Show Explanatory Sources

This patient's onset of hypertension at a young age suggests a secondary cause.  The weakness and paresthesia indicate an associated electrolyte or acid-base disturbance.  These findings, along with suppressed plasma renin, suggest primary hyperaldosteronism (ie, mineralocorticoid excess).  Primary hyperaldosteronism is most commonly caused by a unilateral adrenal adenoma (Conn syndrome) or bilateral adrenal hyperplasia (idiopathic hyperaldosteronism).

Hyperaldosteronism is characterized by increased distal Na⁺ reabsorption in the renal collecting ducts.  This creates a negative charge in the lumen, pulling H⁺ and K⁺ from tubular cells and leading to their urinary excretion.  As a result, hypokalemia is common.  Increased H⁺ excretion by alpha-intercalated cells promotes bicarbonate production and increased activity of the basolateral HCO₃⁻/Cl⁻ exchanger, resulting in elevated serum bicarbonate and metabolic alkalosis (Choice E).

Despite increased Na⁺ reabsorption, overt volume overload (eg, pedal edema) is rarely seen due to a phenomenon known as aldosterone escape.  Increased intravascular volume increases pressure natriuresis and augments atrial natriuretic peptide release, thereby limiting net sodium retention and overt volume overload.  Hypernatremia is also not typically seen because the temporary increase in serum osmolality triggers a compensatory rise in antidiuretic hormone (ADH) release.

(Choice A)  Loop or thiazide diuretic use can cause metabolic alkalosis, hypokalemia, and hyponatremia (mostly with thiazides) due to urinary losses of H⁺, K⁺, and Na⁺.  Na⁺ loss leads to hypovolemia, which can exacerbate hyponatremia (due to nonosmotic stimulus for ADH secretion) and alkalosis (due to increased bicarbonate reabsorption).

(Choice C)  Primary adrenal insufficiency reduces urinary excretion of H⁺ and K⁺ and promotes renal Na⁺ loss due to low aldosterone.  As a result, metabolic acidosis, hyperkalemia, hyponatremia, and hypovolemia develop.

(Choice D)  Mineralocorticoid receptor antagonists (eg, spironolactone) block aldosterone receptors, thereby impairing urinary excretion of H⁺ and K⁺.  Common adverse effects therefore include metabolic acidosis and hyperkalemia.  Na⁺ excretion is only mildly increased, and serum Na⁺ concentration is usually not significantly affected.

Educational objective:
Primary hyperaldosteronism increases distal Na⁺ reabsorption (secondary hypertension), leading to increased urinary excretion of H⁺ and K⁺ (metabolic alkalosis and hypokalemia).  Overt volume overload is not seen due to aldosterone escape, and serum Na⁺ concentration is typically normal due to preserved antidiuretic hormone function.