Multiple myeloma is a malignant plasma cell dyscrasia characterized by bone marrow plasmacytosis (1). Malignant plasma cells produce an abnormal monoclonal immunoglobulin, the laboratory hallmark of the disease process, as well as cytokines, which stimulate cells of the bone marrow microenvironment (2)(3). The neoplastic clone and its products cause the dysfunction of several organs, including bone pain or fractures, renal failure, anemia, susceptibility to infection, hyperviscosity, and hypercalcemia (1). However, the most characteristic feature of multiple myeloma and other monoclonal gammopathies is the presence of a serum and/or urinary monoclonal (M) component on immunofixation (4). Approximately two-thirds of patients with a serum M component also have Bence Jones proteins (BJPs) in the urine. In almost 20% of myelomas, only immunoglobulin light chains are present in the serum and/or urine and are often designated as light chain multiple myeloma (LCMM).
Renal failure occurs in ∼25% of myeloma patients, and there is some renal pathology in more than one-half (1)(5)(6). The number of patients with renal disease varies considerably depending on the criteria used to define renal impairment. Serum creatinine concentrations remain in the reference interval until the glomerular filtration rate is reduced by almost 50%; therefore, the data obtained with blood creatinine concentrations most likely underestimate the incidence of renal involvement in myeloma. Data using the estimated creatinine clearance rate (7), which takes into account various variables, including patient age, weight, and gender, indicate that approximately one-half of patients have renal insufficiency at the time of diagnosis (5). The nature of the M component is also associated with the prevalence of renal disease (5)(8)(9). In light chain myeloma, 65% of patients have impaired renal function at the time of diagnosis when estimated creatinine clearance is used as the variable (5). The …
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