Sodium retention by uPA-plasmin-ENaC in nephrotic syndrome-Authors reply
Acta Physiol (Oxf)
.
2020 Apr;228(4):e13432.
doi: 10.1111/apha.13432.
Epub 2020 Jan 9.
Authors
Gitte R Hinrichs
1
,
Kathrin Weyer
2
,
Ulla G Friis
1
,
Per Svenningsen
1
,
Ida Katrine Lund
3
,
Rikke Nielsen
2
,
Géraldine Mollet
4
,
Corinne Antignac
4
5
,
Claus Bistrup
6
7
,
Boye L Jensen
1
,
Henrik Birn
2
8
Affiliations
1
Department of Molecular Medicine, Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark.
2
Department of Biomedicine, Aarhus University, Aarhus, Denmark.
3
The Finsen Laboratory, Biotech Research & Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark.
4
Laboratory of Hereditary Kidney Diseases, Paris Descartes-Sorbonne Paris Cité University, Paris, France.
5
Department of Genetics, Necker Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France.
6
Department of Nephrology, Odense University Hospital, Odense, Denmark.
7
Department of Clinical Research, University of Southern Denmark, Odense, Denmark.
8
Department of Renal Medicine, Aarhus University Hospital, Aarhus, Denmark.
PMID:
31845496
DOI:
10.1111/apha.13432
No abstract available
Publication types
Letter
Comment
MeSH terms
Epithelial Sodium Channels*
Fibrinolysin
Humans
Nephrotic Syndrome*
Sodium
Urokinase-Type Plasminogen Activator
Substances
Epithelial Sodium Channels
Sodium
Fibrinolysin
Urokinase-Type Plasminogen Activator