Bortezomib-induced glomerular microangiopathy complicated with monoclonal immunoglobulin deposition disease.

A 75-year-old man admitted with IgG λ-type myeloma with creatinine level of 2.3 mg/dL. Serum lactate dehydrogenase level and platelet count were normal. Urinalysis demonstrated massive proteinuria dominated by albuminuria. Weekly bortezomib and dexamethasone therapy were started to treat myeloma but failed to be continued because of rapid deterioration of renal function and increase in proteinuria 1 week after the treatment. His renal function exacerbated to require hemodialysis for a month. There was no clinical evidence of tumor lysis syndrome or thrombocytopenia throughout the course of his acute kidney injury (AKI). After he became dialysis independent, a renal biopsy was performed to clarify myeloma-related renal involvement and the cause of AKI. As a result, IgG2-λ monoclonal immunoglobulin deposition disease (MIDD) and severe endothelial injury were revealed. There was no evidence of cast nephropathy. Bortezomib-induced glomerular microangiopathy (GMA) superimposed on MIDD. Bortezomib has a potential risk to cause drug-induced GMA without systemic thrombotic microangiopathy, in which vascular endothelial growth factor-nuclear factor-κ B pathway could be involved. This is the first case of biopsy-proven bortezomib-induced GMA. If proteinuria (mainly albuminuria) increases after using bortezomib, GMA should be suspected as an adverse effect of bortezomib even absent of clinical signs of systemic thrombotic microangiopathy.