Enteric Oxalate Secretion Mediated by Slc26a6 Defends against Hyperoxalemia in Murine Models of Chronic Kidney Disease.
Slc26a6
aristolochic acid I
chronic kidney disease
intestine
oxalate
Journal
Journal of the American Society of Nephrology : JASN
ISSN: 1533-3450
Titre abrégé: J Am Soc Nephrol
Pays: United States
ID NLM: 9013836
Informations de publication
Date de publication:
09 2020
09 2020
Historique:
received:
28
01
2020
accepted:
01
05
2020
pubmed:
15
7
2020
medline:
4
3
2021
entrez:
15
7
2020
Statut:
ppublish
Résumé
A state of oxalate homeostasis is maintained in patients with healthy kidney function. However, as GFR declines, plasma oxalate (P Feeding a diet high in soluble oxalate or weekly injections of aristolochic acid induced CKD in age- and sex-matched wild-type and Fecal oxalate excretion was enhanced in wild-type mice with CKD. This increase was abrogated in Slc26a6-mediated enteric oxalate secretion is critical in decreasing the body burden of oxalate in murine CKD models. Future studies are needed to address whether similar mechanisms contribute to intestinal oxalate elimination in humans to enhance extrarenal oxalate clearance.
Sections du résumé
BACKGROUND
A state of oxalate homeostasis is maintained in patients with healthy kidney function. However, as GFR declines, plasma oxalate (P
METHODS
Feeding a diet high in soluble oxalate or weekly injections of aristolochic acid induced CKD in age- and sex-matched wild-type and
RESULTS
Fecal oxalate excretion was enhanced in wild-type mice with CKD. This increase was abrogated in
CONCLUSIONS
Slc26a6-mediated enteric oxalate secretion is critical in decreasing the body burden of oxalate in murine CKD models. Future studies are needed to address whether similar mechanisms contribute to intestinal oxalate elimination in humans to enhance extrarenal oxalate clearance.
Identifiants
pubmed: 32660969
pii: ASN.2020010105
doi: 10.1681/ASN.2020010105
pmc: PMC7461683
doi:
Substances chimiques
Antiporters
0
Oxalates
0
Slc26a6 protein, mouse
0
Sulfate Transporters
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1987-1995Subventions
Organisme : NIDDK NIH HHS
ID : P30 DK079310
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK033793
Pays : United States
Organisme : NIDDK NIH HHS
ID : R37 DK033793
Pays : United States
Informations de copyright
Copyright © 2020 by the American Society of Nephrology.
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