism are very rare but have been reported. 2–4 Modern diag- nostic approaches can often make the distinction between APA and IHA. This is important because, although the treatment for IHA is medical manage- ment alone, patients with APA are considered sur- gically curable and are treated by either unilateral adrenalectomy or enucleation. We present an in- teresting and rare case of primary hyperaldosteron- ism in which a unilateral hypersecreting aldoster- onoma coexisted with a large, contralateral adrenal mass ultimately found to be consistent with ade- noma. This diagnostic and therapeutic dilemma will also demonstrate simple enucleation of aldo- steronoma as a viable alternative to total adrenal- ectomy. CASE REPORT A 57-year-old man presented to the clinic with poorly controlled, chronic hypertension despite various regimens of antihypertensive medications including triamterene and hydrochlorothiazide (Dyazide), prazosin, verapamil, propranolol hy- drochloride (Inderal), nifedipine, and doxazosin. Physical examination was remarkable only for an average blood pressure of 170/100 mm Hg. Labo- ratory examinations yielded potassium levels of 3.1 to 3.3 mEq/mL. Plasma aldosterone concentra- tion (PAC) was 13.8 ng/dL (normal 1.0 to 16.0). Plasma renin activity (PRA) was 0.1 ng/mL/hr (normal 1.0 to 6.0) yielding a PAC/PRA ratio of 138 (greater than 25 suggests primary aldosteron- ism). Twenty-four hour urine aldosterone on a normal salt diet was 74.6 g (normal 6.0 to 25.0). Intravenous saline infusion failed to suppress plasma aldosterone levels significantly. Upright posture for 90 minutes suppressed plasma aldoste- rone concentration to 11.6 ng/dL. An 18-OH-cor- ticosterone level was 21 ng/dL (normal 9 to 58). A computed tomography (CT) scan was obtained, which showed a 5.0  5.0  4.5-cm right adrenal mass seemingly replacing the entire gland and a 0.8  0.8  0.8-cm left adrenal mass in an other- wise radiographically normal gland (Figs. 1 and 2). The discordance between the postural study and CT (suggesting APA) and 18-OH-corticosterone level (consistent with IHA) did not allow differen- tiation between the two entities at this point. Selec- tive adrenal venous sampling was performed and revealed the following basal aldosterone levels: in- From the Departments of Urology and Surgery, Northwestern University Medical School, Chicago, Illinois and Surgical Ser- vice, Veterans Affairs Chicago Health Care System-Lakeside Di- vision, Chicago, Illinois Reprint requests: Jason D. Engel, M.D., Department of Urol- ogy, Northwestern University Medical School, 300 East Superior Street, Tarry 11-715, Chicago, IL 60611 Submitted: January 12, 1998, accepted (with revisions): April 10, 1998 CASE REPORT © 1998, ELSEVIER SCIENCE INC. 0090-4295/98/$19.00 ALL RIGHTS RESERVED PII S0090-4295(98)00223-4 711