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Complement activation products in plasma after heart transplantation in humans
H Vallhonrat1, W W Williams, G W Dec
1Renal Unit, Massachusetts General Hospital, Boston 02114, USA.
Insights
Plasma levels of complement fragments C4d and SC5b-9 are not useful for detecting acute rejection or graft atherosclerosis after heart transplantation. Early complement activation may still contribute to allograft injury.
Area of Science:
- Immunology
- Transplantation Medicine
- Cardiology
Background:
- Complement activation is linked to cardiac allograft dysfunction.
- Early and late allograft dysfunction are significant concerns in heart transplantation.
Purpose of the Study:
- To evaluate plasma C4d and SC5b-9 as noninvasive markers for acute rejection and accelerated graft atherosclerosis (AGA) in cardiac transplant recipients.
Main Methods:
- Plasma levels of C4d (classical pathway) and SC5b-9 (terminal pathway) were measured in heart transplant recipients during routine endomyocardial biopsy.
- Patients were studied in the immediate post-transplant period (0-100 days) and >6 months post-transplant.
Main Results:
- No correlation was found between plasma complement fragments and biopsy-proven acute rejection or AGA.
- Plasma C4d and SC5b-9 were elevated in most patients in the immediate post-transplant period, decreasing over the first 4-6 weeks.
Conclusions:
- Plasma C4d and SC5b-9 are not effective noninvasive markers for detecting acute rejection or AGA post-heart transplantation.
- Elevated complement activation in the early post-transplant period suggests a potential pathogenic role in allograft injury.
Background:
Complement activation has recently been implicated as a contributing factor to early and late allograft dysfunction in cardiac transplantation. The current study was designed to determine whether measurement of plasma complement fragments C4d and SC5b-9 would be useful in detecting acute rejection or accelerated graft atherosclerosis (AGA) in cardiac allograft recipients.
Methods:
We measured complement activation products, C4d (classical pathway) and SC5b-9 (terminal pathway), at the time of routine endomyocardial biopsy in heart transplant recipients. Ten patients in the immediate posttransplantation period (0-100 days) and 19 patients more than 6 months after transplantation were studied.
Results:
No correlation was found between plasma levels of complement activation fragments and the presence of biopsy-proven acute allograft rejection or AGA (assessed by coronary angiography). However, plasma C4d and SC5b-9 were significantly elevated in 9 of 10 and 7 of 10 patients, respectively, in the immediate posttransplantation period. This was followed by progressive decrease in the levels of C4d and SC5b-9 fragments during the first 4-6 weeks after transplantation.
Conclusion:
We conclude that measuring plasma levels of fragments C4d and SC5b-9 is not a useful noninvasive method for detecting acute rejection or AGA after heart transplantation. However, this study provides further evidence that early complement activation after heart transplantation may play a pathogenic role in allograft injury.