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Copyright ©The Author(s) 2016.
World J Gastroenterol. May 14, 2016; 22(18): 4438-4445
Published online May 14, 2016. doi: 10.3748/wjg.v22.i18.4438
Table 2 Current data for donor-specific HLA-antibody-associated injuries in kidney and liver transplantation
Kidney transplantationLiver transplantation
DSA specificity and levels↑ risk hyperacute rejection[44]; ↑ DSA in new onset late kidney allograft dysfunction[45]; acute AMR is associated with high posttransplant DSA levels[45]↑ DSA in recipients with CR, presence of IgG3 subclass associated with ↑ risk of graft loss[40]
C4d deposition in microvasculatureGraft failure significantly worse in the presence of C4d+ staining[44]; C4d+ is a marker of antibody-mediated injury[44,46]C4d+ staining nonspecific; In the presence of DSA, linear portal capillary and sinusoidal staining observed in ACR; DSA negative C4d+ staining found in biliary strictures and recurrent liver disease[47]
DSA subtypes, C1q binding↓ graft survival and ↑ risk for AMR with C1q-binding DSA[48,49]Limited data[50]
Microvascular inflammationPeritubular capillaritis is a possible predictor of chronic AMR[51]; subclinical AMR may contribute to development of CAN[52]No current data
EC activation by light microscopyEC and BM ultrastructural abnormalities in glomerular and peritubular capillaries are early markers of TXG[53]No current data
Gene expression profile of chronic AMRDefined genetic profile in AMR[54,55]No current data
Therapeutic-trials to prevent DSA-associated injuryBortezomib (plasma cell-targeted therapy) as a possible antihumoral therapy[56]; plasma exchange for AMR[57,58]No current data