Table 2.

The metabolic alkaloses

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-β (OH) steroid dehydrogenase activity

Chronic licorice/carbenoxolone ingestion

Congenital AME syndrome (11-β HSD type 2 inactivating mutation)

Renin-secreting tumors

Some forms of congenital adrenal hyperplasia

11-β hydroxylase deficiency

17-α 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

ECF, extracellular fluid; ACTH, adrenocorticotropic hormone; AME, apparent mineralocorticoid excess; HSD, hydroxysteroid dehydrogenases