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Kidney Week

Abstract: SA-PO210

Renal Thrombotic Microangiopathy with Multiple Myeloma: Resolution with Chemotherapy

Session Information

  • Trainee Case Reports - V
    October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

  • 103 AKI: Mechanisms

Authors

  • Ehren, Lindsey, University of South Florida, Tampa, Florida, United States
  • Lee, Dae Hyun, University of South Florida, Tampa, Florida, United States
  • Shirley, Kayla, University of South Florida, Tampa, Florida, United States
  • Mirza, Abu-Sayeef, University of South Florida, Tampa, Florida, United States
  • Obi, Onyekachi C., University of South Florida, Tampa, FL, Florida, United States
  • Bassil, Claude, University of South Florida, Tampa, FL, Florida, United States
  • Baz, Rachid, H. Lee Moffitt Cancer Center & Research Institute, Tampa, Florida, United States
  • Wheeler, Donald E., University of South Florida, Tampa, Florida, United States
Introduction

Thrombotic microangiopathy (TMA) is a clinical entity described by systemic microvascular occlusion, causing hemolytic anemia and thrombocytopenia resulting in end-organ ischemia. Numerous mechanisms may cause the condition including direct immunoglobulin deposition or chemotherapy. TMA is a pathological diagnosis characterized by fibrin thrombi within arterial vessels including the capillaries. Recent literature shows up to 13.7% of patients with thrombotic microangiopathy have monoclonal immunoglobulin. We present a case in which renal TMA-associated acute kidney injury responded to multiple myeloma treatment.

Case Description

A 43-year-old male with history of recent Bell’s palsy and peripheral neuropathy presented with abdominal distension, dyspnea and unintended weight loss. Initial evaluation was significant for anemia (Hgb 8.9g/dL), normal platelet count (265,000/mm3), normal LDH (139 U/L) and acute kidney injury (Creatinine 2.2mg/dL). CT of abdomen and pelvis demonstrated large-volume ascites and nonspecific sclerotic density in left iliac bone. Subsequent workup included a bone marrow biopsy significant for 30% plasma cells with 90% cellularity, and serum protein electrophoresis of positive IgA lambda monoclonal gammopathy (IgA 928mg/dL, M spike 0.5g/dL). Diagnosis of plasma cell myeloma was made. Renal biopsy was consistent with chronic thrombotic microangiopathy without immunoglobulin deposits by IFM or EM. The patient was treated with cyclophosphamide and prednisone (50mg). Renal function improved within the first three weeks of treatment to 1.3mg/dL.

Discussion

Very few cases have reported renal TMA with multiple myeloma to date. Distinct from the typical light-chain associated renal tubular injury of multiple myeloma, AKI due to TMA is also described. Our patient is one of few reported cases in which myeloma treatment resulted in improvement in renal TMA-induced renal insufficiency. Further investigation is needed to establish management guidelines for renal failure in this setting.