Anti-CD40 Abs purified from the sera of recurrent FSGS patients were particularly pathogenic in human podocyte cultures and injection of anti-CD40/rFSGS Ab enhanced suPAR-mediated proteinuria in wild-type mice, but no sensitizing effect was noted in mice deficient in CD40 or in wild-type mice that received blocking Ab to CD40, supporting the fact that suPAR might be formed by immunologically mediated mechanisms in FSGS [99]. This evidence concerns the gene CD40 and focal segmental glomerulosclerosis.