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Primary Aldosteronism due to Unilateral Adrenal Hyperplasia^*

A. GANGULY, P. G. ZAGER and J. A. LUETSCHER

Endocrine Division, Department of Medicine, Stanford University School of Medicine Stanford, California 94305

Address requests for reprints to: John A. Luetscher, M.D., Endocrine-Hypertension Laboratory, Stanford University Medical Center, Room M-204, Stanford, California 94305.

A 45-yr-old man with hypertension, hypokalemia, low plasma renin, and hyperaldosteronism was studied. Plasma and urine aldosterone were consistently above normal, remaining abnormally high even on a 300-meq sodium intake. Plasma aldosterone had a marked circadian rhythm, which was correlated with plasma cortisol. Aldosterone secretion was temporarily suppressed after dexamethasone administration and was stimulated by exogenous ACTH. The effect of posture was variable in the eight studies performed, possibly due to episodic secretion of aldosterone observed near the sampling times of 0800 and 1200 h. Blood from the right adrenal vein contained 50–100 times more aldosterone than the left adrenal venous samples. The right adrenal gland was excised and found to contain many microscopic subcapsular nests of clear cells. Plasma aldosterone, renin, and potassium returned to normal after surgery, and blood pressure fell to 120/75 over the next 8 months. Three years later, the patient is normotensive without drugs.

^* This work was supported by a research grant from the National Heart, Lung, and Blood Institute (HL-13917).

Supported by NIH Training Grant AM-05021.

Recipient of Research Career Award AM-14176 from the NIAMDD.

Received March 28, 1980.

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