[Immunotherapy mechanisms in glomerulonephritis]

Abstract

The pathogenetic mechanisms of glomerulonephritis are numerous and complex, involving both humoral and cell-mediated immune responses. The ability of drugs to interfere with immune pathways has not been completely understood and the treatment of glomerulonephritis is therefore still empirical and based on clinical studies. Corticosteroids are the most commonly used drugs; their mechanism of action is variable and can be modulated by the prescribed dosage. Immunosuppressive drugs employed for the treatment of glomerulonephritis include alkylating agents such as cyclophosphamide and antimetabolites such as mycophenolate-mofetil and azathioprine. These drugs have a powerful immunosuppressive effect but are associated with several dangerous side effects. Cyclosporin A is a calcineurin inhibitor belonging to the class of immunomodulators and is able to interfere with the immune response. Another group of drugs are monoclonal antibodies, the most popular among which is rituximab. It is an antibody directed against the transmembrane protein CD20, specifically espressed on the surface of B lymphocytes. Its use is limited to cases in which the usual therapy with steroids and immunosuppressive drugs was ineffective. The clinical studies conducted so far look promising.