Conn’s syndrome, also called primary hyperaldosteronism, is characterized by an increased production of aldosterone. In 80% of cases this is due to an adrenal adenoma. Other causes include hypertrophy of the zona glomerulosa of the adrenal cortex and adrenal carcinoma, although the latter is extremely rare. The excessive secretion of aldosterone leads to the increased retention of Na+ and loss of K+ by the kidneys. Most of the clinical features, muscle weakness, tetany, paresthesiae, polydipsia and polyuria, are due to the hypokalemia whereas the excessive Na+ retention causes hypertension.
Investigating the possibility of Conn’s syndrome involves determining the concentrations of Na+ and K+ in the serum and urine of the patient. Plasma Na+ can be high, slightly increased or normal, whereas that of K+ is always reduced. Measurements of plasma aldosterone and renin in patients with Conn’s syndrome often show a high aldosterone concentration and a low renin activity. Conn’s syndrome is managed by treating its underlying cause. Often this is a tumor that must be removed surgically. Other approaches involve using diuretics, such as spironolactone, an antagonist to aldosterone that helps to control hypertension. This is particularly useful when the cause of Conn’s syndrome is adrenal hyperplasia.
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