A 47-year-old woman is evaluated for difficult-to-control hypertension. She was previously treated for hypokalemia.

On physical examination, temperature is 36.0 °C (96.8 °F), blood pressure is 178/100 mm Hg, pulse rate is 58/min, respiration rate is 16/min, and BMI is 29. No abdominal bruit is detected. Funduscopic examination shows mild arteriolar narrowing.

Laboratory studies:
Electrolytes
Sodium
143 meq/L (143 mmol/L)
Potassium
3.5 meq/L (3.5 mmol/L) (after replacement therapy)
Chloride
101 meq/L (101 mmol/L)
Bicarbonate
33 meq/L (33 mmol/L)
Aldosterone
Baseline
23 ng/dL (635 pmol/L)
3 Days after high salt intake
15 ng/dL (414 pmol/L)
Renin activity
Baseline
3 Days after high salt intake
Aldosterone to renin activity ratio
>50

Which of the following is the most appropriate next step in management?

Correct

Answer and Critique (Correct Answer: C)

Educational Objective:Manage primary hyperaldosteronism.

Key Point

  • Primary hyperaldosteronism is characterized by an elevated serum aldosterone level that is not suppressed by high salt intake and is associated with suppressed plasma renin activity; the anatomic/pathologic cause of the disease is determined by a CT scan.

The most appropriate next step is CT of the patient’s adrenal glands, with and without contrast. This patient has severe and difficult-to-control hypertension associated with laboratory findings characteristic of primary hyperaldosteronism. She had spontaneous, unprovoked hypokalemia and has metabolic alkalosis. The evaluation of unexplained hypertension and unprovoked hypokalemia begins with measurement of the plasma renin activity and aldosterone level. A serum aldosterone to plasma renin activity ratio greater than 20 and a serum aldosterone level greater than 15 ng/dL (414 pmol/L) strongly suggest primary hyperaldosteronism. On follow-up testing, the patient has an elevated serum aldosterone level that was not suppressed by high salt intake; plasma renin activity was suppressed. These are the biochemical features of primary hyperaldosteronism. After hyperaldosteronism is confirmed, a search for the anatomic or pathologic cause should begin. CT of the adrenal glands is the appropriate initial step in identifying the anatomic cause of the disease.

Aldosterone-producing adenomas respond to unilateral adrenalectomy. Within the first postoperative year, 67% of patients are normotensive and 90% are normokalemic. Medical therapy is the treatment of choice for adrenal hyperplasia. Neither partial nor complete adrenalectomy is indicated, however, until the anatomic and pathologic features have been defined by a CT scan.

Although bilateral adrenal vein catheterization and sampling can be helpful in defining the source of excessive aldosterone secretion (unilateral versus bilateral), the procedure is invasive, is technically difficult, and should not be performed before a CT scan is obtained.

Duplex ultrasonography of the renal arteries is used to investigate the possibility of renal artery stenosis. Such testing is not indicated in this patient, nor would it be helpful. The biochemical features of her case (suppressed plasma renin activity but elevated serum aldosterone level) practically rule out the possibility of renal artery stenosis.

Bibliography

  • Funder JW, Carey RM, Fardella C, et al; Endocrine Society. Case detection, diagnosis, and treatment of patients with primary aldosteronism: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2008;93(9):3266-3281. [PMID:18552288] - See PubMed
Incorrect

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