Abstract: SA-PO262
Therapeutic Plasma Exchange in Carfilzomib Associated Thrombotic Microangiopathy
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
- Krate, Jonida, St. Joseph's Hospital and Medical Center Phoenix, Arizona, Phoenix, Arizona, United States
- Qaqish, Ibrahim, St. Joseph's Hospital and Medical Center Phoenix, Arizona, Phoenix, Arizona, United States
Introduction
Thrombotic microangiopathy (TMA) was reported to be associated with second generation proteasome inhibitors. The role of therapeutic plasma exchange(TPE) in management of carfilzomib induced TMA is not clear. Here we present our experience on TPE use in management of carfilzomib induced TMA.
Case Description
61 year old man with past medical history of congestive heart failure, type 2 diabetes mellitus, hypertension, chronic kidney disease, diagnosed with kappa light chain multiple myeloma in February 2016. He was started on Cybor-D chemotherapy in March 2016. His chemotherapy was interrupted several times due to acute kidney injury (AKI). Subsequently, he progressed and he was transitioned to carfilzomib, revlimid, and dexamethasone combination of chemotherapy in May 2017. Two months after initiation of carfilzomib therapy patient developed markedly elevated BUN and serum creatinine. Patient underwent kidney biopsy, which revealed abundant glomerulosclerosis (8/10 globally sclerotic) and ~ 70% of interstitial fibrosis and tubular atrophy. Some non-sclerotic glomeruli showed global capillary thrombosis and necrosis.
Patient underwent eight sessions of TPE. Lactate dehydrogenase improved after termination of carfilzomib and continued to improve after TPE. Haptoglobin improved after TPE. Platelet count did improve despite termination of chemotherapy and TPE. Unfortunately, because of severity of AKI patient never regained kidney function and required chronic hemodialysis.
Discussion
We presented case of TMA after initiation of carfilzomib for the treatment of multiple myeloma. Patient did not have ADAMTS 31 deficiency. TPE was held to assess for platelet response, which remained stable then increased and therefore TPE was not resumed. In our patient platelete transfusion given prior to renal biopsy confounded interpretation of total TPE. Given the pattern of minimal hematological and clinical response in our patient to TPE compared to the response in patients with idiopathic TTP, we speculate the optimum role of TPE is minimal or not established in Carfilzomib associated TMA. Discontinuation of the drug remains an important management strategy and the role of TPE is still not categorized by ASFA.
Clinicians should be aware of rare association between carfilzomib underlying TMA. Discontinuation of the drug, future drug avoidance and supportive care is the corner stone of management.