This patient’s presentation is consistent with primary hyperaldosteronism (Conn’s syndrome) due to a benign adenoma in the zona glomerulosa layer of the adrenal cortex. Hypertension and low plasma renin activity are characteristic findings of this condition.
Primary hyperaldosteronism is characterized by hypertension, decreased plasma renin activity, muscle weakness, tetany, hypokalemia, and metabolic alkalosis. Benign adenoma in the zona glomerulosa layer of the adrenal cortex is the most common cause. Autonomous secretion of excess aldosterone leads to bicarbonate retention (metabolic alkalosis), potassium wasting (hypokalemia), and sodium / water retention (hypernatremia and hypertension). Renin activity is suppressed in the setting of aldosterone excess.
Viera et al describe the approach to hyperaldosteronism: “In middle-aged adults, aldosteronism is the most common secondary cause of hypertension, and the recommended initial diagnostic test is an aldosterone / renin ratio. If the aldosterone/renin ratio is above 20, and is accompanied by an aldosterone level above 15 ng per dL, the patient should be referred to an endocrinologist for confirmatory testing with one of several salt suppression tests.”
Sukor reviews the management of primary hyperaldosteronism: “The detection of primary aldosteronism is of utmost importance not only because it provides an opportunity for a targeted treatment, but also because it has been demonstrated that patients with primary aldosteronism are more prone to cardiovascular events and target organ damage than essential hypertensives. Normalization of circulating aldosterone or mineralocorticoid blockade is necessary to prevent aldosterone-induced tissue damage that occurs independent of blood pressure.”
Figure A shows an axial CT image with a hypodense fat-containing mass (arrow) in the right adrenal consistent with an adrenal adenoma. Illustration A depicts a flow chart of the diagnosis and management of primary hyperaldosteronism.
Answer 1: Primary hyperaldosteronism is characterized by low plasma renin activity.
Answer 2: Deficiency of the 21-hydroxylase enzyme would reduce adrenal production of mineralocorticoids (aldosterone) and glucocorticoids, shunting precursors instead towards increased androgen production.
Answer 3: Hypertension, not hypotension, would be expected in a state of aldosterone excess.
Answer 5: Decreased excretion of sodium would be anticipated in the setting of increased aldosterone; hypernatremia is a rare finding but is consistent with hyperaldosteronism.
Viera AJ, Neutze DM. Diagnosis of secondary hypertension: an age-based approach. Am Fam Physician. 2010 Dec 15;82(12):1471-8.
Sukor N. Primary aldosteronism: from bench to bedside. Endocrine. 2012 Feb;41(1):31-9. Epub 2011 Nov 1.
PMID:21166367 (Link to Abstract)