**6.2. Chronic antibody mediated rejection**

Chronic AMR is now included in the newest update of the Banff 07 classification of renal allograft pathology with the following criteria: [1]morphological changes as glomerular double contours compatible with transplant glomerulopathy (TPG) and severe PTC basement membrane multilayering, interstitial fibrosis and tubular atrophy with or without PTC loss, and fibrous intimal thickening in arteries without internal elastica duplication; [2] diffuse C4d deposition in PTCs; and [3] presence of DSA (Solez et al.,2008). Not all these criteria are always fulfilled in an individual patient at every given time point (Fehr et al., 2009).

PTC basement membrane multilayering correlates highly with TPG, and most of TPG have evidence of either C4d-positive staining or DSA. However, the proposed criteria do not apply to all situations of chronic active antibody-mediated rejection. Chronic AMR is distinct from acute AMR in that no acute inflammation (neutrophils, edema, necrosis, thrombosis) is present. However, cellular activity is often reflected by increased mononu‐ clear cells in glomerular capillaries and PTC (Colvin, 2007). The Banff criteria require PTC C4d positivity for diagnosis of ABMR as well as microcirculation injury. However, C4d is not a sensitive marker of chronic ABMR, and in many patients with transplant glomerulopathy, C4d staining is negative in the presence of anti-HLA DSA. Therefore, the recent update of the Banff classification introduced the diagnostic category of "suspi‐ cious for ABMR." It is defined with the presence of morphologic evidence of antibodymediated tissue injury and positive anti-HLA antibody with negative C4d, or PTC C4d positivity in the absence of alloantibody (Solez et al., 2008).
