Table 2.

Revised classification of antibody-mediated rejection.

Acute/active ABMR
1	Evidence of acute tissue injury, including one or more of the following
	Microvascular inflammation (g > 0 and/or ptc > 0)
	Intimal or transmural arteritis (v > 0)
	Acute thrombotic microangiopathy, in the absence of any other cause
	Acute tubular injury, in the absence of any other cause
2	Evidence of current/recent antibody interaction with vascular endothelium, including at least one of the following:
	Linear C4d staining in ptc
	Moderate microvascular inflammation(g + ptc ≧ 2)
	Increased expression of gene transcripts indicative of endothelial injury
3	Serologic evidence of DSAs
Chronic/active ABMR
1	Evidence of chronic tissue injury, including one or more of the following
	Transplant glomerulopathy(cg > 0)
	Severe ptc basement membrane multilayering (requires EM)
	Arterial intimal fibrosis of new onset, excluding other causes
2	Evidence of current/recent antibody interaction with vascular endothelium, including at least one of the following
	Linear C4d staining in ptc
	moderate microvascular inflammation(g + ptc ≧ 2)
	Increased expression of gene transcripts indicative of endothelial injury
3	Serologic evidence of DSAs

The bold font showed the most important factor to diagnose ABMR (Acute and Chronic).

DSAs, donor-specific HLA antibodies; EM, electron microscopy.

Furthermore, in the revised criteria, ABMR phenotypes have been classified as acute/active; chronic/active corresponding to the diagnostic criteria, which have been listed in detail.