Document Detail


Renal transport of uric acid: evolving concepts and uncertainties.
MedLine Citation:
PMID:  23089270     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In addition to its role as a metabolic waste product, uric acid has been proposed to be an important molecule with multiple functions in human physiologic and pathophysiologic processes and may be linked to human diseases beyond nephrolithiasis and gout. Uric acid homeostasis is determined by the balance between production, intestinal secretion, and renal excretion. The kidney is an important regulator of circulating uric acid levels by reabsorbing about 90% of filtered urate and being responsible for 60% to 70% of total body uric acid excretion. Defective renal handling of urate is a frequent pathophysiologic factor underpinning hyperuricemia and gout. Despite tremendous advances over the past decade, the molecular mechanisms of renal urate transport are still incompletely understood. Many transport proteins are candidate participants in urate handling, with URAT1 and GLUT9 being the best characterized to date. Understanding these transporters is increasingly important for the practicing clinician as new research unveils their physiologic characteristics, importance in drug action, and genetic association with uric acid levels in human populations. The future may see the introduction of new drugs that act specifically on individual renal urate transporters for the treatment of hyperuricemia and gout.
Authors:
Ion Alexandru Bobulescu; Orson W Moe
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Advances in chronic kidney disease     Volume:  19     ISSN:  1548-5609     ISO Abbreviation:  Adv Chronic Kidney Dis     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-10-23     Completed Date:  2013-04-10     Revised Date:  2013-11-06    
Medline Journal Info:
Nlm Unique ID:  101209214     Medline TA:  Adv Chronic Kidney Dis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  358-71     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
Affiliation:
Departments of Internal Medicine and Physiology and the Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX 75390-8856, USA. alexandru.bobulescu@utsouthwestern.edu
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MeSH Terms
Descriptor/Qualifier:
Biological Transport
Glucose Transport Proteins, Facilitative / metabolism
Gout / metabolism*,  physiopathology
Humans
Hyperuricemia / complications,  metabolism*
Kidney / metabolism*
Kidney Tubules, Proximal / metabolism*
Organic Anion Transporters / metabolism
Organic Cation Transport Proteins / metabolism
Uncertainty
Uric Acid / metabolism*
Grant Support
ID/Acronym/Agency:
K01 DK090282/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Glucose Transport Proteins, Facilitative; 0/Organic Anion Transporters; 0/Organic Cation Transport Proteins; 0/SLC22A12 protein, human; 0/SLC2A9 protein, human; 69-93-2/Uric Acid
Comments/Corrections

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