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

Background Urinary plasmin activates the epithelial Na + channel (ENaC) in vitro and may possibly be a mechanism of sodium retention in nephrotic syndrome (NS). This study used a paired design to test the hypothesis that remission of NS is associated with a decreased content of urinary plasmin and reduced ability of patients’ urine to activate ENaC. Methods Samples were collected during active NS and at stable remission from 20 patients with idiopathic NS, aged 9.1 ± 3.2 years. Plasminogen–plasmin concentration was measured with an enzyme-linked immunosorbent assay. Western immunoblotting for plasminogen–plasmin was performed in paired urine samples. The patch clamp technique was used to test the ability of urine to evoke an inward current on collecting duct cells and human lymphocytes. Results The urinary plasminogen–plasmin/creatinine ratio was 226 [95 % confidence interval (CI) 130–503] μg/mmol in nephrotic urine versus 9.5 (95 % CI 8–12) μg/mmol at remission ( p