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Aldosterone facilitates the exchange of sodium for potassium in the distal nephron and plays a key role in the regulation of the body's fluid and electrolyte composition. The secretion of aldosterone from the adrenal cortex is normally determined by the renin-angiotensin system in response to changes in the

Figure 8-3. A 70-year-old woman with chronic severe hypertension and hypokalemia. Workup showed a serum aldosterone level of 24, a renin activity level of 0.27, and a ratio of 88. A thin-cut computed tomographic scan showed a 1.8 cm left adrenal tumor (arrow) and a normal right adrenal gland. A, She underwent a laparoscopic left adrenalectomy. Pathology showed adrenal cortical adenoma and nodular adrenal cortical hyperplasia. B, Her hypertension improved after the operation with fewer medications required.

Figure 8-3. A 70-year-old woman with chronic severe hypertension and hypokalemia. Workup showed a serum aldosterone level of 24, a renin activity level of 0.27, and a ratio of 88. A thin-cut computed tomographic scan showed a 1.8 cm left adrenal tumor (arrow) and a normal right adrenal gland. A, She underwent a laparoscopic left adrenalectomy. Pathology showed adrenal cortical adenoma and nodular adrenal cortical hyperplasia. B, Her hypertension improved after the operation with fewer medications required.

body's serum sodium concentration. Hypersecretion of aldosterone leads to decreased serum potassium levels, increased body sodium, and resultant hypertension. Through negative feedback, it also lowers renin production from the kidneys. The biochemical hallmarks of primary hyperaldosteronism are hypokalemia, elevated plasma aldosterone, and low plasma renin activity. Secondary hyperaldostero-nism is characterized by elevated plasma renin activity in response to an extra-adrenal stimulus for min-eralocorticoid secretion and is usually seen in the setting of renal vascular disease or in patients treated with certain antihypertensive medications.2

Primary hyperaldosteronism should be suspected in patients presenting with hypertension and hypokalemia (potassium < 3.2 mg/dL). In most cases, the diagnosis of primary hyperaldosteronism is delayed for months to years, and these patients will usually be taking one or more antihypertensive med-ications.1,2 Because some of these medications (diuretics, angiotensin-converting enzyme inhibitors) may affect the renin-angiotensin system, patients undergoing workup for primary hyperaldosteronism should

stop their antihypertensive medications for at least 2 weeks prior to biochemical testing. This is usually not dangerous as malignant hypertension is rare in these patients. The finding of elevated plasma aldosterone and decreased plasma renin activity in a hypertensive patient with hypokalemia is highly suggestive of primary hyperaldosteronism; a plasma aldosterone-to-plasma renin activity ratio of greater than 30 to 1 is considered by many to be diagnostic for this disease. Hypokalemia following a sodium challenge (1 g sodium chloride with meals for 4 days) is also characteristic of primary hyperaldosteronism.1

Differentiating between solitary adenoma and bilateral adrenal hyperplasia in patients with primary hyperaldosteronism is of utmost importance because adenomas are generally responsive to surgical treatment, whereas hyperplasia is best managed medically (Figure 8-4).8 In previous decades, endocrinologists relied on various stimulatory tests to differentiate between adenoma and hyperplasia; adenomas tend to secrete aldosterone autonomously, whereas hyperplasias appear to retain normal control by the renin-angiotensin system. The most com monly used stimulatory test is the measurement of plasma aldosterone levels in response to postural change.9 In this test, the plasma aldosterone level is first measured while the patient is in the supine position; the plasma aldosterone is then measured again after the patient has been upright for 4 hours. In patients with hyperplasia, the plasma aldosterone level will typically increase after standing because of the normal renin-angiotensin system control, whereas patients with an aldosterone-secreting adenoma will exhibit a paradoxical decrease or no change in plasma aldosterone level because the tumor is autonomously functioning. Despite the widespread use of postural stimulation studies in past decades, this test unfortunately results in a high false-negative rate in patients with adenomas (from 15 to 40% in various reports) and thus cannot be relied on as the single diagnostic test for differentiating between hyperplasia and adenomas in patients with primary hyperaldosteronism. Improved localization studies within the past decade have facilitated the identification of adrenal tumors and have reduced the role of stimulatory biochemical testing in the differentiation between adenomas and hyper-plasia in patients with primary hyperaldosteronism.

All patients who are diagnosed with primary hyperaldosteronism on the basis of biochemical tests should undergo a localization study to distinguish between adrenal adenoma and hyperplasia. High-resolution (3 mm sections) abdominal CT scanning is the initial localization study of choice (see Figures 8-1 to 8-4).3 The sensitivity of CT in identifying adrenal adenomas in patients with primary hyperaldosteronism ranges from 82 to 97%. The typical appearance of an aldosteronoma on CT scan is a unilateral, homogeneous tumor measuring between 0.5 and 2 cm in diameter. Although CT is highly sensitive for identifying adrenal adenomas, it cannot be used alone to diagnose hyperplasia. Patients with bilateral adrenal tumors identified on CT, as well as those with no enlargement of their adrenal glands, should undergo further localization studies. We recommend the measurement of plasma aldosterone levels via selective adrenal vein catheterization to differentiate bilateral hyperplasia from a small unilateral adenoma in patients with negative or equivocal CT scans.1011 Cortisol must be measured concurrently with aldosterone during the adrenal venous sampling to correct for the position of the catheter. Other authors have recommended the use of the NP-59 (iodomethylnorcho-lesterol) scan, which is an adrenal isotope scan using radiolabeled iodine.3 Prior to undergoing NP-59 scanning, patients require suppression of the normal adrenal cortex with dexamethasone as well as thyroid blockade to prevent iodine uptake in the thyroid gland. Because the accuracy of NP-59 is lower for adenomas smaller than 1 cm in diameter, it is considered to be less useful in patients who have a negative abdominal CT scan.

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