Document Detail


Pathophysiology of metabolic alkalosis: a new classification based on the centrality of stimulated collecting duct ion transport.
MedLine Citation:
PMID:  21849227     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Metabolic alkalosis is a unique acid-base disorder because it can be induced and sustained by functional alterations in renal ion transport. This review summarizes more than 50 years of research into the pathophysiologic processes causing this disorder. The evidence reviewed supports the hypothesis that virtually all forms of metabolic alkalosis are sustained by enhanced collecting duct hydrogen ion secretion, induced by stimulation of sodium uptake through the epithelial sodium channel (ENaC). Enhanced collecting duct hydrogen ion secretion in metabolic alkalosis occurs most commonly secondary to changes in ion transport earlier along the nephron, but also can occur as the result of primary stimulation of ENaC. In both these settings, potassium secretion is stimulated, and abnormal potassium losses cause depletion of body potassium stores. Potassium depletion has a key role in sustaining metabolic alkalosis by stimulating renal hydrogen ion secretion, enhancing renal ammonium production and excretion, and downregulating sodium reabsorption in the loop of Henle and early distal tubule. A new classification of the causes of metabolic alkalosis is proposed based on these pathophysiologic events rather than response to treatment.
Authors:
F John Gennari
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Publication Detail:
Type:  Journal Article; Review     Date:  2011-08-17
Journal Detail:
Title:  American journal of kidney diseases : the official journal of the National Kidney Foundation     Volume:  58     ISSN:  1523-6838     ISO Abbreviation:  Am. J. Kidney Dis.     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-09-29     Completed Date:  2011-11-21     Revised Date:  2012-02-17    
Medline Journal Info:
Nlm Unique ID:  8110075     Medline TA:  Am J Kidney Dis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  626-36     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
Affiliation:
University of Vermont College of Medicine, Burlington, VT, USA. fgennari@uvm.edu
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MeSH Terms
Descriptor/Qualifier:
Aldosterone / physiology
Alkalosis / classification,  etiology,  physiopathology*
Chlorides / metabolism
Diuretics / pharmacology
Epithelial Sodium Channel / metabolism*
Genetic Diseases, Inborn / metabolism
H(+)-K(+)-Exchanging ATPase / metabolism
Humans
Hydrogen / metabolism
Ion Transport* / drug effects
Kidney Tubules, Collecting / metabolism*
Kidney Tubules, Proximal / metabolism
Membrane Transport Proteins / metabolism
Models, Biological
Potassium / metabolism
Proton-Translocating ATPases / metabolism
Sodium / metabolism
Sodium Chloride Symporters / metabolism
Sodium-Hydrogen Antiporter / metabolism
Sodium-Potassium-Chloride Symporters / metabolism
Chemical
Reg. No./Substance:
0/Chlorides; 0/Diuretics; 0/Epithelial Sodium Channel; 0/Membrane Transport Proteins; 0/SLC26A4 protein, human; 0/Sodium Chloride Symporters; 0/Sodium-Hydrogen Antiporter; 0/Sodium-Potassium-Chloride Symporters; 1333-74-0/Hydrogen; 52-39-1/Aldosterone; 7440-09-7/Potassium; 7440-23-5/Sodium; EC 3.6.1.10/H(+)-K(+)-Exchanging ATPase; EC 3.6.3.14/Proton-Translocating ATPases
Comments/Corrections
Comment In:
Am J Kidney Dis. 2012 Feb;59(2):315; author reply 315-6   [PMID:  22243948 ]
Am J Kidney Dis. 2012 Feb;59(2):315; author reply 315-6   [PMID:  22243949 ]

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