Novel opportunities for C3 glomerulopathy treatment: what do we know to date

C3 glomerulopathy (С3G) is a group of ultra-rare diseases with the incidence about 13 cases per 1 million population per year. Major role in the C3G pathogenesis play disturbances of the complement activation, deposition and degradation, resulting in the glomerular deposition of C3, which, in turn, leads to glomerular damage and inflammation in the kidney tissue. C3G commonly associated with the progressive course, poor kidney outcomes and high rate of recurrence after kidney transplantation. Efficacy of the current conventional approaches to C3G treatment, including nephroprotective measures and glucocorticoids and mycophenolic acid analogues is insufficient; the usage of targeted anti-B-cell therapy with rituximab also did not provide sustainable effect. Unsatisfactory results of the current clinical practice and a rapid progress in the development of new targeted medications recently lead to the active investigation of a number of molecules, targeting several factors of the complement cascade, which may enrich therapeutic armamentarium for the treatment of C3G and other glomerular diseases, associated with the complement dysregulation. Several studies, aiming the evaluation of blockade of various complement system components – C5, C5a receptor, factor D, factor B, C3, and mannose-binding lectin-associated serine proteases type 1 and type 2 for С3G treatment are currently in progress. This review of literature presents available data from the current clinical trials and discusses new options of the targeted treatment of C3G.