Title : Remission of nephrotic syndrome diminishes urinary plasmin content and abolishes activation of ENaC.

Pub. Date : 2013 Aug

PMID : 23503750






2 Functional Relationships(s)
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1 BACKGROUND: Urinary plasmin activates the epithelial Na(+) channel (ENaC) in vitro and may possibly be a mechanism of sodium retention in nephrotic syndrome (NS). Sodium plasminogen Homo sapiens
2 CONCLUSIONS: These findings support the hypothesis that aberrantly filtered plasminogen-plasmin may contribute to ENaC activation and mediate primary renal sodium retention during active childhood NS. Sodium plasminogen Homo sapiens