Immune-mediated kidney diseases are characterized by an adaptive immune response directed against various self-antigens. B cells, as progenitors of autoantibody-producing plasma cells and as antigen-presenting cells, play a crucial role in the pathogenesis of these diseases. Despite significant advancements in B-cell-targeting therapies, relapses are common among patients. Evidence of insufficient B-cell depletion by monoclonal antibodies such as rituximab, and the inability to deplete plasma cells, suggest that a more robust and complete B-cell depletion may be necessary for immune-mediated kidney diseases.