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.

Background: Currently, colorectal cancer (CRC) ranks as the third most common cancer and the second leading cause of cancer-related mortality worldwide. CRC frequently metastasizes to the liver (50%), lungs (10–15%), peritoneum (4%), bones (10.7%–23.7%), brain (0.3%–6%), and spinal cord. Approximately 35% of CRC cases are diagnosed before distant metastasis, 36% upon lymph node involvement, and 23% after distant organ metastasis. Although several studies have established primary tumor models in mice in our country, there are limited studies on experimental lung metastasis models, prompting the need for this research. Aim: To establish and evaluate a lung metastasis model of colorectal cancer in C57BL/6J mice using the MC38 cell line. Materials and Methods: This study was conducted at the Institute of Biomedical Sciences, Mongolian National Uni versity of Medical Sciences. Approval was obtained from the Ethics Review Board of the Mongolian National Univer sity of Medical Sciences (2023/3-09) and all laboratory safety regulations and protocols were strictly followed. Male C57BL/6J mice bred at the Experimental Animal Center of Mongolian National University of Medical Sciences were used. MC38 murine colorectal carcinoma cells were cultured and injected intravenously (via the tail vein) at a concen tration of 0.25×10⁶ cells per mouse (n=12) to induce lung metastasis. Histological analysis was subsequently performed. Results: Histological examination revealed significant alterations in lung tissue architecture, characterized by areas of dense infiltration by pleomorphic, hyperchromatic cells, disrupting the normal alveolar structure. No histological abnor malities were observed in other organs. Conclusion Intravenous injection of MC38 colorectal adenocarcinoma cells into the tail vein of C57BL/6J mice success fully induced lung metastases, characterized by hyperchromatic, pleomorphic cell infiltrates forming glandular structures within the lung parenchyma.

Background: According to the World Health Organization (WHO), 99 percent of the world’s population is exposed to air that exceeds WHO recommendations, with low- and middle-income countries being the most affected. The main causes of indoor air pollution include human activities such as fuel burning, cooking, cleaning, and smoking; housing character istics such as walls, floors, ceilings, and furniture; ventilation; and outdoor air pollution. Aim : To assess PM1 and PM10 concentrations in 120 selected households in Ulaanbaatar. Materials and Methods : Indoor PM1 and PM10 concentrations were measured using Purple Air real-time sensors in randomly selected Ulaanbaatar households between October 2023 and January 2024. Supplementary data on factors af fecting the PM2.5 concentration were collected via questionnaires. Each measurement was taken in 10-minute intervals, yielding 51,309 data for analysis. Results : PM1 concentrations were measured at 55.5±53.2 μg/m³ in gers, 54.9 ± 46.7 μg/m³ in houses, and 31.6±40.1 μg/ m³ in apartments (p<0.001) and measuring PM10 concentrations were 110.6±108.6 μg/m³ in gers, 110.6±96.7 μg/m³ in houses, and 62.2±83.0 μg/m³ in apartments (p<0.001) When considering the concentration of PM1, PM10 by heating type, PM1 was 55.3±50.1 μg/m³ and PM10 was 110.6±103.0 μg/m³ in households with stoves and furnaces, and PM1 was 31.6±40.1 μg/m³ and PM10 was 62.2±83.0 μg/m³ in households connected to the central heating system (p<0.001). Regarding the months of measurement, the highest concentration was observed in December 2023, at 77.1±94.1 μg/ m³. The highest concentrations for both PM₁ and PM₁₀ were recorded in January 2024, at PM₁: 64.8±55.1 μg/m³, PM₁₀: 131.4±116.0 μg/m³. Conclusion 1. Indoor PM10 concentrations in residential environments in Ulaanbaatar city were within the MNS4585:2016 Air Quality Standard, however, it was exceeded the WHO air quality guidelines, indicating an excessive risk of increas ing morbidity and mortality among the population. 2. Indoor PM1 and PM10 concentrations in residential environments in Ulaanbaatar varies depending on location, type of housing, type of heating, and month of measurement.