Rituximab in immunologic glomerular diseases

Figures & data

Figure 1 Rituximab mode of action: apoptosis and ADCC. Rituximab mediated apoptosis is thought to be a consequence of caspase-3 activation. Complement activation by the Fc portion of the antibody leading to cell lysis is another mode of action of rituximab. Rituximab also induces ADCC mediated by a variety of effector cells (natural killer cells, granulocytes and macrophages). ADCC in the presence of rituximab represent killing of B cells by effector cells that are activated by binding to the Fc portion of the chimeric anti-CD20 molecule.

Table 1 Proposed role of rituximab in glomerular diseases

Lupus nephritis

Induction of remission

Relapsing or refractory disease

Inadequate data on role as maintenance therapy

ANCA-associated vasculitides

Induction of remission

Combination therapy with cytoxan for induction of remission

Poor response in granulomatosis manifestations (orbital/pachymeningitis)

Inadequate data on role as maintenance therapy or timing of retreatment to prevent relapse

Cryoglobulinemic vasculitis

Hepatitis C-related

Non-Hepatitis C-related

Non-cryoglobulinemic glomerulonephritis

Idiopathic membranous nephropathy

Anti-PLA2-related diseases

Overcome dependency on calcineurin inhibitors

Autoimmune thrombotic thrombocytopenic purpura

Beneficial in patients with poor response to standard therapy

Suggestion of benefit as first-line therapy in acute TTP

Focal segmental glomerulosclerosis

Recurrent FSGS in transplanted kidney

Uncertain benefit in primary FSGS