Causes of Metabolic Alkalosis: Differential Diagnosis

ECF volume contracted: urine chloride concentration <20 meq/L

 • Gastric alkalosis: vomiting/ nasogastric suction

 • Chloride-rich diarrhea (congenital chloridorrhea)

 • Status/ postchronic hypercapnia (acute reversal of chronic respiratory acidosis)

 • Cystic fibrosis with major sweating

 • Thiazide or loop diuretics after renal tubule diuretic effect has dissipated

 • Some villous adenomas

ECF volume expanded: urine chloride concentration > 20 meq/L

 • Primary hyperaldosteronism (unilateral adenoma/ bilateral hyperplasia/ glucocorticoid-sensitive hyperaldosteronism)

 • Severe Cushing syndrome (especially because of ectopic ACTH)

 • Exogenous mineralocorticoids

 • Reduced 11-ß (OH) steroid dehydrogenase activity: Chronic licorice/carbenoxolone ingestion, Congenital AME syndrome (11-ß HSD type 2 inactivating mutation)

 • Renin-secreting tumors

 • Some forms of congenital adrenal hyperplasia: 11-ß hydroxylase deficiency, 17-a hydroxylase deficiency

 • Liddle syndrome

ECF volume contracted: but urine chloride concentration > 20 meq/L (generally indicates a renal tubule reabsorptive defect)

 • Thiazide or loop diuretics actively working

 • Bartter syndrome (defective Na reabsorption in loop of Henle, furosemide-like lesion)

 • Gitelman syndrome (defective Na reabsorption at the thiazide-sensitive site)

Metabolic alkalosis: other

 • Severe potassium deficiency

 • Milk (calcium) alkali syndrome

 • NaHCO3 loads with markedly reduced GFR

 • Refeeding after fasting



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