Mice lacking plasma kallikrein [30], or plasminogen/plasmin [31] or urokinase-plasminogen activator (uPA) were not protected from Na+ retention in experimental nephrotic syndrome [32], although Hinrichs and coworkers reported a urokinase-dependent intratubular plasminogen activation and γENaC cleavage in a podocin-deficient nephrotic mouse model [33]. This evidence concerns the gene NPHS2 and nephrotic syndrome.