Sodium retention in nephrotic syndrome is independent of the activation of the membrane-anchored serine protease prostasin (CAP1/PRSS8) and its enzymatic activity
Daniel Essigke(University Children's Hospital Tübingen), Ferruh Artunç(Deutsches Diabetes-Zentrum e.V.)
Cited by 17
Related Papers
FAN1 mutations cause karyomegalic interstitial nephritis, linking chronic kidney failure to defective DNA damage repair
|Nature Genetics|2012|244
Proteolytic activation of the epithelial sodium channel (ENaC) by factor VII activating protease (FSAP) and its relevance for sodium retention in nephrotic mice
|Pflügers Archiv - European Journal of Physiology|2021|25