Deterioration

of the renal allograft function after the biopsies was seen in 31 patients (62%), of which 11 lost their graft. We suggest that histopathological changes of transplant glomerulopathy might be accompanied by inflammation of the microvasculature, such as transplant glomerulitis and peritubular capillaritis, thickening of the peritubular capillary basement membrane, and circulating anti-HLA antibodies. C4d deposition in the PTC is not always present in biopsy specimens of TG. We speculated that C4d deposition in the GC, rather than that in the PTC might be a more characteristic manifestation of TG. Many of the patients with TG had a history of AR. Anti-HLA antibody Class II, particularly when the antibody was DSA Class II, appeared to be associated with the development of TG. The prognosis of grafts exhibiting TG was not too good even under the currently used immunosuppressive protocol. Transplant glomerulopathy (TG) is Akt inhibitor a morphologic pattern of chronic kidney allograft injury and is

generally associated with poor renal allograft survival.[1] TG is characterized by double contours of the glomerular basement PLX-4720 order membranes (GBM), often accompanied by increased mesangial matrix.[2] TG is included as a criterion of chronic active antibody-mediated rejection (c-AMR) in the Banff ‘09 classification.[3] In this report, we discuss the clinical and pathological analyses of patients developing TG after renal transplantation. During the period from January

2006 to October 2012, TG was diagnosed in 86 renal allograft biopsy specimens (BS) obtained from 50 renal transplant recipients who were followed up at our institute. The data of these 86 BS and 50 patients were retrospectively reviewed from the clinical records in this study. The immunosuppressive protocol mainly consisted of triple-drug therapy, including methylprednisolone (MP), cyclosporine (CYA) or tacrolimus (TAC) and mizoribine (MZ), azathioprine (AZ) or mycophenolate mofetil (MMF) (Table 1). In some cases, basiliximab and rituximab had been given in addition (Table 1). Renal allograft biopsy was performed as part of the diagnostic workup for graft dysfunction 4��8C and proteinuria, or as protocol biopsy. The biopsy specimens were examined by light, electron and immunofluorescence microscopy. The biopsies were diagnosed and scored according to the Banff ‘09 classification.[3] TG was diagnosed by light microscopy based on the finding of double contours of the GBM.[2] Patients with hepatitis C virus-associated glomerular disease and thrombotic microangiopathy were excluded from this study. We used the ptcbm score, which showed thickening of the peritubular capillary basement membrane and was evaluated by light microscopy (LM) in place of diagnosing of peritubular capillary basement membrane multilayering (PTCBMML) by electron microscopy (EM).