Abstract: SA-PO258
Vancomycin Associated AKI: Think of 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
- Bhalla, Anshul, Tufts Medical Center, BOSTON, Massachusetts, United States
- Wacker, Matthias, Tufts Medical Center, BOSTON, Massachusetts, United States
- Goyal, Nitender, Tufts Medical Center, BOSTON, Massachusetts, United States
Introduction
Vancomycin-induced renal toxicity is common and thought to be due to interstitial nephritis or direct tubular toxicity. Vancomycin can also induce an immunological response, leading to production of drug-dependent anti-platelet antibodies and cause immune-mediated thrombocytopenia. A similar antibody mediated process can be associated with drug-induced thrombotic microangiopathy (TMA) and AKI.
Case Description
A 51 year old woman, who recently completed a 2 week course of Levofloxacin for pneumonia, was diagnosed with a lung abscess and empyema and initiated on Vancomycin, Cefepime and Metronidazole along with a chest tube placement. She remained hemodynamically stable with kidney function at baseline. On hospital day 5, she developed oliguric AKI with supratherapeutic vancomycin levels. She was also noted to be thrombocytopenic. Hemolysis labs were abnormal with LDH 730 and haptoglobin <10. Peripheral smear showed 10-12 schistocytes/hpf. Liver function tests, disseminated intravascular coagulation workup, complement levels, auto-immune and vasculitis serologies were within normal limits. ADAMTS13 activity was markedly low (<5%) and ADAMTS13 inhibitor presence was confirmed with Bethesda assay. Vancomycin-dependent anti-platelet antibody (tested at Blood Center of Wisconsin) was positive. Diagnosis of acquired TTP was made and managed with discontinuation of vancomycin and initiation of plasma exchange for a total of 4 exchanges and prednisone with improvement in platelet count, hemolysis parameters and kidney function. (Table 1).
Discussion
We report a case of acquired TTP with ADAMTS13 inhibitor and vancomycin-dependent antiplatelet antibody. A previous study reported one patient with suspected vancomycin-induced TMA with presence of anti-platelet antibodies but ADAMTS13 activity was not tested. In our case, timing of TMA and AKI after 5 days of vancomycin exposure along with presence of the antibody point towards a vancomycin associated immune mediated process. It is difficult to ascertain if the antiplatelet antibody was detected as the ADAMTS13 inhibitor or if both antibodies co-existed. TMA should be identified as a cause of vancomycin associated AKI.