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.

BackgroundIgA nephropathy and MPGN are common glomerulonephritis in the world that progresses slowly andrenal function can even remain unchanged for decades. Clinically, it presents by isolated hematuria,proteinuria. Histologically, IgA nephropathy presents with acute glomerular damage, mesangial cellproliferation, endocapillary leucocyte infiltration, and crescent formations, these lesions can undergoresolution with sclerotic healing. Since 2013, renal biopsy has been done at the First Central Hospitalof Mongolia a few times. However, the confirmative diagnosis of IgA nephropathy and MPGN remainunknown in Mongolia by renal biopsy. Therefore, we intended to test renal biopsy techniques andconfirm its diagnosis by renal biopsy at the Second Central Hospital of Mongolia.MethodsUltrasound guided renal biopsy had been done for four patients by nephrologist at the Departmentof Nephrology of the Second Central Hospital of Mongolia. All four specimens were evaluated assatisfactory which show more than 8 glomerulus under the light microscopy. Each renal cortical tissuewas divided into two tips: one piece for routine H&E stain and special stains, including Masson’strichrome, and PAS stain; another piece for immunofluorescence by frozen section, which werestained with IgG, IgM, IgA and complement component 3 (C3). Each case was screened by threepathologists.Results:The case which shows mesengial widening, mesengial hypercellularity under the light microscopyor mesangial granular deposition of IgA and C3 by immunofluorescence was diagnosed as IgAnephropathy. We obtained crescent formation with glomerular adhesion in most cases. In addition, weobserved secondary MPGN in one case, which is caused by hepatitis C virus infection.Conclusion: Probably, it is a new step for developing pathologic diagnosis for nephrology in Mongolia.We needs further study for improving renal biopsy technique and confirming the diagnosis of IgAnephropathy and MPGN using electron microscopy and pathological report by oxford classification forIgA nephropathy.