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Published on: August 12, 2017
The role of complement-fixing donor-specific antibodies identified by a C1q assay after heart transplantation
M Farrero Torres1, M J Pando2, C Luo3
1Heart Failure and Heart Transplantation Program, Cardiovascular Institute, Hospital Clinic, Barcelona, Spain.
Insights
Detecting complement-fixing donor-specific antibodies (DSA) using the C1q assay can help predict acute rejection after heart transplantation. This monitoring aids in understanding transplant outcomes and patient survival.
Area of Science:
- Transplantation immunology
- Cardiovascular surgery
- Clinical diagnostics
Background:
- Donor-specific antibodies (DSA) against human leukocyte antigens (HLA) are linked to heart transplant rejection and graft failure.
- However, not all DSA possess the ability to fix complement, a key factor in immune response.
Purpose of the Study:
- To investigate the association between complement-fixing DSA and outcomes in heart transplant recipients.
- To evaluate the utility of the C1q assay in identifying complement-fixing DSA.
Main Methods:
- Retrospective analysis of 121 adult heart transplant recipients.
- Utilized C1q solid-phase assay to detect complement-fixing DSA alongside standard IgG assays.
Main Results:
- Post-transplant DSA were associated with higher rates of acute cellular rejection and antibody-mediated rejection.
- Complement-fixing DSA (C1q+) correlated with increased antibody-mediated rejection compared to non-complement-fixing DSA (C1q-).
- Patients with DSA showed higher mortality, primarily due to acute rejection, but no survival difference was observed between C1q+ and C1q- DSA groups.
Conclusions:
- Routine monitoring of DSA post-heart transplantation is crucial.
- Characterization of DSA using the C1q assay provides valuable prognostic information for acute rejection.
- This approach can aid in personalized patient management and improve transplant outcomes.
Background:
The development of donor-specific antibodies (DSA) to human leukocyte antigens (HLA) has been associated with acute rejection and allograft failure after heart transplantation. Not all DSA, however, can fix complement.
Methods:
To determine the association between complement-fixing DSA and heart transplant outcomes, we retrospectively analyzed results obtained using the C1q solid-phase assay that specifically detects complement-fixing DSA in parallel with the standard IgG assay in 121 adult heart transplant recipients.
Results:
The 52 recipients who developed post-transplant DSA had a higher incidence of acute cellular rejection (58% vs 19%, P < .001) and antibody-mediated rejection (29% vs 7%, P < .001) than the 69 recipients without DSA. The 24 recipients with C1q+ DSA had more antibody-mediated rejection than the 28 recipients with C1q- DSA (46% vs 14%, P = .012), but there was no difference in the incidence of acute cellular rejection between these two groups. Patients with post-transplant DSA had higher mortality than patients with no DSA (29% vs 13%, P = .031), mainly due to increased incidence of acute rejection. No differences in survival were found between recipients with C1q+ DSA and C1q- DSA.
Conclusions:
Routine monitoring of DSA post-transplant, and their characterization using the C1q assay, may provide prognostic information for acute rejection after heart transplantation.
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