Complement disinhibition is pathogenic: DAF/CD55 loss unleashes C3 convertase, activating C3a/C3aR and an IL-1β/IL-1R1 loop that lowers nephrin and remodels actin; low DAF with C3d positivity and high urinary C3a coincide with FSGS-like lesions and proteinuria [33]. Here, IL1B is linked to focal segmental glomerulosclerosis.