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NDT Advance Access originally published online on May 21, 2007
Nephrology Dialysis Transplantation 2007 22(7):1819-1822; doi:10.1093/ndt/gfm072
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Agonistic antibody-triggered stimulation of Angiotensin II type 1 receptor and renal allograft vascular pathology

Duska Dragun

Department of Nephrology and Intensive Care Medicine Campus Virchow-Klinikum and Center for Cardiovascular Research Medical Faculty of the Charité, Berlin, Germany

Correspondence and offprint requests to: Duska Dragun, Department of Nephrology and Intensive Care Medicine, Charite Campus Virchow Clinic, Augustenburger Platz 1, 13353 Berlin, Germany. Email: duska.dragun@charite.de

Keywords: Angiotensin receptors; apheresis; humoral immunity; kidney transplantation; vascular rejection

The first 150 words of the full text of this article appear below.



   Introduction
 
Despite the substantial improvements in post-transplantation management and novel immuno-suppressive modalities that have resulted in improved overall survival, rejection with vascular involvement remains a challenging problem in organ allotransplantation. Acute vascular rejections have an aggressive clinical course and frequently lead to a loss of allograft [1]. The histopathology of vascular rejection applies to a wide variety of vascular lesions in the allograft, ranging from thrombosis, fibrinoid vascular necrosis and endarteritis to myointimal proliferation with fibrosis [2]. A definitive causal relationship that would explain whether overwhelming anti-donor T-cell response, or alloantibodies, or both are responsible for the development of vascular allograft lesions is still missing. Resistance to therapy with anti-lymphocyte antibody preparations or steroids [3], implicates the contribution of anti-donor humoral reactivity against human leukocyte antigens (HLA) and vascular rejection. Donor-specific anti-HLA alloantibodies initiate rejection through complement-mediated and antibody-dependent, cell-mediated, cytotoxicity [4]. The . . . [Full Text of this Article]



   Non-HLA antibodies in transplant patients
 


   Angiotensin II type 1 receptor agonistic antibodies and vascular rejection—clinical and morphological features
 


   Diagnostic and therapeutic options
 


   How AT1R-AA mediate vascular rejection
 

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