Minireviews
Copyright ©The Author(s) 2024.
World J Transplant. Mar 18, 2024; 14(1): 89772
Published online Mar 18, 2024. doi: 10.5500/wjt.v14.i1.89772
Table 1 Types of acute rejection and clinical manifestations
T cell-mediated rejectionAntibody-mediated rejection
Time of occurrenceWithin 90 d after LT with a median onset of 8 d[47]Within the first few weeks after LT
Incidence10%–30%[92,93]0.3%–2%[94]
Clinical manifestationsElevation of serum aminotransferases, alkaline phosphatase, gamma-glutamyl transpeptidase and/or bilirubinElevated aminotransferases; Graft injury with refractory thrombocytopenia, hyperbilirubinemia, low serum complements levels; Rapid allograft failure, hemorrhagic necrosis
Diagnostic criteria (histology needed)Quantitative scoring - Rejection activity index (RAI): Portal inflammation - mixed (predominantly mononuclear activated lymphocytes, neutrophils, and eosinophils); Bile duct inflammation/damage; Venous endothelial inflammation; Each of these parameters is scored as 1 to 3 and thus a maximum score of 9 is possible; 0–2 is no rejection,3 borderline (consistent with), 4–5 is mild, 6–7 is moderate and 8–9 as severe ACR[49]Histology: endothelial cell hypertrophy, portal capillary dilatation, microvasculitis with monocytes, eosinophils and neutrophils, and portal/peri-portal edema. Microvascular involvement involving the central veins can distinguish acute AMR from other types of injury early after LT; Elevated DSA; Diffuse C4d deposition of microvasculature in ABO-compatible tissues, or portal stroma in ABO-incompatible tissues; Exclusion of other liver diseases[49]