A Man With Hypokalemia, Sleep Apnea, and Resistant Hypertension

Minh Chung; Eric Warren, DO; Darshan Rola; Brian Zacharias; Jennifer Broyles, MD


July 20, 2022

Primary hyperaldosteronism is defined as an inappropriately elevated aldosterone level despite a low plasma renin level.[5] The excess aldosterone is produced through one of two main mechanisms: an aldosterone-producing adenoma of the right or left adrenal gland or bilateral hyperaldosteronism.[5]

Aldosterone, a product of the renin-angiotensin-aldosterone system in normal physiology, activates mineralocorticoid receptors expressed in various sites throughout the body, including endothelial cells, the hypothalamus, cardiomyocytes, and the kidneys.[5] The renal effect of mineralocorticoid receptor activation by aldosterone is the primary mechanism by which a hyperaldosterone state will lead to hypertension. Aldosterone acts at the distal tubule and cortical collecting duct to reabsorb sodium and water, which expands intravascular volume. This mechanism also drives the urinary secretion of potassium. In addition, aldosterone acts at the H+-ATPase of the alpha-intercalated cell at the cortical collecting duct, which stimulates the renal loss of hydrogen ions.[5]

Screening for primary hyperaldosteronism should be performed in high-risk patients, which includes those with resistant hypertension, hypertension and a family history of early-onset hypertension or a cerebrovascular accident at age younger than 40 years, hypertension and hypokalemia, and/or hypertension with an adrenal mass, according to the 2017 American College of Cardiology (ACC)/American Heart Association (AHA) hypertension guidelines.[6] Screening is widely performed with a serum aldosterone-to-renin ratio. A ratio > 20 is commonly accepted as a positive screening result.[5]

A positive screen warrants referral to an endocrinologist or other hypertension specialist to confirm the diagnosis of primary hyperaldosteronism and, if necessary, to identify the subtype. Confirmatory assessment is performed with the saline infusion test, which expands the intravascular volume. In a patient with normal physiology, volume expansion suppresses endogenous aldosterone production, whereas in a patient with primary hyperaldosteronism, the aldosterone level remains elevated.[5]


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