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Updated: Sep 19, 2025

Murine Kidney Transplant Technique
Published on: October 20, 2015
Kidney transplant arteriopathy revisited
Katharina Wirths1,2, Michael Thomas3, Georg Dieplinger3
1Department of Internal Medicine, Faculty of Medicine, University Bonn, Venusberg-Campus 1, 53127, Bonn, Germany. katha@ish.de.
Background:
Transplant arteriopathy involves a spectrum of Leukocyte Common Antigen-positive, hypoelastotic, foam cell intimal fibrosis. Transplant arteriopathy has been associated with both Chronic Active T Cell-Mediated Rejection and Antibody-Mediated Rejection chronicity. Aim of this study was to find clinicopathological correlates of transplant arteriopathy in a single centre retrospective cohort.
Methods:
We retrieved 46 biopsies showing transplant arteriopathy from 33 patients, out of a total of 784 biopsies carried out between 2005 and 2014. We retrospectively evaluated Banff Lesion Scores and Additional Diagnostic Parameters as well as the transplant arteriopathy descriptors Leukocyte Common Antigen-positive, hypoelastotic, foam cell, and correlated these findings with clinical data and death-censored transplant survival.
Results:
Transplant arteriopathy was frequently associated with antibody-mediated rejection-associated Banff Lesions Scores and Additional Diagnostic Parameters. Hypoelastotic, leukocyte common antigen-positive and foam cell lesions were often combined, with hypoelastotic lesion being the most frequent finding in transplant arteriopathy. Leukocyte common antigen-positive lesion appeared earlier and was associated with Banff Lesion Score v ≥ 1. About half were positive for donor-specific antibodies, about a third had concurrent transplant glomerulopathy, and about a sixth were C4d-positive. Twelve of thirty-three transplants were lost during follow-up, concurrent transplant glomerulopathy was associated with shorter transplant survival.
Conclusions:
The frequent coincidence of transplant arteriopathy and indicators of antibody-mediated rejection suggests that this arterial remodelling could indeed be antibody-mediated rejection chronicity. The transplant community should re-examine transplant arteriopathy with an expanded definition including the previously ignored hypoelastotic lesion in order to re-confirm or reject with confidence transplant arteriopathy as Additional Diagnostic Parameter of Antibody-Mediated Rejection chronicity, and to learn about its prognostic and therapeutic implications.
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