From the Research
Non-anion gap metabolic alkalosis with elevated bicarbonate is most commonly caused by diuretic use, particularly loop diuretics like furosemide and thiazides like hydrochlorothiazide, as well as vomiting or nasogastric suction, and excessive mineralocorticoid activity. The use of diuretics, such as thiazides and loop diuretics, can lead to increased renal bicarbonate reabsorption due to volume contraction and potassium depletion, resulting in metabolic alkalosis 1. Other causes of non-anion gap metabolic alkalosis include:
- Vomiting or nasogastric suction, which lead to loss of hydrochloric acid and subsequent retention of bicarbonate
- Excessive mineralocorticoid activity, as seen in primary hyperaldosteronism, Cushing's syndrome, or exogenous steroid use, which promotes sodium reabsorption and hydrogen ion secretion in the distal tubule
- Severe potassium depletion (hypokalemia) from any cause, which can independently drive bicarbonate retention
- Milk-alkali syndrome from excessive calcium and absorbable alkali intake
- Post-hypercapnic states where the kidneys have adapted to chronic respiratory acidosis by retaining bicarbonate
- Bartter and Gitelman syndromes, genetic disorders affecting renal tubular function, which also present with metabolic alkalosis
These conditions all share the common feature of either increasing bicarbonate generation or decreasing its excretion while maintaining a normal anion gap, distinguishing them from anion gap metabolic alkalosis caused by accumulation of organic acids 2, 3. It is essential to identify and address the underlying cause of non-anion gap metabolic alkalosis to provide appropriate treatment and prevent complications.