Abstract
Graft thrombosis is a devastating complication after renal transplantation. We recently described the association of anti-beta-2-glycoprotein-I (IgA-ab2GP1) antibodies with early graft loss mainly caused by thrombosis in a monocenter study. Multicenter prospective observational cohort study. Seven hundred forty patients from five hospitals of the Spanish Forum Renal Group transplanted from 2000 to 2002 were prospectively followed-up for 10 years. Early graft loss and graft loss by thrombosis. The presence of IgA anti-B2GP1 antibodies in pretransplant serum was examined using the same methodology in all the patients. At transplantation, 288 patients were positive for IgA-B2GP1 (39%, Group-1) and the remaining were negative (Group-2). Graft loss at 6 months was higher in Group-1 (12.5 vs. 4.2% p < 0.001), vessel thrombosis being the most frequent cause of early graft loss, especially in Group-1 (6.9 vs. 0.4% p < 0.001). IgA-aB2GP1 was the most important independent risk factor for graft thrombosis (hazard ratio: 13.83; 95% CI: 3.17-60.27, p < 0.001). Furthermore, the, presence of IgA-aB2GP1 was associated with early graft loss and delayed graft function. At 10 years, survival figures were also lower in Group-1: graft survival was lower compared with Group-2 (60.4 vs. 76.8%, p < 0.001). Mortality was significantly higher in Group-1 (19.8 vs. 12.2%, p = 0.005). Patients were obtained during a 3-year period (1 January 2000-31 December 2002) and kidneys were only transplanted from brain-dead donors. Nowadays, the patients are older and the percentage of sensitized and retransplants is high. In a prospective observational multicenter study, we were able to corroborate that pretransplant presence of IgA-aB2GP1 was the main risk factor for graft thrombosis and early graft loss. Therefore, a prospective study is needed to evaluate the efficacy and safety of prophylactic anticoagulation to avoid this severe complication.
Highlights
The introduction of modern immunosuppression, advances in the control of infections, better methodologies, and improvement in histocompatibility tests in recent decades have substantially increased short- and long-term results after renal transplantation
We previously described that the presence of pretransplant IgAaB2GP1 is an independent risk factor for early graft loss in two unicenter studies [7, 14] and graft thrombosis [14] after renal transplantation
We have been able to demonstrate in an observational, multicenter, and prospective study including 740 renal transplant patients from five hospitals of Spain that preformed IgA-anti-beta-2 glycoprotein-I (aB2GP1) is an independent risk factor for early graft thrombosis
Summary
The introduction of modern immunosuppression, advances in the control of infections, better methodologies, and improvement in histocompatibility tests in recent decades have substantially increased short- and long-term results after renal transplantation. The percentage of patients who suffer graft loss in the first months posttransplant (mainly by thrombosis) has remained unchanged (5–8%) [1]. Humoral immune response to the allograft after kidney transplantation is one of the main factors responsible for the deterioration of graft function, or even graft loss. It has been recently described that antibody-based autoimmune responses may affect the outcome of renal transplantation [3]. The main antigens associated with an autoimmune-mediated allograft response are angiotensin 1 receptor [4], endotelin 1 receptor [5], LG3 fragment of perlecan [6], and β2 glycoprotein I (B2GP1) [7]. We recently described the association of anti-beta-2-glycoprotein-I (IgA-ab2GP1) antibodies with early graft loss mainly caused by thrombosis in a monocenter study
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call