A 39-year-old man is evaluated in the office for a 6-year history of difficult-to-control hypertension. Initially, he was treated with hydrochlorothiazide, but within 1 week, he developed profound muscle weakness; follow-up potassium concentration was 2.1 meq/L. Hydrochlorothiazide was discontinued, and he has not been on a diuretic for 6 years. He has struggled with obesity throughout his life and has a 7-year history of type 2 diabetes mellitus. His current medications are lisinopril, diltiazem, pravastatin, metformin, glipizide, and aspirin.
On physical examination, his blood pressure is 189/92 mm Hg, heart rate is 87/min, and BMI is 32.8. There is no jugular venous distention, and his lungs are clear. Cardiac examination reveals an S4. He has no edema.
Sodium 141 meq/L
Potassium 3.1 meq/L
Chloride 104 meq/L
Bicarbonate 33 meq/L
BUN 11 mg/dL
Creatinine 0.9 mg/dL
24 hour urine:
Sodium 90 meq
Potassium 57 meq
Free cortisol 36 µg/24 h (normal <55 µg/24 h)
Which of the following is the most likely cause of this patient's hypertension?
A Cushing's syndrome
B Essential hypertension
E Renovascular hypertension
* The diagnosis of primary hyperaldosteronism is made by showing increased autonomous aldosterone synthesis with suppression of the renin-angiotensin system.
* Primary hyperaldosteronism is diagnosed in as many as 50% of patients with unprovoked hypokalemia.
Answer and Critique (Correct Answer = C)
This hypertensive patient has unprovoked hypokalemia, and his high urine potassium level indicates excessive renal potassium losses (in the presence of ongoing hypokalemia, a urine potassium concentration >30 meq/24 h identifies excessive renal potassium loss). These findings make hyperaldosteronism the most likely diagnosis listed. Hyperaldosteronism is included in the differential diagnosis of hypertension and hypokalemia. Unprovoked hypokalemia is highly suggestive of hyperaldosteronism—primary hyperaldosteronism has been identified in as many as 50% of patients with unprovoked hypokalemia. Severe hypokalemia following administration of a non–potassium sparing diuretic also is suggestive of hyperaldosteronism. Some patients with primary hyperaldosteronism are persistently normokalemic; thus, screening is also indicated in patients with early-onset, severe hypertension or resistant hypertension.
The diagnosis of primary hyperaldosteronism is made by showing increased autonomous aldosterone synthesis with suppression of the renin-angiotensin system. Although this test can be performed under random conditions, accuracy is increased if the sample is obtained after hypokalemia has been corrected and, preferably, in the absence of drugs that alter the renin-aldosterone axis, such as spironolactone (the effects of spironolactone can last 2 to 3 weeks), other diuretics, β-blockers, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin receptor blockers (ARBs). For a diagnosis of primary hyperaldosteronism, the plasma aldosterone concentration should be >15 ng/dL and plasma renin activity should be <1.0 ng/mL/h.
Cushing's syndrome is a reasonable consideration for a patient with difficult-to-control hypertension, obesity, and diabetes. However, this patient's 24-hour urine free cortisol is normal, ruling out Cushing's syndrome. Essential hypertension is not associated with hypokalemia, renal potassium wasting, or metabolic alkalosis. These findings more strongly suggest hyperaldosteronism. Pheochromocytoma is a very rare neoplasm that is associated with paroxysmal or sustained hypertension; however, pheochromocytoma is not associated with hypokalemia, renal potassium wasting, or metabolic alkalosis, making pheochromocytoma unlikely in this patient. Renovascular hypertension is often associated with older age and signs of other peripheral vascular disease, such as carotid bruits, claudication, diminished pulses, and coronary artery disease. Although the physical examination may be normal in patients with renovascular hypertension, the presence of abdominal, femoral, or carotid bruits increases its pretest probability. Atherosclerotic renovascular disease may be associated with renal impairment (which may worsen with ACE inhibitor or ARB therapy), which is absent in this patient. Finally, renovascular hypertension is not associated with hypokalemia, renal potassium wasting, or metabolic alkalosis.
1. Bornstein SR, Stratakis CA, Chrousos GP. Adrenocortical tumors: recent advances in basic concepts and clinical management. Ann Intern Med. 1999;130:759-71. [PMID: 10357696] [PubMed]
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