Treatment of proliferative glomerulonephritis with monoclonal Ig deposits

Ig: immunoglobulin; VCD: bortezomib, cyclophosphamide, dexamethasone; RCD: rituximab, cyclophosphamide, dexamethasone; BR: bendamustine, rituximab; IgM: immunoglobulin M; ACE: angiotensin-converting enzyme; ARB: angiotensin receptor blocker.
* Treatment should be selected and administered in consultation with a hematologist or oncologist who is experienced in the use of antimyeloma and antilymphoma agents.
¶ In patients who have monoclonal Ig deposition in the kidney, no detectable monoclonal protein in the serum or urine, and normal kidney function and proteinuria <1 g/day, the decision to aggressively treat with chemotherapy is more difficult since there is no clear evidence that a pathologic clone is responsible for the kidney disease. In such patients, a more conservative approach to treatment is preferred.
Δ In patients who have non-IgM monoclonal protein deposits in the kidney, it is difficult to infer whether the patient has a hypothetical plasma cell clone or a B cell clone. In such patients, it is reasonable to initiate empiric treatment with either plasma cell- or B cell-directed therapy after discussing the potential risks and benefits of these therapies with the patient.