Low mannose-binding lectin and increased complement activation correlate to allograft vasculopathy, ischaemia, and rejection after human heart transplantation

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Abstract
Aims Transplant-associated coronary artery disease (TxCAD) is a major cause of post-transplant graft failure. The aim of this study was to investigate a possible role of mannose-binding lectin (MBL) deficiency and complement activation in TxCAD. Methods and results In a prospective study of heart transplant recipients (n=38) with a follow-up of 5.3±1.3 years (range: 0.9–6.6), angiographically verified TxCAD (n=6) was correlated to plasma MBL, complement activation, and endothelial activation (soluble E-selectin). MBL deficiency (P=0.020). Furthermore, one or more acute rejection episodes were observed in 6/6 of the MBL-deficient patients and in 15/32 of the MBL-sufficient patients (χ2; P=0.016). Complement activation (C4bc) correlated with soluble E-selectin (r=0.36; P=0.027), both being significantly higher in patients with ischaemia detected in the first biopsy (C4bc: 13.4±6.1 AU/mL; E-selectin: 96±13 ng/mL) than in those without ischaemia (C4bc: 6.3±0.5; E-selectin: 51±6; P=0.037 and 0.002). Finally, terminal complement complex correlated closely with mortality (P=0.002). Conclusion Low MBL was related to the development of TxCAD and acute rejection and increased complement activation correlated to histopathologic ischaemia and mortality after heart transplantation.