The complement pathway is a central part of the innate immune system and also modulates adaptive immunity. It is implicated in the pathogenesis of glomerular disease by a number of clinical findings. These include the presence of complement components in renal biopsy samples, decreases in circulating levels indicating consumption, the presence of autoantibodies to complement proteins and the association of genetic mutations with disease either in individuals or within families. Further support and mechanistic insights comes from animal models. This review provides an overview of the role of complement in glomerular diseases and discusses the data from patients and animal models with reference to specific diseases. These include atypical haemolytic uraemic syndrome, C3 glomerulopathy, anti-neutrophil cytoplasmic antibody vasculitis, lupus nephritis and membranous nephropathy. The implications for therapy are also discussed.