Kidney Week

Abstract: SA-PO263

Reversible Dialysis Dependent AKI Due to Carfilzomib Induced Thrombotic Microangiopathy (TMA)

Session Information

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

Category: Trainee Case Reports

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Patel, Abhishek J., University of Tennessee Health Science Center, Memphis, Tennessee, United States

Abhishek J. Patel,

• Dasari, Aravind, University of Tennessee Health Science Center, Memphis, Tennessee, United States

Aravind Dasari,

• Vo, Hieu Q., University of Tennessee Health Science Center, Memphis, Tennessee, United States

Hieu Q. Vo,

• Wall, Barry M., Veterans Affairs Medical Center, Memphis, Tennessee, United States

Barry M. Wall,

Group or Team Name

• University of Tennessee Health Science Center, Memphis, TN, United States

Introduction

Renal complications of carfilzomib, a second-generation proteasome inhibitor used in treatment of relapsed or refractory multiple myeloma, are typically mild and reversible. However, severe acute kidney injury (AKI) related to TMA and tumor lysis have also been reported. We report an additional patient with kidney biopsy confirmed TMA leading to dialysis dependent AKI that fully resolved after discontinuing caflizomib without the use of immunosuppressive medications or plasmapheresis.

Case Description

56 year old male with stage 1 IgG kappa light chain restricted multiple myeloma with 50-60% of bone marrow replacement with CD138+ plasma cells with t(11;14) translocation received intial treatment with bortezomib, lenalidomide and dexamethasone with minimal response. He was then treated with one cycle of carfilzomib (20 mg/m² on 2 consecutive days), lenalidomide, and dexamethasone. He subsequently presented two weeks later with non-oliguric AKI with a serum creatinine of 10.3 mg/dL (pre-treatment creatinine, 0.9 mg/dl). He was euvolemic by clinical examination and no kidney abnormalities were noted on kidney ultrasound. Additional laboratory included: uric acid 11.7mg/dL, serum calcium 7.5mg/dL, phosphorus 4.8mg/dL and potassium 3.6mg/dL. Hemoglobin had decreased from 13.8 to 9.8 g/dl, platelet count decreased from 384 to 72 K/ul, and schistocytes were noted on the peripheral blood smear. AKI worsened despite discontinuing carfilzomib and the administration of intravenous fluids and rasburicase. Temporary hemodialysis support was required for one week. Renal biopsy revealed thrombotic microangiopathy, acute tubular injury, moderate arteriosclerosis and arteriolar hyalinosis. AKI rapidly resolved with follow up serum creatinine of 1.1 mg/dL. Similarly, hemoglobin and plateltet count gradually returned to pre- treatment values. He is currently being evaluated for autologous stem cell transplantation and has not been rechallenged with carfilzomib.


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Discussion

Our patient had renal biopsy proven TMA following a single cycle of carfilzomib treatment that resulted in dialysis dependent non-oliguric AKI with associated microangiopathic anemia and thrombocytopenia. AKI was reversible after discontinuing carflizomab without concomitant use of plasmapheresis or immunosuppressive medications, consistent with direct drug induced toxicity.