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Complement activation and long-term graft function in ABO-incompatible kidney transplantation.

Marit S van Sandwijk1, Astrid Klooster2, Ineke Jm Ten Berge3

  • 1Department of Nephrology, Amsterdam University Medical Centers, Amsterdam NL-1105 AZ, Netherlands. m.s.vansandwijk@amsterdamumc.nl.

World Journal of Nephrology
|October 31, 2019
PubMed
Summary
This summary is machine-generated.

ABO-incompatible kidney transplants show similar survival but lower early function due to T-cell mediated rejection. Complement activation by anti-ABO antibodies may impair long-term graft function through T-cell co-stimulation.

Keywords:
ABO-incompatibleComplementGraft functionKidney transplantationRejection

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Area of Science:

  • Nephrology
  • Immunology
  • Transplantation Science

Background:

  • ABO-incompatible kidney transplantation is generally successful in the short term, attributed to graft accommodation.
  • The mechanism of accommodation, potentially involving complement inhibition, remains unclear.
  • Incomplete complement inhibition might explain inferior long-term graft function in ABO-incompatible transplants compared to ABO-compatible ones.

Purpose of the Study:

  • To investigate the link between pre-transplant anti-ABO antibodies, complement activation, and long-term kidney transplant outcomes.
  • To elucidate the role of complement activation in ABO-incompatible kidney transplantation.

Main Methods:

  • A cohort study comparing 27 ABO-incompatible kidney transplantations with 108 ABO-compatible controls (2008-2013).
  • Analysis of graft and patient survival, kidney function (creatinine clearance, MDRD), and rejection rates.
  • Correlation of pre-transplant anti-ABO IgG titers with complement activation markers (C5b-9) and T-cell mediated rejection.

Main Results:

  • No significant differences in overall graft or patient survival were observed.
  • ABO-incompatible recipients exhibited lower kidney function at three months post-transplant (P=0.02) due to higher rates of early T-cell mediated rejection (33% vs 15%, P=0.03).
  • Elevated pre-transplant anti-ABO IgG titers correlated with C5b-9 staining and T-cell mediated rejection, suggesting a role for complement activation in rejection.

Conclusions:

  • Complement activation by anti-ABO antibodies, potentially through C5a-mediated T-cell co-stimulation, may contribute to impaired long-term graft function in ABO-incompatible kidney transplantation.
  • Understanding this mechanism could lead to improved strategies for ABO-incompatible kidney transplantation.