Abcc6 deficiency prevents rhabdomyolysis-induced acute kidney injury.
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
06 Dec 2023
06 Dec 2023
Historique:
received:
06
03
2023
accepted:
20
11
2023
medline:
11
12
2023
pubmed:
7
12
2023
entrez:
6
12
2023
Statut:
epublish
Résumé
Rhabdomyolysis is a risk factor for acute kidney injury, transition towards chronic kidney disease, and death. The role of calcium phosphate deposits in the mechanisms of rhabdomyolysis-induced acute kidney injury (RAKI) is still unclear. Better insight of the role calcium in RAKI could lead to new therapeutic avenues. Here, we show in a mice model of RAKI that calcium phosphate deposits were frequent in the kidney (hydroxyapatite) and partly correlated with the severity of the kidney injury. However, the intensity of deposits was highly heterogeneous between mice. Treatment with sodium chloride, sodium bicarbonate or inorganic pyrophosphate (PPi; an inhibitor of the calcium phosphate crystallization), or combinations thereof, did not improve kidney outcomes and hydroxyapatite deposition during RAKI. Unexpectedly, Abcc6 knockout mice (ko), characterized by PPi deficiency, developed less severe RAKI despite similar rhabdomyolysis severity, and had similar hydroxyapatite deposition suggesting alternative mechanisms. This improved kidney outcome at day 2 translated to a trend in improved glomerular filtration rate at month 2 in Abcc6
Identifiants
pubmed: 38057332
doi: 10.1038/s41598-023-47894-z
pii: 10.1038/s41598-023-47894-z
pmc: PMC10700332
doi:
Substances chimiques
Sodium Bicarbonate
8MDF5V39QO
Sodium Chloride
451W47IQ8X
Calcium Phosphates
0
Hydroxyapatites
0
Abcc6 protein, mouse
0
Multidrug Resistance-Associated Proteins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
21513Subventions
Organisme : Université Toulouse III - Paul Sabatier
ID : Ecole doctorale BSB
Organisme : ERA PerMed-JTC 2018
ID : ANR-18-PERM-0003
Organisme : ERA PerMed-JTC 2018
ID : ANR-18-PERM-0003
Organisme : Fondation pour la Recherche Médicale
ID : DEQ20170336759
Informations de copyright
© 2023. The Author(s).
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