Document Type

Conference Proceeding

Publication Date


Publication Title

J Gen Intern Med


CASE: A 58-year-old man with a past medical history significant for long-standing hypertension, coronary artery disease, cerebrovascular accident, and a 43 pack-year smoking history, who presented to the clinic for evaluation of resistant hypertension. The patient's blood pressure was persistently elevated with systolic above 160 mmHg and diastolic above 100 mmHg despite adherence to 10 mg amlodipine, 40 mg benazepril, and 25 mg chlorthalidone as well as compliance to a low-salt diet. He had no family history of resistant hypertension and denied any illicit drug use. The patient was asymptomatic on presentation. Basic metabolic panel showed normal electrolytes and kidney function, while renal ultrasound showed no sonographic evidence suggesting renal artery stenosis. Metanephrine and normetanephrine levels, random cortisol levels, and thyroid stimulating hormone were within normal limits. Aldosterone level was elevated at 23.7 ng/dL and direct renin level was low at <2.1 pg/mL. The aldosterone to direct renin ratio was 11.3. Given suspicion for primary hyperaldosteronism, the patient underwent saline infusion test and aldosterone was non-suppressed (12.4 ng/dL -measured after saline infusion). Computed tomography of adrenal glands showed a lobulated left adrenal gland with negative Hounsfield units - likely indicating a lipid-rich adenoma. The patient was started on spironolactone and had improvement in blood pressure. However, repeat aldosterone to direct renin ratio remained elevated at 12.8. The patient was referred for adrenal vein sampling for evaluation of a functional left adrenal adenoma.

IMPACT/DISCUSSION: The prevalence of hypertension secondary to primary hyperaldosteronism was thought to account for less than 1% of hypertension etiology. However, some studies have suggested a much higher detection rate with the use of screening tests such as plasma aldosterone/renin activity ratio. (1) Currently, it is recommended that patients with severe hypertension or resistant hypertension undergo testing for endocrine etiologies. However, it is important to promptly test these patients as they frequently present with end-organ damage and cardiovascular events. (2) Although the classic triad of hyperaldosteronism includes hypertension, hypokalemia, and metabolic alkalosis, most patients are actually normokalemic. This case presents a patient who was normokalemic with resistant hypertension. Therefore, it is important to have high clinical suspicion and test these patients early to avoid development of complications.

CONCLUSION: 1. Patients with resistant hypertension should be promptly screened for endocrine hypertension to avoid the development of complications. 2. A normal potassium does not preclude patients from having underlying hyperaldosteronism. 3. Mineralocorticoid receptor antagonists are an effective initial therapeutic option in patients with hyperaldosteronism for both resistant hypertension and hypokalemia if present.



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