Angiotensin II Type 1 Receptor Antibody-Mediated Kidney Rejection Unresponsive to Treatment

Abstract

Allograft rejection is a significant cause of renal transplant failure which needs prompt diagnosis and treatment for graft salvage. Angiotensin II type 1 receptor antibody-mediated rejection (AT1R-AMR) is increasingly being identified as the etiology of antibody-mediated rejection in kidney transplant recipients with allograft rejection but without detectable human leukocyte antigen (HLA) antibodies. While some reports have suggested that AT1R-AMR may be refractory to standard therapy, others have reported improvement or stabilization of graft function. We present two patients in which anti-rejection therapy including therapeutic plasma exchange was unable to salvage the allograft.

Immune monitoring in pediatric kidney transplant

“…There are currently no recommended screening protocols for AT1R, but further study is needed given the simple hypothesized intervention of an angiotensin receptor blocker. 45 ETAR is a G protein-coupled receptor located in the vascular smooth muscle, mesangial cells, pericytes of descending vasa recta bundle cells, and renal tubules that induces vasoconstriction. 46 In rat models, expression of ETAR is increased in ischemia.…”