The patient’s presenting symptoms of nocturia and polydipsia, along with the persistent hypertension, are indicative of a fluid and electrolyte imbalance. The elevated plasma sodium and low plasma potassium are consistent with an elevated aldosterone level as the underlying cause. The normal plasma glucose levels exclude diabetes mellitus as a potential cause for the polydipsia and polyuria.
Aldosterone is the primary mineralocorticoid secreted by the adrenal cortex. It stimulates reabsorption of sodium and secretion of potassium in the renal distal tubules. The reabsorption of sodium contributes to the development of hypertension, and the excessive excretion of potassium can lead to muscular weakness and possibly tetany.
Aldosterone secretion is under multiple controls and is increased by elevation in plasma potassium, by an elevation in angiotensin II, and by an elevation in adrenocorticotropic hormone (ACTH) (see Fig. 70-2, p. 190). Plasma potassium is the most potent of the stimuli governing aldosterone release, and aldosterone is the major hormone regulating body potassium balance. The finding of hypokalemia alone does not immediately suggest hyperaldosteronism, because most diuretics used to treat hypertension are potassium wasting and will deplete body potassium stores.
The endocrine and electrolyte profile in this patient suggests primary hyperaldosteronism. Plasma potassium levels are low and therefore are not stimulating adrenal aldosterone synthesis. Plasma renin activity is also low, indicating that angiotensin II is not stimulating aldosterone synthesis. ACTH plays only a minor role in aldosterone release, and ACTH elevation would be characterized by symptoms related to glucocorticoid excess.
Aldosterone directly stimulates renal H+ secretion in the late tubular segments. Consequently, hyperaldosteronism causes a metabolic alkalosis, characterized by an elevation in pH and high plasma bicarbonate levels. Metabolic acid-base disturbances develop slowly, and, consequently, a respiratory compensation by increasing the plasma CO2 levels would be expected.
Treatment for Conn’s syndrome due to unilateral adrenal adenoma is by adrenalectomy. Hyperaldosteronism due to other causes may be medically managed by spironolactone or by dexamethasone.
