Focal segmental glomerulosclerosis (FSGS) is a common cause of proteinuric kidney disease, which comprises both native and transplanted kidneys. Treatment was limited in the past due to the complicated pathogenesis of FSGS, including previously unidentified serum factors. Here, serum soluble urokinase receptor (suPAR) is reported to be elevated in FSGS patients but not in patients with other primary glomerular diseases. Higher pre-transplantation suPAR levels are associated with risk for FSGS recurrence in kidney grafts. Renal disease only develops when suPAR sufficiently activates podocyte β3 integrin. Thus, disease pathogenesis can be stopped or slowed by ex vivo removal of suPAR from a subject's circulation. Removal may be measured by comparing the level (e.g., amount or concentration) of suPAR before and after such treatment.
