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Abstract: FR-PO789

Non-human Leukocyte Antigen (Non-HLA) Antibodies Against GSTT1 Are Associated With Homozygote Status for the Null Allele and With Histological Changes of Antibody Mediated Rejection

Session Information

Category: Transplantation

  • 2002 Transplantation: Clinical

Authors

  • Obrisca, Bogdan, Fundeni Clinical Institute, Bucharest, Romania
  • Leca, Nicolae, University of Washington, Seattle, Washington, United States
  • Chou-Wu, Elaine, Bloodworks Northwest, Seattle, Washington, United States
  • Ismail, Gener, Fundeni Clinical Institute, Bucharest, Romania
  • Gimferrer, Idoia, Bloodworks Northwest, Seattle, Washington, United States
Background

The presence of anti-GSTT1 Abs have been detected in patients with Antibody Mediated Rejection (AMR) after liver and kidney transplantation (KTx). We aimed to evaluate the relation between anti-GSTT1 Abs and AMR in a cohort of KTx patients.

Methods

Pre and Post-transplant samples from 87 KTx recipients were analyzed by Immunocor’s non-HLA Luminex assay. We included 29 patients with AMR due to HLA-DSA (AMR/DSA+), 28 patients with non-HLA mediated AMR (AMR/DSA-) and 30 patients without rejection with stable allograft function (control).

Results

At an MFI cut-off of 3,000, the overall prevalence of anti-GSTT1 Abs was 14%. The prevalence was higher among AMR/DSA- patients (25%), compared to the control group (13.3%) and AMR/DSA+ group (3.4%)(p=0.06). 81/87 patients underwent GSTT1 genotyping, 16 (19.75%) were negative: 9 AMR/DSA- patients (33.3%), 6 controls (22.2%) and 1 AMR/DSA+ (3.7%) (p=0.02). In the ABMR/DSA- group, the anti-GSTT1 ab MFI was significantly higher in patients negative compared to patients positive for GSTT1 gene (Figure 1). In two multivariate logistic regression models, negativity for GSTT1 gene (OR 43.2; 95%CI, 2.6-716) and anti-GSTT1 Ab positivity (OR 11.9; 95%CI, 1.1-129) were strongly associated with AMR. 14/57 patients with AMR (24.5%) lost their allograft at a median 6.1 years (IQR: 3.7-7.7). Patient with anti-GSTT1 Abs had AMR earlier (17 vs 35 months) than patients without GSTT1 Abs (p=0.02). Despite this, there were no differences in graft loss. When taking into consideration the GSTT1 gene status, among subjects displaying homozygote null status those without allograft failure had an overall higher MFI levels of anti-GSTT1 ab compared to those that lost their allograft (Figure 1).

Conclusion

Presence of GSTT1 Abs and GSST1 gene negative status are associated with AMR, but do not appear to lead to increased graft loss, possibly being a marker of favorable response to rejection treatment.

Figure 1