Kidney transplantation is the best alternative treatment for end-stage renal disease and health-related quality of life and survival of the patients are improved compared with dialysis. Worldwide, more than 1.4 million patients with CKD receive renal replacement therapy with incidence growing by approximately 8% annually.1 Unfortunately, despite significant improvement in graft function, kidney transplants can still fail due to acute rejection and chronic allograft nephropathy.2 Kidney biopsy after transplantation, which has evaluated by Banff 09 classification is usefull method for diagnose of transplanted kidney disease.3,4Kidney graft rejection was diagnosed in 10 renal allograft biopsy specimens (bs) obtained from transplant patients followed up at our institute between 2015 and 2016. All specimens were evaluated as satisfactory which show more than 8 glomerulus under the light microscopy. Each renal cortical tissue was divided into two tips: one piece for routine H&E stain and special stains, including Masson’s trichrome, and PAS stain; another piece for immunofluorescence by frozen section, which were stained with IgA, IgM, IgG and complement component (C3, C4, C1q, C4d). All the renal biopsies were examined by the same pathologist.Out of 117 transplantations, 10 episodes of rejection selected. Among the 10 patients, 30% had an acute T cell rejection and 70% had a chronic allograft nephropathy. Interstitial inflammation (i1-7) was present in 7 bs (70%), tubulitis (t1-4,t2-2) in 6 bs (60%), transplant glomerulitis (g1-1, g2-2, g3-1) in 4 bs (40%), transplant interstitial fibrosis (ci1-2, ci2-2, ci3-2) in 6 bs (60%), tubular atrophy (ct1-6, ct2-2, ct3-1) in 9 bs (90%), mesangial matrix increase (mm1-5) in 5 bs (50%), vascular fibrosis intimal thickeness (cv1-3) in 3 bs (30%), arteriolar hyaline thickening (ah1-5) in 5 bs (50%), tubulitis (ti1-6, ti2-3, ti3-1) in 10 bs (100%) and peritubular capillaritis (ptc1-1, ptc2-2, ptc3-1) in 4 bs (40%). C4d deposition was present very mild in wall of the vessels and peritubular capillaries. Because of not good working Methenamin silver stain, we couldn’t demostrate glomerular basement membrane changes (cg) fully.We suggest that histopathological changes of transplant glomerulopathy might be accompanied by inflammation of the microvasculature, such as transplant glomerulitis and peritubular capillaritis. C4d deposition in the wall of the vessels and peritubular capillaritis is not always present in biopsy specimens of transplant glomerulopathy.