IL1A and glomerulonephritis: As previously observed in experimental anti-GBM disease and in patients with antineutrophil cytoplasmic autoantibody vasculitis–associated glomerulonephritis,25 the increased bioavailability of plasma HGFs, TPO and SCF; and proinflammatory cytokines, IL1α and IL6, is also a hallmark of anti-GBM disease in patients.