Table 2.

Genetic and acquired diseases associated with hypokalemic metabolic alkalosis.

	Bartter	Gitelman	Liddle	AME	Geller	Congenital Adrenal Hyperplasia	Familial Hyperaldosteronism
Potassium	Low	Low	Low	Low	Low	Low	Normal or Low
Sodium Bicarbonate	High	High	High	High	High	High	High
Renin	High	High	Low	Low	Low	Low	Low
Aldosterone	High	High	Low	Low	Low	Low	High
Hypertension	No	No	Yes	Yes	Yes	Yes	Yes
Cortisol/ACTH	−	−	−	N/N	−	Low/High
Age of onset	Infancy	Childhood/Adulthood	Childhood/Adulthood	Every age	Adulthood	Infancy	Childhood/Adulthood
Transmission	AD-AR	AR	AD	AR	AD	AD	AD
Alteration	NaKCl cotransporter 2 Renal outer medullary K channel Cl channel Barttin Ca sensing receptor	NaCl cotransporter Cl channel Kb	Epithelial Na channel gain of function	Defect in11-beta-hydroxysteroid dehydrogenase type 2	Gain of function mutation of mineralocorticoid receptor	Steroid synthesis defect with gain of function of mineralocorticoid receptor	Increased levels of 18-oxocortisol and 18-hydroxycortisol
Gene	SLC12A1 KCNJ1 CLCNKB BSND CASR	SLC12A3 CLCNKB	SCNN1B SCNN1G	HSD11B2	NR3C2	CYP21A2	CYP11B1/CYP11B2 CLCN2 KCNJ5 CACNA1H

AME: apparent excess of mineralcorticoid; ACTH: adreno cortico tropin hormone; N: normal; AR: autosomic recessive; AD: autosomic dominant.