Association of AT1R expression with transplant glomerulopathy and interstitial fibrosis in kidney transplant recipients - Summary - MDSpire

Association of AT1R expression with transplant glomerulopathy and interstitial fibrosis in kidney transplant recipients

  • By

  • Katarzyna Jakuszko

  • Piotr Donizy

  • Agnieszka Sas

  • Guido Moll

  • Rusan Catar

  • Renata Trzeciak-Snopczyńska

  • Justyna Zachciał

  • Sławomir Zmonarski

  • Magdalena Kuriata-Kordek

  • Agnieszka Hałoń

  • Maciej Wuczyński

  • Krzysztof Kujawa

  • Dariusz Janczak

  • Mirosław Banasik

  • July 14, 2026

Share

Objective:

To evaluate AT1R expression in kidney allograft biopsies and the presence of anti-AT1R antibodies in kidney transplant recipients, and to assess their association with chronic allograft dysfunction.

Approach:
  • Study Design: A longitudinal study involving 77 kidney transplant recipients who underwent indication biopsies within 60 months post-transplantation.
  • Assessment Methods: AT1R expression was assessed by immunohistochemistry, and serum anti-AT1R antibody levels were measured using ELISA.
  • Follow-Up: Histopathological findings and long-term graft outcomes were evaluated over a median follow-up of 126 months.
Key Findings:
  • AT1R expression in tubular epithelium was observed in 44.2% of patients.
  • Transplant glomerulopathy (TG) and interstitial fibrosis (IF) were significantly more frequent in patients with positive AT1R expression (24% vs. 7%, p=0.042; 56% vs. 27%, p=0.011).
  • IF severity was higher in the AT1R-positive group (p=0.028).
  • Anti-AT1R antibody levels did not differ between groups.
  • The presence of multiple risk factors, including AT1R expression and histopathological lesions, was associated with worse long-term graft survival.
Interpretation:

AT1R expression is associated with the presence and severity of interstitial fibrosis and transplant glomerulopathy in kidney transplant recipients.

Limitations:
  • The study had a loss of 22 patients during follow-up.
  • The analysis was limited to a specific cohort of kidney transplant recipients.
Conclusion:

These findings suggest a role of AT1R-mediated pathways in chronic allograft injury.

Original Source(s)

Related Content