{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T14:01:33Z","timestamp":1788184893322,"version":"build-2803163510"},"reference-count":33,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T00:00:00Z","timestamp":1783987200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1882694","type":"journal-article","created":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T04:22:30Z","timestamp":1784002950000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Association of AT1R expression with transplant glomerulopathy and interstitial fibrosis in kidney transplant recipients"],"prefix":"10.3389","volume":"17","author":[{"given":"Katarzyna","family":"Jakuszko","sequence":"first","affiliation":[{"name":"Department of Nephrology, Transplantation Medicine and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University","place":["Wroclaw, Poland"]},{"name":"University Clinical Hospital in Wroclaw","place":["Wroclaw, 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Humboldt-Universit\u00e4t zu Berlin, and Berlin Institute of Health (BIH)","place":["Berlin, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Renata","family":"Trzeciak-Snopczy\u0144ska","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Transplantation Medicine and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University","place":["Wroclaw, Poland"]},{"name":"University Clinical Hospital in Wroclaw","place":["Wroclaw, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justyna","family":"Zachcia\u0142","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Transplantation Medicine and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University","place":["Wroclaw, Poland"]},{"name":"University Clinical Hospital in Wroclaw","place":["Wroclaw, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S\u0142awomir","family":"Zmonarski","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Transplantation Medicine and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University","place":["Wroclaw, Poland"]},{"name":"University Clinical Hospital in Wroclaw","place":["Wroclaw, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Magdalena","family":"Kuriata-Kordek","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Transplantation Medicine and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University","place":["Wroclaw, Poland"]},{"name":"University Clinical Hospital in Wroclaw","place":["Wroclaw, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Agnieszka","family":"Ha\u0142o\u0144","sequence":"additional","affiliation":[{"name":"University Clinical Hospital in Wroclaw","place":["Wroclaw, 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