Document Detail

Acid-base metabolism: implications for kidney stones formation.
MedLine Citation:
PMID:  16411127     Owner:  NLM     Status:  MEDLINE    
The physiology and pathophysiology of renal H+ ion excretion and urinary buffer systems are reviewed. The main focus is on the two major conditions related to acid-base metabolism that cause kidney stone formation, i.e., distal renal tubular acidosis (dRTA) and abnormally low urine pH with subsequent uric acid stone formation. Both the entities can be seen on the background of disturbances of the major urinary buffer system, NH3+ <--> NH4+. On the one hand, reduced distal tubular secretion of H+ ions results in an abnormally high urinary pH and either incomplete or complete dRTA. On the other hand, reduced production/availability of NH4+ is the cause of an abnormally low urinary pH, which predisposes to uric acid stone formation. Most recent research indicates that the latter abnormality may be a renal manifestation of the increasingly prevalent metabolic syndrome. Despite opposite deviations from normal urinary pH values, both the dRTA and uric acid stone formation due to low urinary pH require the same treatment, i.e., alkali. In the dRTA, alkali is needed for improving the body's buffer capacity, whereas the goal of alkali treatment in uric acid stone formers is to increase the urinary pH to 6.2-6.8 in order to minimize uric acid crystallization.
Bernhard Hess
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Publication Detail:
Type:  Journal Article; Review     Date:  2006-01-13
Journal Detail:
Title:  Urological research     Volume:  34     ISSN:  0300-5623     ISO Abbreviation:  Urol. Res.     Publication Date:  2006 Apr 
Date Detail:
Created Date:  2006-03-23     Completed Date:  2006-12-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0364311     Medline TA:  Urol Res     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  134-8     Citation Subset:  IM    
Internal Medicine and Nephrology, Klinik Im Park, Bellariastrasse 38, 8038, Zurich, Switzerland.
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MeSH Terms
Acidosis, Renal Tubular / etiology,  metabolism
Acids / chemistry,  metabolism*
Alkalies / chemistry,  metabolism*
Bicarbonates / metabolism
Hydrogen-Ion Concentration
Kidney Calculi / etiology*,  metabolism
Urine / chemistry
Reg. No./Substance:
0/Acids; 0/Alkalies; 0/Bicarbonates

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