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Plasma cell myeloma is a malignancy of plasma cells (see Chapter 13-34) that can cause a variety of renal disorders. “Myeloma kidney” (formally called cast nephropathy) is the most common kidney disease in plasma cell myeloma and occurs when light chain immunoglobulins (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 and hematuria are not present. Hypercalcemia and hyperuricemia are frequently seen. Glomerular amyloidosis can develop in patients with plasma cell myeloma; in these patients, dipstick protein tests are positive due to glomerular epithelial cell foot process effacement and albumin “spilling” into the Bowman capsule with resultant albuminuria; 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 attributed to plasma cell myeloma includes correction of hypercalcemia, volume repletion, and chemotherapy for the underlying malignancy. Plasmapheresis has been proposed to reduce the burden of circulating monoclonal proteins, but results have been equivocal and its use is controversial.

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