RT Book, Section A1 Dirkx, Tonja C. A1 Woodell, Tyler B. A2 Papadakis, Maxine A. A2 McPhee, Stephen J. A2 Rabow, Michael W. A2 McQuaid, Kenneth R. SR Print(0) ID 1184183507 T1 Plasma Cell Myeloma T2 Current Medical Diagnosis & Treatment 2022 YR 2022 FD 2022 PB McGraw-Hill Education PP New York, NY SN 9781264269389 LK accessmedicine.mhmedical.com/content.aspx?aid=1184183507 RD 2024/04/25 AB Plasma cell myeloma is a malignancy of plasma cells (see Chapter 13) that can cause a variety of renal disorders. Injury is due to the toxic effects of monoclonal immunoglobulins or light chain components produced by plasma cells. “Myeloma kidney” (formally called cast nephropathy) is the most common kidney disease in plasma cell myeloma and occurs when light chains (Bence Jones protein) in the urine cause renal toxicity and tubular obstruction by precipitating in the distal tubules. Plasma cell myeloma may also cause Fanconi syndrome, a type 2 proximal renal tubular acidosis characterized by hypophosphatemia and inappropriate glycosuria. Proteinuria in “myeloma kidney” is exclusively tubular; hence, urine dipstick findings are minimal since glomerular proteinuria is not present. Hypercalcemia and hyperuricemia are frequently seen. Glomerular amyloidosis with nephrotic syndrome can develop in patients with plasma cell myeloma; in these patients, urine dipstick is positive due to glomerular epithelial cell foot process effacement and albumin “spilling” into the Bowman capsule; hematuria may or may not be present. Other conditions resulting in kidney dysfunction include plasma cell infiltration of the renal parenchyma and hyperviscosity syndrome compromising renal blood flow. The presence of myeloma-related kidney disease does not itself preclude use of contrast dye for imaging studies; standard precautions for the use of intravenous contrast and gadolinium in patients with reduced GFR apply to patients with myeloma-related kidney disease. Therapy for AKI (see Acute Kidney Injury, above) attributed to plasma cell myeloma includes correction of hypercalcemia; volume repletion; and chemotherapy for the underlying malignancy, typically with bortezomib-based agents. Plasmapheresis has been proposed to reduce the burden of circulating monoclonal proteins, but results have been equivocal and its use is controversial.