Abstract: SA-PO209
Influenza Triggered Thrombotic Microangiopathy
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
- Pitts, Eric, UT Health Science Center, Houston, Houston, Texas, United States
- Tchakarov, Amanda, University of Texas Medical School at Houston, Houston, Texas, United States
- Kala, Jaya, UT Health Science Center, Houston, Houston, Texas, United States
Introduction
Thrombotic microangiopathy(TMA) is a clinical entity characterized by intravascular microangiopathic hemolytic anemia,thrombocytopenia and acute kidney injury. Influenza virus triggered TMA(iTMA) has been rarely reported. Paucity in literature of this clinical entity prompted this report of iTMA. With this report we would like to highlight the importance of understanding other potential causes of TMA in a patient on proteasome inhibitor, also known to cause TMA.
Case Description
A 69 year old lady with diabetes mellitus,hypertension,chronic kidney disease and multiple myeloma on chemotherapy, presented with fever, weakness, shortness of breath and cough for past one day. She received her 14th cycle of carfilzomib and dexamethasone, two days prior to presentation. Her blood pressure was 188/98 mm Hg. Laboratory testing showed creatinine at baseline of 2.2 mg/dl but revealed positive Influenza A. She was admitted for hypertensive urgency and sepsis due to influenza. She was started on Osteltamivir and cancer chemotherapy was held. On day 4 of admission, nephrology was consulted for elevated creatinine of 3.18 mg/dl. Despite volume resuscitation her creatinine continued to rise to 6.88 mg/dl. Further evaluation showed that her hemoglobin drop to 7.7gm/dl, platelets 34,000/uL, lactate dehydrogenase elevated at 849U/l, undetectable haptoglobin. This in addition to hypertensive urgency prompted the diagnosis of TMA. ADAMSTS 13 activity was normal. Hemodialysis was started for worsening renal function and oliguria. Renal biopsy suggested presence of TMA. She received a course of ostelamivir and needed dialysis for a week. After the therapy she stayed off dialysis and returned to baseline creatinine in 2 weeks. Our patient was on carfilzomib for the last 11 months, known to cause TMA, however she developed it only after the influenza infection. She couldn't restart carfilzomib due to financial issues.
Discussion
Influenza associated TMA is a rare entity. It has been reported to occur around 4 days after the onset of infection, like in our patient. The outcome of iTMA is generally favorable with supportive care.. Our patient was on carfilzomib for 11months and the only apparent trigger for the TMA was influenza. Identification of the etiology and differentiation between drug induced complement dysregulation and influenza associated HUS without identifiable complement abnormalities are crucial for treatment.