2015 Volume 3 Issue 2 Pages 147-154
Antibody-mediated rejection (ABMR) is acute and chronic immune responses of endothelial cells induced by donor-specific antibody (DSA). Endothelial cells are covering entire vascular surface of the kidney graft and always exposed to DSA, complement and inflammatory cells derived from the recipient. Preformed and de novo DSA can injure endothelial cells through three different pathways ; i) complement activation, ii) direct endothelial activation after ligation of DSA to corresponding antigens and iii) indirect endothelial activation by inflammatory cells stimulated by DSA via Fc receptor. Therefore, ABMR can be defined as “endothelial injury” induced by DSA. The pathological features of ABMR are determined by the severity and duration of endothelial injury ranging from thrombotic microangiopathy, a most severe form of lethal endothelial injury, to transplant glomerulopathy and capillaropathy, a chronic form of sublethal endothelial stimulation resulting in peculiar microvascular remodeling. Early diagnosis and treatment for ABMR are necessary to achieve more long-term allograft survival. We need a more specific marker besides C4d for histological diagnosis of ABMR. At the present time, periodic surveillance biopsy and detection of DSA are indispensable to establish early diagnosis of ABMR.
