Abstract
Recently it was reported that urinary plasmin activates the epithelial sodium channel (ENaC) and may mediate sodium retention. The present study investigates if remission of nephrotic syndrome (NS) affects glomerular filtration of plasminogen, its activation to plasmin, and the ability of the patients urine to activate ENaC.A paired design study was conducted collecting samples during active nephrotic syndrome and at stable remission. Single cell patch clamp experiments were performed on single collecting duct cells (CDC) with urine samples from six patients investigating the potential to generate an ENaC mediated current.Urine samples from active NS significantly increased the inward current in CDC (201 ± 31%, n=6), whereas at remission, the observed current was significantly lower (29 ± 10%, n=6). The ability of nephrotic urine to enhance inward current was abolished by amiloride (2 μM) (19 ± 10%, n=6).Our data demonstrate significantly increased inward (ENaC) current induced by urine collected during active NS compared to remission, suggesting ENaC inhibition by amiloride to be a new therapeutic target for oedema control.
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