Urokinase‐type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)‐mediated sodium retention in experimental nephrotic syndrome

In nephrotic syndrome, aberrantly filtered plasminogen (plg) is converted to active plasmin by tubular urokinase‐type plasminogen activator (uPA) and thought to lead to sodium retention by proteolytic activation of the epithelial sodium channel (ENaC). This concept predicts that uPA is an important factor for sodium retention and that inhibition of uPA might be protective in nephrotic syndrome.

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