Abstract: PUB316
Thrombotic Thrombocytopenia With Acute Graft Thrombosis (AGT) After Kidney Transplantation
Session Information
Category: Transplantation
- 2002 Transplantation: Clinical
Author
- Steinberg, Julie, Cohen Children's Medical Center, Queens, New York, United States
Introduction
Our case is a patient with AGT of multiple failed kidney transplants.
Case Description
A 15 year old F with Nephronphthisis and ESKD had a living unrelated kidney transplant (LUKT), when poor graft perfusion prompted arterial reanastomosis with improvement. After closure intrarenal doppler waveforms were poorly visualized. Given decreasing serum creatinine (SCr) and good urine output, she was observed. Hours later SCr rose with intrarenal blood flow (BF) on doppler. The graft was found mottled with AGT and thrombi in the right (Rt) external iliac artery, renal artery (RA) and vein (RV). Graft was removed, flushed with heparin/alteplase and reimplanted with doppler-confirmed BF. After closure BF was not detected with diminished Rt lower extremity pulses. The graft was necrotic and removed. Thrombi were removed from the Rt common/ iliac, femoral and popliteal arteries. HD was restarted with heparin. Within hours, thrombocytopenia worsened. Elevated D-dimer and positive platelet factor-4 antibodies (PF-4Ab) suggested heparin-induced thrombocytopenia (HIT) despite negative serotonin release assay (SRA). Heparin was changed to argatroban then apixiban. Following resolved thrombocytopenia and negative PF-4 Ab, she had a second LUKT on therapeutic argatroban. She again had AGT with intrarenal, RV and RA thrombi requiring graft removal. Workup showed positive Coombs and negative heparin Ab, suggestive of Ab-mediated consumptive coagulopathy consistent with vaccine induced thrombotic thrombocytopenia (VITT).
Discussion
Initially HIT was presumed, and heparin discontinued, yet AGT occurred despite heparin avoidance. Thus, symptoms were more consistent with VITT, a syndrome that can occur after COVID-19 vaccines with adenovirus vector. Yet, she was not vaccinated. Like HIT, VITT is thought to be from IgG binding to the PF-4-heparin complex, activating platelets and initiating a hypercoagulable cascade with platelet consumption. Although clinically similar, HIT and VITT are treated differently, thus it is vital to differentiate the two.