Abstract: SA-PO1197
Which Thrombotic Microangiopathy Came First? A Differential of Delayed Kidney Graft Function
Session Information
- Transplantation: Clinical - Complications, Pediatrics, and Multi-Organ Considerations
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Jameson, Robert L., Baylor College of Medicine, Houston, Texas, United States
- Walther, Carl P., Baylor College of Medicine, Houston, Texas, United States
- Ajmal, Muhammad Suleman, Baylor College of Medicine, Houston, Texas, United States
- Murthy, Bhamidipati V.R., Baylor College of Medicine, Houston, Texas, United States
Introduction
Delayed graft function (DGF) can present a diagnostic and clinical quandary during a critical time of patient’s renal recovery. Should an aggressive condition be suspected, the decisions for treatment and testing are not benign. Here we present a patient who after transplantation had multiple clinical complications, predominately a DGF from thrombotic microangiopathy (TMA) suspected from calcineurin use, with a differential of atypical hemolytic uremic syndrome (HUS) and T-cell mediated rejection (TCMR).
Case Description
The patient was a 60-year-old Pakistani male with kidney failure due to hypertension, CAD with stent placement, chronic combined heart failure, and a history of spontaneous left renal hematoma development (Wunderlich syndrome) eight years prior requiring embolization who underwent a deceased donor kidney transplant with basiliximab induction. The kidney donor profile index was 27% and terminal creatinine (Cr, mg/dL) was 1.0 without a graft biopsy. The patient’s panel-reactive antibody was 12% without donor specific antibodies (DSA). Warm ischemic time was 30 minutes, with cold ischemia time of 35 hours.
The patient had DGF, and thrombocytopenia post-transplant. An allograft biopsy performed on post-op day 6 revealed extensive TMA and Banff IIA rejection (i2, v1, g2, ptc2, C4d0) with signs of peritubular capillaritis, glomerulitis, and tubulitis. C4d staining was negative and DSA were absent making tacrolimus-induced TMA more likely than antibody mediated rejection. While the histopathology findings suggested possible TCMR. He received anti-thymocyte globulin and plasmapheresis, and as the patient’s DGF persisted he was also given eculizumab for possible atypical HUS. He later developed perinephric and retroperitoneal hematomas requiring operative evacuations. Initially tacrolimus was changed to sirolimus, and later to cyclosporine to improve post-operative wound healing. His Cr was 2.0 upon discharge after over a month post-transplant. In the interim, he was found to have a complex post-surgical fluid collection with similar Cr upon discharge. Months later in clinic his Cr fluctuated from 2.2 to 2.8.
Discussion
This case shows how post-transplant TMA reduces diagnostic certainty and emphasizes patient involved decision-making. Our case had a mixed presentation of tacrolimus usage vs Banff IIa mixed TCMR by histology, in addition to possible atypical HUS given his prior episode of Wunderlich syndrome