ArticleFrontiers in immunology2026
Association of AT1R expression with transplant glomerulopathy and interstitial fibrosis in kidney transplant recipients.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Editorial: Methods in alloimmunity and transplantation: 2025.Frontiers in immunology · 2026Article
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14 authors.
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Abstract
Background: Chronic allograft dysfunction (CAD) remains a major cause of late kidney transplant failure and is driven by both immune and non-immune mechanisms. Transplant glomerulopathy (TG) and interstitial fibrosis (IF) are key histopathological features associated with chronic antibody-mediated injury and long-term graft loss. Experimental and clinical data suggest that angiotensin II type 1 receptor (AT1R) signaling, including activation by anti-AT1R antibodies, may contribute to fibrotic processes within the kidney. Methods: In this longitudinal study, 77 kidney transplant recipients who underwent indication biopsies within 60 months post-transplantation were analyzed. AT1R expression in allograft tissue was assessed by immunohistochemistry, and serum anti-AT1R antibody levels were measured using ELISA. Histopathological findings and long-term graft outcomes were evaluated over a median follow-up of 126 months. Results: AT1R expression in tubular epithelium was observed in 44.2% of patients. TG and IF were significantly more frequent in patients with positive AT1R expression compared to those without (24% vs. 7%, p=0.042; 56% vs. 27%, p=0.011, respectively), and IF severity was higher in the AT1R-positive group (p=0.028). Anti-AT1R antibody levels did not differ between groups. In survival analyses, neither AT1R expression nor anti-AT1R antibodies alone were associated with allograft survival. However, the presence of multiple risk factors, including AT1R expression, anti-AT1R antibodies, and histopathological lesions, was associated with significantly worse long-term graft survival. Conclusions: AT1R expression is associated with the presence and severity of interstitial fibrosis and transplant glomerulopathy in kidney transplant recipients. While AT1R-related markers alone did not predict graft survival, their combination with histopathological abnormalities identifies patients at higher risk of long-term allograft loss. These findings support a potential role of AT1R-mediated pathways in chronic allograft injury.
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