Plasma cell myeloma is a malignancy of plasma cells (see Chapter 13). Renal involvement occurs in about 25% of all patients. “Myeloma kidney” is the presence of light chain immunoglobulins (Bence Jones protein) in the urine causing renal toxicity. Bence Jones protein causes direct renal tubular toxicity and results in tubular obstruction by precipitating in the tubules. The earliest tubular damage results in Fanconi syndrome (a type II proximal renal tubular acidosis). The proteinuria seen with plasma cell myeloma is primarily due to light chains that are not detected on urine dipstick, which mainly detects albumin. Hypercalcemia and hyperuricemia are frequently seen. Glomerular amyloidosis can develop in patients with plasma cell myeloma; in these patients, dipstick protein determinations are positive due to glomerular epithelial cell foot process effacement and albumin “spilling” into the Bowman capsule with resultant albuminuria. Other conditions resulting in kidney dysfunction include plasma cell infiltration of the renal parenchyma and a hyperviscosity syndrome compromising renal blood flow. Therapy for AKI attributed to plasma cell myeloma includes correction of hypercalcemia, volume repletion, and chemotherapy for the underlying malignancy. Plasmapheresis had been considered appropriate to decrease the burden of existing monoclonal proteins while awaiting chemotherapeutic regimens to take effect. However, in the largest randomized prospective trial to date, plasmapheresis did not provide any renal benefit to these patients. Pheresis therapy still remains controversial.








Content 3

Content 13

Content 11




USMLE Reviewer (Subscription Required)