Vessel thrombosis is a severe complication after renal transplantation. Antibodies anti-β-2 glycoprotein-I of IgA isotype (IgA-aB2GP1) have been linked to thrombotic events and mortality in hemodialysis patients.
All kidney transplanted patients from 2000 to 2011 (n = 1375) in our hospital were followed up for 2 years, evaluating 3 time periods.
At transplantation, 401 patients were positive for IgA-aB2GPI (29.2%, group 1), and the remaining patients were negative (group 2). Graft loss at 6 months posttransplantation was higher in group 1 (18% vs 7.2%; P < 0.001). The most frequent cause of early graft loss was vessel thrombosis, especially in group 1 (12.2% vs 2.6% of patients; P < 0.001). In fact, vessel thrombosis was the most important cause of graft loss in the 3 time periods, irrespective of demographic changes and introduction of transplantation with asystolic donors.
Notably, IgA-aB2GP1 was an independent risk factor for graft thrombosis (odds ratio, 5.047; P < 0.001). Furthermore, the presence of IgA-aB2GP1 was associated with early graft loss and delayed graft function. Mortality at 24 months was also higher in group 1.
In conclusion, pretransplant IgA-aB2GP1 was the main risk factor for graft thrombosis and early graft loss. Further research should be made on whether anticoagulation in antibody-positive patients could ameliorate this catastrophic complication.
Reviewing their experience in 1375 kidney transplant recipients, the authors suggest that IgA anti-beta-2 glycoprotein1 antibodies at time of transplantation is an independent factor of graft loss mainly due to artery and vein thrombosis. Supplemental digital content is available in the text.
1 Department of Immunology, Instituto de Investigación Hospital Universitario, Madrid, Spain.
2 Department of Nephrology, Instituto de Investigación Hospital Universitario, Madrid, Spain.
3 Department of Urology, Instituto de Investigación Hospital Universitario, Madrid, Spain.
4 Department of Pathology, Instituto de Investigación Hospital Universitario, Madrid, Spain.
5 Immunology Section, Universidad San Pablo-CEU, Madrid, Spain.
6 Facultad de Medicina, Universidad Complutense, Madrid, Spain.
Received 25 November 2015. Revision received 17 February 2016.
Accepted 20 February 2016.
This work was supported by grants from Fondo de Investigaciones Sanitarias and cofinanced by European Regional Development Fund (grants: PI12-0108, PIE13/0045 and PI14-0360).
The authors declare no conflicts of interest.
J.M.M., M.S., and J.A.M.F. collaborated equally to this work.
A.S. conceived the project. A.S. and J.M.M. designed the research and wrote the article. A.S., M.S., and J.A.M.F. made the antiphospholipid determinations and were responsible for the database and the statistical analysis. J.M.M., F.G., E.M., A.R.A., E.Gu., E.Go., M.P., and A.A. were responsible for the patients care and clinical data collection. M.A.M. and M.A. made the histopathologic studies. M.J.C., E.S., D.P., and E.P.A. were responsible for the histocompatibility data and coordination of the Organ Transplant Waiting List Serum Bank. All authors contributed to the data interpretation and report preparation.
Correspondence: Antonio Serrano, Instituto de Investigación, I + 12 Hospital Universitario, 12 de Octubre Avda. de Andalucía s/n, 28041, Madrid, Spain. (firstname.lastname@example.org).
Supplemental digital content (SDC) is available for this article. Direct URL citations appear in the printed text, and links to the digital files are provided in the HTML text of this article on the journal’s Web site (www.transplantjournal.com).