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Abstract: FR-PO1180

Clinical Outcomes of HLA-Identical Transplants in the Tacrolimus Era

Session Information

Category: Transplantation

  • 1902 Transplantation: Clinical

Authors

  • D'Costa, Matthew R., Mayo Clinic, Rochester, Minnesota, United States
  • Merzkani, Massini, Mayo Clinic, Rochester, Minnesota, United States
  • Park, Walter, Mayo Clinic, Rochester, Minnesota, United States
  • Alexander, Mariam P., Mayo Clinic, Rochester, Minnesota, United States
  • Smith, Byron H., Mayo Clinic, Rochester, Minnesota, United States
  • Gandhi, Manish, Mayo Clinic, Rochester, Minnesota, United States
  • Schinstock, Carrie A., Mayo Clinic, Rochester, Minnesota, United States
  • Bentall, Andrew J., Mayo Clinic, Rochester, Minnesota, United States
  • Stegall, Mark D., Mayo Clinic, Rochester, Minnesota, United States
Background

HLA identical living donor transplants (LDKT) have excellent graft survival. It remains unclear if causes of death/graft loss, histology or complications associated with tacrolimus-era immunosuppression are different when compared to non-HLA identical recipients.

Methods

We performed a nested case control study of HLA identical full sibling LDKT recipients (cases) and non-HLA identical LDKT recipients (controls) matched for age, sex and year of transplant from 1999 to 2018. Baseline characteristics, overall survival and death censored graft survival (DCGS), histology, and complications were compared.

Results

184 recipients were in each cohort with similar baseline characteristics except for induction regimens: cases were more likely to receive anti-CD25 and alemtuzumab and less likely to receive thymoglobulin (p=<0.01). Cases had longer median follow-up [7.6 (3.7-11.9) vs 5.7 (2.8-10.1) years, p=0.01], better overall survival (81% vs. 71%, p<0.001) and better DCGS (94% vs. 77%, p<0.001). Protocol biopsies at 1, 2, 5, and 10 years showed more tubulitis, peritubular capillaritis and glomerulitis in controls. Acute cellular rejection, chronic antibody-mediated rejection, and BK nephropathy were more common in controls (Table 1). Causes of DCGS and death were similar between groups (Table 1). Time to DCGS from alloimmune injury was shorter in controls (p=0.01); all events in cases (n=3) occurred in the absence of immunosuppression (two were non-adherent and one had PTLD). Rates of leukopenia, proteinuria, and urinary tract infections were similar.

Conclusion

HLA identical LDKT recipients had better patient survival and DCGS when compared to a non-HLA identical cohort. Causes of DCGS and death were similar. Time to DCGS from alloimmune injury was shorter in controls. Controls had higher rates of both cellular and antibody-mediated injury and BK nephropathy. These results suggest a potential role for reducing immunosuppression in HLA identical sibling LDKT.