Abstract
Azotemia associated with the use of lenalidomide, a new and effective therapy for multiple myeloma, has not been reported in patients with multiple myeloma. We describe five patients with plasma cell dyscrasias and renal insufficiency (AL amyloidosis, monoclonal gammopathy of undetermined significance with Fanconi syndrome, and multiple myeloma) treated with lenalidomide and dexamethasone who developed progressive azotemia. Onset of azotemia after initiation of lenalidomide was variable (2 weeks to several months) and was irreversible in four patients. Four patients required hemodialysis after exposure to lenalidomide; two previously were untreated for their plasma cell dyscrasia. The mechanism of azotemia is unknown, but the combination of potentially nephrotoxic paraproteins and lenalidomide, which is immunomodulatory and anti-angiogenic, may underlie this process. We conclude that azotemia is an uncommon, but serious, potential complication of lenalidomide therapy in plasma cell dyscrasias with associated renal insufficiency. We advise careful monitoring of renal function after initiation of lenalidomide in this setting.