Abstract: PUB521
Clinical and Histopathological Features of Anti-AT1 Receptor Antibody-Mediated Acute Rejection in Kidney Transplant Recipients: A Case Series
Session Information
Category: Transplantation
- 2102 Transplantation: Clinical
Authors
- Olano, Claudia Guadalupe, Harbor UCLA Medical Center, Torrance, California, United States
- Urrutia, Andrea Leonor, Harbor UCLA Medical Center, Torrance, California, United States
- Akram, Sami M., Loma Linda University, Loma Linda, California, United States
Introduction
According to US renal Data System (USRDS), one in five patients will lose their kidney allograft within 5 years of transplantation, and over half will experience allograft loss by 10 years (1). Allograft loss is associated with a high burden of psychologic and medical morbidity, with patients faring poorly across many traditional measures of quality of care, including anemia management and phosphate control (2, 3). The most common cause of graft loss during life is alloimmunity (5).
Case Description
Patients: There were four kidney transplant recipients between the ages 34 – 60 (table 1). There were two males and two females. Blood groups are shown in Table 1. The causes of primary renal disease and the comorbidities recorded in Table 1. One patient had biopsy proven TMA as the cause of renal failure. There was one case of second renal transplant. One patient had Living unrelated donor kidney transplant (case 1) and the three others had deceased donor kidney transplant. The case number 2 received donation after cardiac death (DCD). No patient had zero mismatch organ (table 1). In all cases, complement-dependent T-cell and B-cell cross match were negative prior to the operation. T cell antibody and B cell antibody cross match was done with pronase tested donor cells. In case #1 of living unrelated donor, cross match was performed using multiple techniques, automated flow, and serology. Case one and four had zero panel reactive antibodies (PRA), while cases two and three were severe and moderately sensitized respectively (case 2 PRA 85/75, case 3 PRA 45/62).
In case number two there were both Class I DSA and Anti AT1R. Relapse of her underlying TMA was reason. This patient was prescribed Ultimiris resulting in stabilizing of serum creatinine.
Discussion
In conclusion, testing for anti AT1R antibody should be done early if not prior to kidney transplantation. Injury in Acute Rejection mediated by anti AT1R antibodies may be due to mitochondrial dysfunction. Repertoire to treat Acute rejection by inhibiting ERK ½ signaling pathway is about to grow explosively. There is an opportunity to influence the therapy of acute rejection and improve graft as well as patient survival