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Angiotensin II Type 1–Receptor Activating Antibodies in Renal-Allograft Rejection
Angiotensin II Type 1–Receptor Activating Antibodies in Renal-Allograft Rejection
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Angiotensin II Type 1–Receptor Activating Antibodies in Renal-Allograft Rejection
Angiotensin II Type 1–Receptor Activating Antibodies in Renal-Allograft Rejection

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Angiotensin II Type 1–Receptor Activating Antibodies in Renal-Allograft Rejection
Angiotensin II Type 1–Receptor Activating Antibodies in Renal-Allograft Rejection
Journal Article

Angiotensin II Type 1–Receptor Activating Antibodies in Renal-Allograft Rejection

2005
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Overview
Although some kidney-transplant recipients with severe vascular rejection have antibodies against HLA antigens, others do not. Severe vascular rejection accompanied by accelerated hypertension, and even convulsions, resembles preeclampsia. Activating antibodies targeting the angiotensin II type 1 receptor have been found in preeclampsia, and the authors sought and detected such antibodies in patients with severe vascular rejection. These results suggest that a pathway mediated by a non-HLA, angiotensin II type 1 receptor may be involved in vascular rejection. The results suggest that a pathway mediated by a non-HLA, angiotensin II type 1 receptor may be involved in vascular rejection. Many aspects of T-cell–mediated responses in allograft rejection have been elucidated, yet humoral mechanisms are relatively unexplored. Vascular rejection that is refractory to intensified immunosuppression is the most important predictor of early and late graft loss. 1 The association of antidonor humoral reactivity against HLA antigens and vascular rejection has been established. 2 Other targets of the allograft-directed host response remain elusive. However, alloantibodies against the polymorphic non-HLA system were found in serum obtained before transplantation from patients in whom refractory rejection developed after they received kidney transplants from HLA-identical siblings. 3 Allograft endothelium may be a primary target of the cytopathic actions . . .