A 43-year-old man was evaluated for uncontrolled hypertension (HTN) despite multiple drug therapy, which included amlodipine 10 mg daily, clonidine 0.3 mg BID, and metoprolol XL 200 mg BID. He had several episodes of hypokalemia (2.7-3.0 mmol/L) over the years that persisted despite oral potassium supplementation and discontinuing diuretics.
On examination, he had elevated blood pressure (BP) in both arms (160/110 mm Hg) with a heart rate of 60 beats/minute. Physical examination was otherwise unremarkable. His laboratory tests showed serum potassium (K) of 2.8 mmol/L, serum bicarbonate of 33 mmol/L, and serum creatinine of 1.48 mg/dL with estimated GFR of 55 mL/min/1.73 m2.
Plasma aldosterone (PAC) was 33 ng/dL and plasma renin activity (PRA) was less than 0.1 µg/L/hour. A 24-hour urine collection with salt loading showed urinary potassium wasting (60 mmol) and high aldosterone excretion (42 µg). An adrenal computed tomography scan revealed a low-density 1.5 × 1.2 cm nodule in the left adrenal gland (Figure 1). He was started on eplerenone 100 mg BID, which controlled his BP (123/78 mm Hg on sitting and 122/70 mm Hg on standing). Serum K normalized (4.0 mmol/L) without need for supplementation.
The patient wished to undergo surgery. Adrenal venous sampling showed lateralization to the left (See table).
Surgical pathology after laparoscopic unilateral left adrenalectomy confirmed the diagnosis of adrenocortical adenoma. Eplerenone was stopped post-operatively. Plasma aldosterone decreased to 3.3 ng/dL with a PRA of 0.8 µg/L/hour. Over the next year, his serum potassium remained normal (4.0-5.0 mmol/L) without supplementation and his BP was well-controlled (below 120/80 mm Hg) on amlodipine 10 mg alone.
Resistant HTN is defined as persistent elevation of BP above goal in spite of concurrent use of three anti-hypertensive agents, each of unique class, including a diuretic, with all drugs at maximally tolerated doses. HTN that is controlled with the use of four or more medications is also considered resistant to treatment. It is so defined to identify patients who are more likely to have reversible causes of HTN.
Consultation with a HTN specialist should be considered if goal BP cannot be achieved. Evaluation for secondary causes should be done in patients with resistant HTN, and a high suspicion of primary aldosteronism (1°A) should be entertained in patients with the following clinical history: 1) spontaneous or unprovoked hypokalemia with renal potassium wasting, 2) severe diuretic-induced hypokalemia (potassium 3.0 mEq/L or less), which does not normalize after discontinuation of diuretics for at least four weeks and is unresponsive to angiotensin blockers, 3) hypertension with adrenal adenoma, and 4) family history of 1°A.
The authors are affiliated with the Cleveland Clinic’s Glickman Urological and Kidney Institute
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