Metabolic alkalosis is induced by increasing body alkali stores and is manifested by a primary increase in serum [HCO 3 ] and a secondary increase in PaCO2. The disorder only becomes clinically significant when the increase in serum [HCO 3 ] is sustained by impaired excretion of the excess HCO 3 by the kidney. Such impairment can occur with kidney failure, but occurs much more commonly as a result of functional changes in collecting duct ion transport, primarily sodium uptake via the epithelial sodium channel (ENaC), which stimulates continued abnormal bicarbonate reabsorption. The most common form of the disorder is caused by combined chloride and potassium depletion, which causes a secondary stimulation of ENaC that appears to be independent of aldosterone. More rarely the disorder is induced and sustained by primary stimulation of ENaC, either due to autonomous aldosterone secretion or due to genetic defects that stimulate ENaC independent of aldosterone. This chapter presents a new classification of the causes of metabolic alkalosis based on pathophysiology rather than response to treatment, and an approach to the diagnosis and treatment of this common disorder.


Congenital Adrenal Hyperplasia Primary Aldosteronism Metabolic Alkalosis Aldosterone Secretion Bartter Syndrome 
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© Springer Science+Business Media New York 2013

Authors and Affiliations

  1. 1.Department of MedicineUniversity of VermontBurlingtonUSA

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