Studies have demonstrated uPAR can lead to foot process effacement and urinary protein loss in puromycin aminonucleoside nephrosis and LPS-induced transient proteinuria in mice, which was also identified in a majority of patients with FSGS as a soluble factor that acts through binding to and activating podocyte β3 integrin to promote cell motility and kidney permeability16, 17. Here, PLAUR is linked to focal segmental glomerulosclerosis.