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Intimal vascular lesions are considered features of acute T-cell-mediated rejection yet can occur in the absence of tubulointerstitial inflammation, termed isolated 'v' lesions. The clinical significance of these lesions is unclear. The diagnosis requires a biopsy with the presence of arteries. The frequency of adequate biopsies was analysed in 89 renal transplant biopsies from 57 paediatric renal allograft recipients, and the incidence of isolated endarteritis was determined. 60 (67%) biopsies contained an artery and of these, isolated 'v' lesions occurred in 6 (10%). 5 (83%) biopsies with isolated 'v' lesions were associated with positive DSA, suggesting that these lesions may represent acute antibody-mediated rejection. Patients with vessel-negative biopsies had an increased decline in eGFR (median −20.5, IQR −24.4 to 1.2 ml/min/1.73 m2 vs. −9.6, IQR −78.7 to −6.8 ml/min/1.73 m2; P = 0.01). Patients with vessel-negative biopsies were more likely to have repeat biopsy for ongoing allograft dysfunction, (25.0% vs. 2.4%; P < 0.01). The data suggest that isolated 'v' lesions are more common than previously thought. A significant proportion of biopsies classified as 'normal' or 'borderline change' in the absence of a large vessel may represent undiagnosed acute rejection. This may result in suboptimal therapy with possible adverse effects on renal outcome. [ABSTRACT FROM AUTHOR]

Background. The term chronic allograft nephropathy (CAN) was deleted in the Eighth Banff Classification and two new categories were introduced: chronic T-cell-mediated rejection (CTMR) and chronic active humoral rejection (CAHR). The aim of this study was to revise our CAN cases diagnosed in the last 4 years, analyse allograft survival rates and identify types of infiltrating cells in the different settings.Methods. Seventy-nine patients with biopsy-proven CAN were examined and classified into four groups according to the Banff 2005 criteria: CTMR, CAHR, chronic calcineurin inhibitor toxicity (CNITOX) and interstitial fibrosis and tubular atrophy not otherwise specified (NOS). CD4, CD8, CD20, CD68, CD103, Foxp3 and IL-17 protein expression and C4d deposits were investigated.Results. We diagnosed 20 CTMR, 13 CAHR, 28 CNITOX, and 18 NOS. Death-censored graft survival at 4 years from renal biopsy was worse in CAHR compared with the other types of chronic injury. Glomerular CD8+ cells were increased in CTMR vs CNITOX and NOS. Interstitial CD4+ and CD8+ cells were increased in CTMR vs CNITOX. CD68+ cells in glomerular and peritubular capillaries were higher in CAHR vs CNITOX, CTMR and NOS. CD103+ cells were higher in cases with tubulitis than in those without. T regulatory and T helper 17 cells were rarely observed in the different settings.Conclusions. Graft survival was worse in patients with CAHR. The presence of any grade transplant glomerulopathy and chronic allograft vasculopathy are poorer prognostic factors. Infiltrating CD8+, CD103+ and CD4+ cells may help to differentiate CTMR from other types of chronic injury, thus improving diagnostic/prognostic features of biopsy in patients with chronic allograft dysfunction. [ABSTRACT FROM AUTHOR]