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Kidney Week

Abstract: FR-PO888

Long Term Follow Up for Antibody Mediated Rejection of Kidney Transplant Due to Angiotensin II Type 1 Receptor Antibodies

Session Information

Category: Transplantation

  • 1802 Transplantation: Clinical

Authors

  • Alasfar, Sami, Johns Hopkins University, Baltimore , Maryland, United States
  • Alachkar, Nada, Johns Hopkins University, Baltimore, Maryland, United States
  • Kraus, Edward S., Johns Hopkins University, Baltimore, Maryland, United States
  • Philogene, Mary Carmelle, Johns Hopkins University , Baltimore, Maryland, United States
Background

A new appreciation for the contribution of non-HLA antibodies (Abs) in kidney transplantation (K-TXP) has arisen as a result of reports of antibody mediated rejection (ABMR) without HLA Abs. Abs directed against the angiotensin II type 1 receptor (AT1R-Ab) have received greater scrutiny because of the existence of a commercially available assay. Studies on the treatment and long term follow up of AT1R-Ab mediated ABMR are lacking

Methods

Among K-TXP patients with positive (≥17 Units/ml) or borderline (10-17 Units/ml) AT1R-Ab, we retrospectively identified those with biopsy proven ABMR by Banff 2017 and had negative or low level HLA Abs at the time of rejection

Results

14 patients were identified. Patients’ characteristics are shown in table 1. Median time of follow up from ABMR is 24 months. Median time from transplant to ABMR is10 months. With regards to treatment, 9 received plasmapheresis and intravenous immunoglobulins +/- high dose corticosteroids (HDCS), 1 received HDCS, and 1 received HDCS and thymoglobulin. Of treated patients, 6 responded. One lost allograft due to recurrence of ABMR. Of all patients, 10 had follow up biopsy. 5 had improvment in histological findings, and the other 5 developed transplant glomuerlopathy. Of the 3 who did not receive any treatment, 1 progressed to allograft loss, 1 had resolution on follow up biopsy, and 1 remained with elevated but stable serum Creatinine. Of the 11 who received treatment, 9 had evidence of reduction in AT1R-Ab titer. Of the three who did not receive treatment, 1 had improvement in AT1R-Ab titer

Conclusion

AT1R-Ab mediated ABMR is seen in HLA sensitized and non sensitized patients. Conventional ABMR treatment reduces AT1R-Ab titer in most patients but not all achieve clinical response. As with HLA antibodies, AT1R-Ab may lead to transplant glomerulopathy

Table 1
Mean age at current transplant (yr)40.8 +/- 3.8
Number of males11/14
Number with previous K-TXP8/14
Deceased donor K-TXP9/14
Mean number of mismatches in ABCDRDQ4/10
Number with HLA sensitization at transplant8/14
Number with HLA DSA at transplant6/14
Number with positive or borderline AT1R-Ab at transplant13/13, one unavilable
Induction immunosuppression with thymoglobulin14/14
Maintenance immunosuppression at time of ABMR14/14 tacrolimus, mycophenolate, and prednisone