CASE 2 Hypertension And Hypokalemia Case Description

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A 45-yr-old male presented for evaluation of hypertension. The patient first came to medical attention 30 yr ago when he was noted to be hypertensive at age 14. This was discovered in high school during a routine physical exam where he was found to have a blood pressure of approximately 190/95 mmHg. A physical exam was performed and no abnormalities were noted except for obesity (body mass index = 34 kg/m2). An electrocardiogram (EKG), basic electrolytes (including potassium), creatinine, and urinalysis were also noted to be normal. A 24-h urine collection for catecholamine excretion was normal. His hypertension was attributed to obesity, and he was instructed to start a weight loss and exercise program; hydrochlorothiazide was started. At age 19, his blood pressure was 170/90 mmHg while on therapy. An intravenous pyelogram (IVP) and nephrogram was performed, but no renal abnormalities were identified. He had lost 25 lbs and his blood pressure was moderately improved; his medication was changed to propranolol. He continued on this medication for the next 15 yr with only moderate control of his hypertension (140-160/85-100 mmHg); he also complained of frequent headaches.

At age 40, he was seen by a new physician for worsening blood pressure control on propranolol treatment. His exam was notable for obesity, but no other abnormalities were identified. He was specifically noted not to be Cushingoid, and no abdominal bruits could be appreciated. However, he was found to be hypokalemic (3.0 mmol/L), and was started on potassium replacement (80 mmoL/d). His blood pressure was now noted to be 200/ 100 mmHg. He denied any excess licorice ingestion.

His past medical history was otherwise notable for peptic ulcer disease, spastic colitis, frequent headaches, and a transient (5 min) episode of left-sided weakness at age 20 that spontaneously resolved. His family history was notable for a maternal grandmother who had hypertension and died of a cerebral hemorrhage at age 66. His mother also had hypertension, as did eight maternal uncles and aunts (all diagnosed in adulthood). He has one brother, 5 yr younger, who had started treatment for hypertension at age 23.

Given the strong family history of hypertension, young age of onset, and appearance of hypokalemia, his physician pursued testing for secondary causes of his hypertension. Twenty-four-hour urine collections for catecholamine and cortisol excretion were normal. Random plasma aldosterone (PA) and plasma renin activity (PRA) levels revealed values of 37.1 ng/dL (normal = 3.0-35.0 ng/dL, normal salt diet) and <0.1 ng/mL/h (normal upright value = 0.4-8.8 ng/mL/h, normal salt diet), respectively. Given these data, a diagnosis of primary hyperaldosteronism was made. He was started on spironolactone 50 mg daily, but additionally required labetalol and losartan for blood pressure conrol. Later, his dose of spironolactone was increased to 200 mg daily. A CT scan with 5-mm slices of the adrenal glands showed no evidence of an adenoma, and was reported as normal. Given the patient's extensive family history of early-onset hypertension, it was thought he may suffer from glucocorticoid-remediable aldosteronism (GRA). However, a blood sample for the chimeric gene duplication characteristic of GRA was negative. He was, therefore, diagnosed with bilateral, idiopathic adrenal hyperplasia as a cause for primary hyperaldosteronism. The patient pursued a second opinion, and was referred to another physician who performed further testing.

To confirm the diagnosis of primary hyperaldosteronism, the patient was asked to undergo a saline suppression test (measurement of aldosterone following administration of two liters 0.9% normal saline over 4 h), which revealed failure of normal aldosterone suppression (aldosterone = 12.0 ng/dL; normal value <5.0 ng/dL). His blood pressure remained poorly controlled on spironolactone, losartan, labetalol, and hydrochlorothiazide. Potassium levels were within normal limits. A repeat CT scan with 1-mm slices revealed bilateral micronodular adrenal glands: two 4-mm nodules were seen in both the right and left adrenal glands, and a 6-mm nodule was seen in the right adrenal gland.

Given the history of early-onset hypertension, hypokalemia, and multiple small, sub-centimeter adrenal nodules seen radiographically, it was felt the exact cause of his hyper-

Table 1

Results of Right and Left Adrenal Vein Sampling with Continuous ACTH Infusion

Table 1

Results of Right and Left Adrenal Vein Sampling with Continuous ACTH Infusion

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