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- Title
Rebuttal to editorial: Sodium retention by uPA in nephrotic syndrome?
- Authors
Bohnert, Bernhard N.; Kanse, Sandip; Haerteis, Silke; Korbmacher, Christoph; Artunc, Ferruh
- Abstract
Moreover, it demonstrates that uPA knockout mice do not compensate the chronic lack of uPA by upregulating other serine proteases with the ability to convert plasminogen into plasmin in nephrotic urine. We also agree that very low concentrations of plasmin are sufficient to cause proteolytic ENaC activation as we have previously shown in vitro.[5] Therefore, we cannot rule out the possibility that in nephrotic uPA knockout mice very low concentrations of urinary plasmin may contribute to proteolytic ENaC activation. In our view, both studies question the current concept of uPA-mediated plasmin generation as a key mechanism of proteolytic ENaC activation and sodium retention in nephrotic syndrome. Urokinase-type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)-mediated sodium retention in experimental nephrotic syndrome.
- Subjects
FOCAL segmental glomerulosclerosis; NEPHROTIC syndrome
- Publication
Acta Physiologica, 2020, Vol 228, Issue 4, p1
- ISSN
1748-1708
- Publication type
Article
- DOI
10.1111/apha.13427