Refinements in the diagnostic criteria for acute and chronic ABMR in renal allografts were proposed in the most-recent Banff congress (11); however, the 3 basic requirements remain: (1) histologic evidence of acute or chronic tissue injury (see Table 1), (2) evidence of current/recent antibody interaction with vascular endothelium (most notably C4d staining but also severe microvascular injury or increased expression of gene transcripts in the biopsy tissue indicative of endothelial injury, if thoroughly validated), and (3) serologic evidence of donor-specific antibodies.
52,53,55) Recently, classification schema for pancreas ABMR and cellular rejection were published under the auspices of the Banff group, based on contemporary data.
After initial case reports of ABMR in pancreas allografts from several groups, (56-58) Torrealba and colleagues (59) published the first study systematically investigating C4d staining in correlation with donor-specific antibody studies, histopathology, treatment, and outcome.
12,55) Chronic, active ABMR encompasses features of acute ABMR, as described, along with graft sclerosis-fibrosis, in the absence of cellular rejection.
66) As in kidney, ABMR has been difficult to recognize and diagnose prospectively.
Evaluating for C4d deposition remains central to the immunophenotypic criteria for ABMR in heart allografts, although it has been supplemented by recommendations for additional stains in either formalin-fixed or frozen tissue (discussed below).
Although C4d remains an essential assay in evaluation of ABMR in cardiac allografts, different companion staining panels were recently recommended by the ISHLT working formulation for frozen/IF and formalin/IHC-IP biopsy specimens.
The proposed reporting scheme for ABMR in heart allografts involves assessment of both histologic and immunophenotypic features.
Acute ABMR in lung allografts has been recognized sporadically, and data in the literature are less established than for kidney and heart.
The ISHLT summary statement put forth C4d as the primary/recommended immunostain in the assessment of pulmonary ABMR.
6% [18 of 236] with major disagreements across all observers), yet the number of cases evaluated by both methods was small (n = 59), and ABMR was very rare in this study group.
Currently, diagnosis of ABMR in lung requires a multidisciplinary approach and synthesis of pathologic findings ([C4d.