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- Title
Sodium retention by uPA‐plasmin‐ENaC in nephrotic syndrome—Authors reply.
- Authors
Hinrichs, Gitte R.; Weyer, Kathrin; Friis, Ulla G.; Svenningsen, Per; Lund, Ida Katrine; Nielsen, Rikke; Mollet, Géraldine; Antignac, Corinne; Bistrup, Claus; Jensen, Boye L.; Birn, Henrik
- Abstract
Sodium retention by uPA-plasmin-ENaC in nephrotic syndrome - Authors reply There is a great interest in exploring the mechanisms of oedema in nephrotic syndrome (NS) as evidenced by two parallel studies published in Acta Physiologica.[[1]] This has generated an editorial comment[3] which we respond to by this rebuttal. This seminal observation indicates that serine protease activity contributes to nephrotic sodium retention in mouse NS [8]; however, the importance of the individual protease(s) remains to be clarified.
- Subjects
NEPHROTIC syndrome; PLASMINOGEN activators; SERINE proteinases; BRUGADA syndrome; SERUM albumin
- Publication
Acta Physiologica, 2020, Vol 228, Issue 4, p1
- ISSN
1748-1708
- Publication type
Article
- DOI
10.1111/apha.13432