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Abstract: SA-PO516

Immunoadsorption and Rituximab Therapy Induces Sustained Reduction of Anti-Pneumococcal IgG in ABO Incompatible Kidney Transplantation

Session Information

Category: Transplantation

  • 1702 Transplantation: Clinical and Translational


  • Faustini, Sian Elizabeth, University of Birmingham, Birmingham, United Kingdom
  • Bentall, Andrew J., Mayo Clinic, Rochester, United States
  • Wall, Nadezhda, University of Birmingham, Birmingham, United Kingdom
  • Shabir, Shazia, University Hospitals Birmingham NHS Foundation Trust, Birmingham, United Kingdom
  • Richter, Alex, University of Birmingham, Birmingham, United Kingdom
  • Ball, Simon T., University Hospitals Birmingham NHS Foundation Trust, Birmingham, United Kingdom

Patients with chronic kidney disease (CKD) have a higher infectious burden than the general population. Immunosuppression in kidney transplantation increases infection risk further. In addition to conventional immunosuppression, ABO incompatible transplantation (ABOi) requires modulation of the recipient antibody (Ab) pool to reduce anti-donor blood group Ab, which may also reduce protective Ab.


This study measures specific-IgG against protein and polysaccharide vaccine antigens in 14 ABOi patients, who undergo immunoadsorption therapy and rituximab (IAR), and 37 patients who undergo ABO compatible (ABOc) transplant with conventional immunosuppression. Plasma samples were analysed for IgG directed against tetanus toxoid (TT) and 12 pneumococcal polysaccharides (PnPs), using a luminex bead based assay, at baseline and 12 months post-transplant for both cohorts and in addition, post-IA/rituximab for ABOi and 3 months post transplant for ABOc patients.


At baseline, the ABOi and ABOc cohorts did not differ significantly in age or proportion of individuals with IgG titres above protective thresholds for TT (79 v 92%) or ≥ 8 Pneumococcal serotypes (50% v 65%). For ABOi, there was a significant reduction in anti-TT and 11/12 anti-PnPs titres from baseline to post-IAR (median reduction in titre of 17% and 27% respectively). For ABOc, there was significant reduction in anti-PnPs IgG titre for 8/12 serotypes tested at 3 months, but anti-TT IgG remained stable. At 12 months, the ABOc cohort had recovered anti-PnPs IgG titres to 10/12 Pneumococcal serotypes. In contrast, anti-PnPs IgG had only recovered for 2 serotypes in the ABOi group, despite anti-TT titres recovering to pre-transplant levels.


Both transplant cohorts had relatively low Pneumococcal, but good TT coverage pre-transplantation. Conditioning with IAR reduced specific IgG directed against non-blood group polysaccharide antigens such as PnPs. The ABOi cohort shower a greater reduction in Pneumococcal IgG coverage than the ABOc group and this did not recover at 12 months. Our findings reveal the impact of IAR on protective antibodies and suggest an opportunity to revisit the timing of vaccination schedules.


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