Question 1 · Hard
A 23-year-old dancer is referred for fatigue and leg cramps. Her blood pressure is 104/68 mm Hg, and she denies vomiting and any diuretic or laxative use. Results: sodium 137, potassium 2.7, chloride 89 and total CO2 36 mmol/L; magnesium normal. Arterial pH 7.49, pCO2 47 mm Hg [6.3 kPa], HCO3- 35 mmol/L. Spot urine: sodium 52 mmol/L, potassium 38 mmol/L, chloride 6 mmol/L, pH 7.5. A urine diuretic screen is negative on two separate samples, and plasma renin and aldosterone are both raised. The most likely cause of her metabolic alkalosis is:
- ASurreptitious diuretic use
- BGitelman syndrome (a salt-losing tubulopathy)
- CConcealed self-induced vomiting
- DPrimary hyperaldosteronism
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Answer: C · Concealed self-induced vomiting
A hypokalemic metabolic alkalosis with normal blood pressure and a high renin points to chloride loss, either from the stomach or into the urine. The urine chloride separates the two: a value below about 20 mmol/L, as here, means the kidney is conserving chloride, as it does after vomiting. Urine sodium is misleadingly high because the kidney is excreting the excess bicarbonate with sodium and potassium, which also makes the urine alkaline. Gitelman syndrome and active diuretic use both keep urine chloride high, and two negative diuretic screens make hidden diuretic use unlikely. Primary hyperaldosteronism causes hypertension with a suppressed renin.
- A: Active diuretic use keeps urine chloride high, and two screens were negative.
- B: Gitelman syndrome wastes chloride in the urine and usually lowers magnesium.
- D: Primary hyperaldosteronism causes hypertension with a suppressed renin.