A 30-year-old woman comes to the office due to generalized weakness and paresthesia. Medical history is unremarkable and she takes no medications. However, the patient says her blood pressure was elevated at a workplace health fair 3 months ago, although she attributed it to being "stressed out" and did not take any action. Blood pressure is 150/95 mm Hg. Cardiac examination is normal with full and symmetric distal pulses and no pedal edema. Laboratory evaluation shows low plasma renin activity and normal serum creatinine levels. CT scan of the abdomen reveals a solitary, hypodense, 1.5-cm right adrenal mass. Which of the following patterns of serum electrolyte concentrations would most likely be seen in this patient?

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11ec160b_3ab9_d0df_9249_8f809c162bfe_MD0001_00 This patient has hypertension at a young age, suggesting a secondary cause. Her weakness and paresthesia indicate an associated electrolyte or acid-base disturbance. These findings, along with a suppressed plasma renin, suggest primary mineralocorticoid excess (hyperaldosteronism). The most common causes of primary hyperaldosteronism include unilateral adrenal adenoma (Conn syndrome) and bilateral adrenal hyperplasia (idiopathic hyperaldosteronism), which can be differentiated on abdominal CT scan. Hyperaldosteronism is characterized by increasedNa⁺ reabsorption in the renal collecting tubules. This creates a negative charge in the lumen, pulling K⁺ and H⁺ from tubular cells and leading to increased excretion of urinary K⁺ and H⁺. As a result, hypokalemia is common. Increased H⁺ excretion by α-intercalated cells promotes bicarbonate production and increased activity of the basolateral HCO₃₋/Cl- exchanger, resulting in elevated serum bicarbonate and metabolic alkalosis. Despite the increase in Na⁺ reabsorption, hypernatremia and pedal edema are rarely observed due to a phenomenon known as aldosterone escape. The increased intravascular volume causes increased renal blood flow (with resulting pressure natriuresis) and augmented release of atrial natriuretic peptide. This limits net sodium retention and prevents the development of overt volume overload and significant hypernatremia. (Choice A) Due to aldosterone escape, serum Na⁺ concentration is normal in hyperaldosteronism. Increased loss of K⁺ and H⁺ in the urine causes hypokalemia and high (not low) serum bicarbonate. (Choice B) Patients with primary adrenal insufficiency have increased renal Na⁺ loss and reduced urinary excretion of K⁺ and H⁺ due to low aldosterone activity. As a result, hypovolemia, hyponatremia, hyperkalemia, and metabolic acidosis develop. Hypovolemia also acts as a nonosmotic stimulus for antidiuretic hormone (ADH) secretion, further accentuating the hyponatremia. (Choice C) Loop or thiazide diuretic use can cause hypovolemia, hyponatremia (mostly with thiazides), hypokalemia, and metabolic alkalosis due to urinary losses of Na⁺, K⁺, and H⁺. Hypovolemia can also exacerbate hyponatremia (due to increased ADH secretion) and alkalosis (due to increased bicarbonate reabsorption). (Choice D) Mineralocorticoid receptor antagonists (eg, spironolactone) block aldosterone receptors and impair urinary excretion of K⁺ and H⁺. Side effects include hyperkalemia and metabolic acidosis. Na⁺ excretion is only mildly increased and serum Na⁺ concentration is usually not significantly affected. Educational objective: Primary hyperaldosteronism causes increased Na⁺ reabsorption in the renal collecting tubules, leading to increased urinary excretion of K⁺ and H⁺. Patients typically have secondary hypertension as well as hypokalemia and metabolic alkalosis. The serum Na+ concentration remains normal due to aldosterone escape. __________ References: Mineralocorticoid hypertension and hypokalemia. (http://www.ncbi.nlm.nih.gov/pubmed/17275580)

A 30-Year-Old Woman Comes to the Office Due to Generalized