ACR Codes: 86.544
Hyperaldosteronism (aldosteronism) is the second classic endocrine cause of HTN, which can either be primary or secondary. The high concentration of aldosterone causes increased exchange of intratubular sodium for potassium in the distal tubules in the nephrons causing a progressive decrease in potassium concentration and increased sodium retention. Sodium balance is ultimately achieved with relative hypervolemia despite continued hyperaldosteronism. Therefore, these patients have increased volume and decreased measured plasma renin.
Primary aldosteronism can be from aldosterone producing adenomas, also termed Conn's syndrome. Approximately 80 percent of patients with Conn's syndrome have a unilateral adrenal cortical adenoma, located twice as frequently on the right as on the left, which rarely exceeds 4 cm in diameter. It is the most common cause of primary hyperaldosteronism and is diagnosed most commonly in patients 20 to 50 years of age. Primary aldosteronism can also be from idiopathic bilateral hyperaldosteronism. This is the second most common cause of primary aldosteronism in adults and the most common cause in children. Other types of primary aldosteronism include glucocorticoid-suppressible hyperaldosternism and aldosterone producing adrenocortical carcinoma. Secondary hyperaldosteronism in hypertensives can be due to either a primary overproduction of renin (primary reninism) or to an overproduction of renin secondary to a decrease in renal blood flow, which is the most common cause of secondary hyperaldosteronism.
Plasma renin activity (PRA) is suppressed in almost all patients with untreated primary hyperaldosteronism. In this patient the PRA was decreased and the aldo/PRA ratio was determined to be 360. This is an elevated ratio, which points towards hyperaldosteronism. The next step for these patients involves measurement of plasma and urine aldosterone level after salt loading. In primary hyperaldosteronism, there will be an increased level of aldosterone, which will not suppress in response to salt loading. In summary, patients with high aldosterone, low plasma renin activity, low plasma potassium, and kaliuresis have primary aldosteronism.
The presence and location of an adenoma may be confirmed by arteriography or venography and adrenal venous sampling. However, because CT is easy to perform, noninvasive, and greater than 80 percent accurate even in the detection of small (0.5 cm) adenomas, it has replaced more invasive techniques. To detect tiny adrenal nodules, 1.5 to 3 mm contiguous CT scan through the entire adrenal gland must be performed. The right adrenal gland is located just dorsal to the inferior vena cava at the level of its intra- and extrahepatic portions. Retroperitoneal fat separates the medial margin of the liver from the right adrenal gland. Most right adrenal glands are positioned 1 to 2 cm superior to the upper pole of the right kidney and course parallel to the crus of the diaphragm.
Interpretation of adrenal appearances on cross-sectional imaging is best done in conjunction with information from biochemical studies. On CT scan, aldosteronomas can appear homogenous and have an attenuation value similar to that of other solid organs, or they may have low CT attenuation values, because they can contain as much as 5.1 percent lipid. Less frequently, aldosteronomas contain calcium and thus have CT high attenuation values. Intravenous administration of contrast material usually does not greatly enhance the aldosteronoma, but contrast may make the lesion more apparent because of enhancement of normal adrenal tissue. In more than 90 percent of cases, CT can distinguish aldosterone-producing adenoma from hyperplasia and thus determine the most effective mode of therapy.
Treatment of aldosterone producing adenoma involves surgical removal of the adenoma. In 70% of cases surgical removal of a unilateral adenoma reverses hypokalemia and frequently cures hypertension. However, in most cases no masses are found in surgery. If surgery fails or is not indicated, dietary sodium restriction (<80 mEq daily) or spironolactone can be used. Spironolactone is the main medical treatment for primary aldosteronism. It is a competitive aldosterone antagonist and has been used in doses from 25 to 400 mg per day. Idiopathic nodular hyperplasia is more difficult to treat since hypertension is rarely improved with bilateral adrenalectomy. Only when there is significant symptomatic hypokalemia, which cannot be controlled with medical therapy, surgery is considered.
Reference(s): 1. Computed Tomography Of The Body With Magnetic Resonance Imaging by Albert A. Moss, 2nd Edition, W. B. Saunders Company, 1992.
2. Ganguly A. Primary aldosteronism. NEJM 339:1828-34, 1998.
3. Young WF, Hogan MJ, Klee GG, Grant CS, van Heerden JA. Mayo Clin Proc 65: 96-110, 1990.
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