MON-164 CLINICAL AND PATHOLOGICAL ANALYSES IN CASES OF TRANSPLANT GLOMERULOPATHY AFTER KIDNEY TRANSPLANTATION IN MONGOLIA

Abstract

Transplant glomerulopathy (TG) is included as one of the criteria of chronic active antibody-mediated rejection (c-AMR) in Banff 09 classification. TG is a morphologic lesion of renal allografts that is characterized histologically by duplication and/or multilayering of the glomerular basement membrane (GBM). TG is well documented to be associated with the presence of donor-specific antibodies (DSAs), most notably against HLA class II antigens, and in the majority of cases is felt to represent a morphologic manifestation of chronic antibody-mediated rejection (ABMR). The First Central Hospital of Mongolia is the only hospital that perform Kidney transplantation (KT) in Mongolia. We perform 20 KT per year and currently we performed total of 164 KT in end stage kidney disease patients in our hospital. In addition, we follow-up nearly 400 kidney transplanted patients in our clinic (including patients had transplantation in overseas). In this report, we discuss the clinical and pathological analyses of cases of TG after renal transplantation. TG was diagnosed in 10 renal allograft biopsy specimens (BS) obtained from transplant patients who was under follow up at our clinic between 2017 and 2018. We checked DSA and stained the specimens with H&E, masson's trichrome, PAS, silver staining and used Banff 09 classification. Immunofluorescence and C4d stainings were also done. Among the 10 patients,20% had a history of acute rejection (AR); of these,10% had acute antibody-mediated rejection (a-AMR).Among the 86 BS of TG,the TG was mild in 35 cases (cg1),moderate in 28 cases (cg2) and severe in 23 cases (cg3).Peritubular capillaritis was present in 74 bs (86%), transplant glomerulitis in 65 (76%),interstitial fibrosis and tubular atrophy (if/ta) in 71 (83%),thickening of the peritubular capillary (ptc) basement membrane in 72 (84%), and interstitial inflammation in 40 (47%).C4d deposition in the ptc was present in 49 bs (57%); 39 of these 49 bs showed diffuse c4d deposits in the ptc (c4d3),while the remaining 10 bs showed focal deposits (c4d2).Diffuse c4d deposition in the glomerular capillaries (GC) was seen in 70 bs (81%), while focal c4d deposition in the GC was seen in 9 (11%). In the assay using plastic beads coated with HLA antigen performed in 67 serum samples obtained in the peri-biopsy period, circulating ant-HLA alloantibody was detected in 55 (82%); in 33 of the 55 (49%) samples, donor-specific antibodies (DSA) were detected. Among our study, the findings in 22 bs (26%) fully met the criteria for c-AMR in banff '09 classification, including TG, c4d deposition in the ptc and presence of DSA, while those in 27 BS were suspicious of c-AMR. Deterioration of the renal allograft function after the biopsies was seen in 31 patients (62%). 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. 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 poor even under the currently used standard triple immunosuppressive regimen.