Banff ’05 Meeting Report: Differential Diagnosis of Chronic Allograft Injury and Elimination of Chronic Allograft Nephropathy (’CAN’)

Clinical and pathological correlations of C4d immunostaining and its infl uence on the outcome of kidney transplant recipients

“…6 Patients were classified as: no rejection (NR), ACR, ABMR or interstitial fibrosis/tubular atrophy (IF/TA). No rejection included biopsies with normal tissue, acute tubular necrosis, calcineurin inhibitor toxicity, or borderline changes.…”

“…[1][2][3][4][5] C4d represents one criterion to the diagnosis of acute and chronic ABMR according to Banff classification. 6 Staining for C4d in peritubular capillaries is present in other histological diagnosis of kidney graft biopsies, such as acute cellular rejection and/or acute graft injury, 3 interstitial fibrosis and tubular atrophy, calcineurin inhibitor toxicity, and even in grafts without dysfunction and with no morphological signs of rejection. 3,4,7 The influence of C4d on graft function and outcome over these different Banff categories is still unclear.…”

Renal Allograft Fibrosis: Biology and Therapeutic Targets

“…IF/TA is a non-specific lesion induced by various immune and non-immune injuries to the graft (9,10) and an independent risk factor for late graft loss, particularly in grafts from expanded criteria donors, irrespective of whether a specific disease was diagnosed in the allograft or not (11)(12)(13)(14)(15). However, ''IF/TA'' should only be diagnosed if the underlying etiology of fibrosis and tubular atrophy is not clear (5). With protocol biopsies and detailed clinical information a cause of graft dysfunction can be recognized in most cases, with the majority being due to chronic rejection (9,10,12,16).…”

“…Tubulointerstitial fibrosis is the final common pathway of most progressive renal diseases and the most potent predictor of outcome (1)(2)(3)(4). In renal allografts, tubulointerstitial fibrosis is jointly assessed with tubular atrophy, given that the two almost inevitably occur in parallel, and is termed ''interstitial fibrosis/tubular atrophy (IF/TA)'' (5). IF/TA is detectable in about 40% of kidney allografts at 3-6 months (6,7) and increases to about 65% at 2 years (8).…”

Diminished Met Signaling in Podocytes Contributes to the Development of Podocytopenia in Transplant Glomerulopathy

“…1 Although interstitial fibrosis and tubular atrophy (IFTA) is multifactorial in origin, transplant vasculopathy and transplant glomerulopathy (TxG) are considered specific lesions of chronic allograft rejection. [2][3][4][5][6][7] The prevalence of TxG increases over time after transplantation from 5% at 1 year to 20% at 5 years. 8 Early, subdiagnostic findings include an "activated" aspect of glomerular endothelial cells (GECs), with accumulation of mitochondria, Golgi apparati, and ribosomes, and a transition from fenestrated to continuous endothelium.…”