The differential diagnosis of metabolic alkalosis divides patients into those that have volume depletion (also called chloride-responsive metabolic alkalosis) and those that do not have volume depletion (also called chloride-resistant metabolic alkalosis).
Chloride-resistant metabolic alkalosis
With hypertension:[2]Galla JH. Metabolic alkalosis. J Am Soc Nephrol. 2000 Feb;11(2):369-75.
http://jasn.asnjournals.org/content/11/2/369.full
http://www.ncbi.nlm.nih.gov/pubmed/10665945?tool=bestpractice.com
[4]Online Mendelian Inheritance in Man (OMIM). Liddle syndrome. MIM#177200. March 2016 [internet publication].
http://www.ncbi.nlm.nih.gov/omim/177200
[5]Khanna A, Kurtzman NA. Metabolic alkalosis. J Nephrol. 2006 Mar-Apr;19(Suppl 9):S86-96.
http://www.ncbi.nlm.nih.gov/pubmed/16736446?tool=bestpractice.com
[6]Morineau G, Sulmont V, Salomon R, et al. Apparent mineralocorticoid excess: report of six new cases and extensive personal experience. J Am Soc Nephrol. 2006 Nov;17(11):3176-84.
http://jasn.asnjournals.org/content/17/11/3176.full
http://www.ncbi.nlm.nih.gov/pubmed/17035606?tool=bestpractice.com
[7]Fleseriu M, Auchus R, Bancos I, et al. Consensus on diagnosis and management of Cushing's disease: a guideline update. Lancet Diabetes Endocrinol. 2021 Dec;9(12):847-75.
https://pmc.ncbi.nlm.nih.gov/articles/PMC8743006
http://www.ncbi.nlm.nih.gov/pubmed/34687601?tool=bestpractice.com
Primary hyperaldosteronism
Secondary hyperaldosteronism, for example, renin-producing tumor
Renal artery stenosis
Cushing syndrome
Licorice ingestion
Tobacco chewing
Apparent mineralocorticoid excess
Liddle syndrome: autosomal-dominant inheritance, early onset hypertension, hypokalemic metabolic alkalosis, low plasma renin activity, and suppressed aldosterone secretion.[4]Online Mendelian Inheritance in Man (OMIM). Liddle syndrome. MIM#177200. March 2016 [internet publication].
http://www.ncbi.nlm.nih.gov/omim/177200
No hypertension:[8]Online Mendelian Inheritance in Man (OMIM). Bartter syndrome, type 4A. MIM#602522. May 2016 [internet publication].
http://www.ncbi.nlm.nih.gov/omim/602522
[9]Online Mendelian Inheritance in Man (OMIM). Gitelman syndrome. #263800. November 2012 [internet publication].
http://www.ncbi.nlm.nih.gov/omim/263800
[10]Blanchard A, Bockenhauer D, Bolignano D, et al. Gitelman syndrome: consensus and guidance from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int. 2017 Jan;91(1):24-33.
https://www.kidney-international.org/article/S0085-2538(16)30602-0/fulltext
http://www.ncbi.nlm.nih.gov/pubmed/28003083?tool=bestpractice.com
[11]Naesens M, Steels P, Verberckmoes R, et al. Bartter's and Gitelman's syndromes: from gene to clinic. Nephron Physiol. 2004;96(3):65-78.
http://www.ncbi.nlm.nih.gov/pubmed/15056980?tool=bestpractice.com
[12]Gennari FJ. Hypokalemia. N Engl J Med. 1998 Aug 13;339(7):451-8.
http://www.ncbi.nlm.nih.gov/pubmed/9700180?tool=bestpractice.com
[13]Hearing SD. Refeeding syndrome. BMJ. 2004 Apr 17;328(7445):908-9.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC390152
http://www.ncbi.nlm.nih.gov/pubmed/15087326?tool=bestpractice.com
Bartter syndrome: autosomal-recessive inheritance, hypokalemic metabolic alkalosis, elevated plasma renin activity and hyperaldosteronism, normal blood pressure (BP), deranged prostaglandin metabolism, and increased urinary chloride excretion
Gitelman syndrome: autosomal-recessive inheritance, hypokalemic metabolic alkalosis, hypocalciuria, and hypomagnesemia
Current loop or thiazide diuretic therapy
Profound potassium depletion
Hypercalcemia of nonhyperparathyroid etiology
Poststarvation refeeding syndrome
Transfusion of blood products (sodium citrate).
Chloride-responsive metabolic alkalosis
Gastrointestinal causes:[2]Galla JH. Metabolic alkalosis. J Am Soc Nephrol. 2000 Feb;11(2):369-75.
http://jasn.asnjournals.org/content/11/2/369.full
http://www.ncbi.nlm.nih.gov/pubmed/10665945?tool=bestpractice.com
[5]Khanna A, Kurtzman NA. Metabolic alkalosis. J Nephrol. 2006 Mar-Apr;19(Suppl 9):S86-96.
http://www.ncbi.nlm.nih.gov/pubmed/16736446?tool=bestpractice.com
[14]Hihnala S, Höglund P, Lammi L, et al. Long-term clinical outcome in patients with congenital chloride diarrhea. J Pediatr Gastroenterol Nutr. 2006 Apr;42(3):369-75.
http://www.ncbi.nlm.nih.gov/pubmed/16641574?tool=bestpractice.com
[15]Bates CM, Baum M, Quigley R. Cystic fibrosis presenting with hypokalemia and metabolic alkalosis in a previously healthy adolescent. J Am Soc Nephrol. 1997 Feb;8(2):352-5.
http://www.ncbi.nlm.nih.gov/pubmed/9048354?tool=bestpractice.com
[16]Dave S, Honney S, Raymond J, et al. An unusual presentation of cystic fibrosis in an adult. Am J Kidney Dis. 2005 Mar;45(3):e41-4.
http://www.ncbi.nlm.nih.gov/pubmed/15754262?tool=bestpractice.com
Vomiting
Gastric drainage
Villous adenoma of colon (usually leads to normal anion gap metabolic acidosis; however, some of these tumors secrete chloride, leading to metabolic alkalosis)
Congenital chloride diarrhea (rare congenital syndrome due to a defect in large bowel chloride absorption, which leads to chronic diarrhea with stool fluid rich in chloride)
Cystic fibrosis.
Renal causes:[2]Galla JH. Metabolic alkalosis. J Am Soc Nephrol. 2000 Feb;11(2):369-75.
http://jasn.asnjournals.org/content/11/2/369.full
http://www.ncbi.nlm.nih.gov/pubmed/10665945?tool=bestpractice.com
[5]Khanna A, Kurtzman NA. Metabolic alkalosis. J Nephrol. 2006 Mar-Apr;19(Suppl 9):S86-96.
http://www.ncbi.nlm.nih.gov/pubmed/16736446?tool=bestpractice.com
Postdiuretic therapy
Posthypercapnia.
Exogenous alkali intake:[2]Galla JH. Metabolic alkalosis. J Am Soc Nephrol. 2000 Feb;11(2):369-75.
http://jasn.asnjournals.org/content/11/2/369.full
http://www.ncbi.nlm.nih.gov/pubmed/10665945?tool=bestpractice.com
[5]Khanna A, Kurtzman NA. Metabolic alkalosis. J Nephrol. 2006 Mar-Apr;19(Suppl 9):S86-96.
http://www.ncbi.nlm.nih.gov/pubmed/16736446?tool=bestpractice.com
[17]Schuman CA, Jones HW 3rd. The 'milk-alkali' syndrome: two case reports with discussion of pathogenesis. Q J Med. 1985 May;55(217):119-26.
http://www.ncbi.nlm.nih.gov/pubmed/4001310?tool=bestpractice.com