ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: PO2198

Immunosuppression Could Influence De Novo Angiotensin II Type Receptor Antibodies Development Early After Kidney Transplantation

Session Information

Category: Transplantation

  • 1902 Transplantation: Clinical

Authors

  • Sorohan, Bogdan Marian, Universitatea de Medicina si Farmacie Carol Davila, Bucharest, Bucharest, Romania
  • Berechet, Andreea Ioana, Institutul Clinic Fundeni, Bucharest, Bucharest, Romania
  • Bucsa, Cristina, Institutul Clinic Fundeni, Bucharest, Bucharest, Romania
  • Tincu, Corina, Institutul Clinic Fundeni, Bucharest, Bucharest, Romania
  • Obrisca, Bogdan, Universitatea de Medicina si Farmacie Carol Davila, Bucharest, Bucharest, Romania
  • Ismail, Gener, Universitatea de Medicina si Farmacie Carol Davila, Bucharest, Bucharest, Romania
Background

Angiotensin II type I receptor antibodies (AT1R-Ab) are non-HLA autoAb associated with graft rejection and detrimental effects on graft function in kidney transplantation (KT). Nevertheless, the data regarding risk factors associated with AT1R-Ab development is scanty. To our knowledge, immunosuppression (IS) has not yet been reported as a potential risk factor. We sought to evaluate the incidence of de novo AT1R-Ab at 1 year after KT and risk factors associated with their formation.

Methods

We performed a prospective study on 58 KT recipients, transplanted between October 2018 and October 2019, who were followed for 1 year. Exclusion criteria: age <18 years and preformed AT1R-Ab. AT1R-Ab were evaluated at 1 year after KT using an ELISA technique and the cut-off value for detection was >10 U/ml. Logistic regression analysis was used to identify risk factors associated with AT1R-Ab formation.

Results

Twelve out of 58 patients (20.6%) had de novo AT1R-Ab at 1 year of follow-up. Mean age of the study cohort was 40.8±10.5 years, 60.3% were males and 17.2% had a preemptive KT. Glomerular diseases was the main cause for CKD (27.6%). Donors mean age was 48.6±15.6 years, 62.1% were cadaveric donors and 31% of patients had ≥4 mismatches. Monoclonal Ab directed against IL-2 receptor (84.5%) was the main induction IS used. Immediate-release tacrolimus (TAC) was used in 53.4% and mycophenolate sodium was preferred in 89.7% of cases. Patients with de novo AT1R-Ab had a significantly decreased BMI (21.4±1.8 vs 23.2±2.9 kg/m2, p=0.04), received significantly more frequently IS with rabbit globulin anti-thymocyte (rATG) (41.7 vs 8.7%, p=0.01), immediate-release TAC (83.3 vs 45.7%, p=0.01) and had a significantly higher mean TAC level at 3 months after KT (13.8±5.6 vs 11.4± 3ng/ml, p=0.04). By multivariate logistic regression we found that rATG was an independent risk factor for de novo AT1R-Ab development (OR= 5.62; 95%CI: 1.11- 28.34, p=0.03) and immediate-release TAC had a trend of association with Ab (OR= 5.02; 95%CI: 0.93- 27.06, p=0.03) at 1 year after KT.

Conclusion

The incidence of de novo AT1R-Ab was 20.6% and rATG induction IS was an independent risk factor for Ab development at 1 year after KT. Our results suggest that IS could influence de novo AT1R-Ab formation.