ABSTRACT
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.
ABSTRACT
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.
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Background Systemic Lupus Erythematous (SLE) is a multi-systemic autoimmune disease with numerous patterns of clinical and immunological manifestations. Renal disease in SLE occurs in 40–75% of patients, most often within five years of disease onset, and is one of the strongest predictors of a poor outcome. Anti-dsDNA antibodies are reported to be more prevalent in patients with SLE who have renal disease. Anti-Sm, anti SSA and anti SSB antibodies are also considered to play a pathogenic role in inducing renal symptoms in SLE, and a strong correlation has been seen in lupus nephritis (LN) between disease activity and anti-dsDNA antibody levels. Objective The aim of our study is to highlight the clinical and laboratory features in SLE patients. Methods This is a three year hospital based case-control study of patients with renal diseases, who were admitted to the nephrology and rheumatology units of the 1st central Hospital and 3rd central hospital, Mongolia. Standard methods were used for laboratory testing. Autoantibodies (C/P-ANCA, anti-dsDNA, anti-Sm, anti-SS-A/Ro, anti-SS-B/La, anti-Scl-70, anti-GBM) measured by Enzyme Immuno Assay (Germany, ORGENTEC Diagnostika GmbH). Renal function was evaluated by the eGFR (estimated glomerular filtration rate) using the Cockcroft-Gault formula. Result The study included 27 patients with lupus nephritis and 78 controls with other types of GN. There were 85.2% of female patients in the lupus nephritis group. Patients with LN were significantly younger than the controls (mean (SD) 31.9 (10.1) years vs. 37.1 (11.9) years; p=0.036). For the serology, a higher proportion of anti dsDNA (46.1%), anti Sm (29.6%), anti SSA (63%) and anti SSB (11.1%) were seen in the group with lupus nephritis (p=0.001; p=0.043; p<0.0001; p=0.096, respectively). The Pearson’s correlation analysis indicated that the level of anti-dsDNA (r=-0.249, p=0.021) and anti SSA (r=-0.195, p=0.048) were significantly correlated with the renal function (eGFR). All had dipstick proteinuria 1+/2+/3+, more than 10 red blood cells/hpf hematuria (n-12, 44.4%) in lupus nephritis group and renal function (mean eGFR (SD) 88.1 (51.3) ml/min vs. 112.3 (67) ml/min; p=0.05) was more decreased in lupus nephritis patients than controls. Conclusion Notably, rising titers of antibodies to dsDNA, SSA may indicate exacerbations of glomerulonephritis.
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Background: Glomerulonephritis (GN) remains a common cause of end stage kidney failure worldwide. The auto antibodies are useful in the patients prognosing, diagnose and treatment of GN. The aim of the study was to compare the prevalence and levels of auto antibodies in the sera of patients with GN in relation to the clinical activity of disease and auto antibodiesMethods: From a hospital-based population, 90 patients with GN (mean age 37.9±12.7) were recruited. Autoantibodies (C/P-ANCA, anti-dsDNA, anti-Sm, anti-SS-A/Ro, anti-SS-B/La, anti-Scl-70, anti-GBM) measured by Enzyme Immuno Assay (Germany, ORGENTEC Diagnostika GmbH). Renal function was evaluated by the eGFR using the Cockcroft-Gault formula.Results: Patients with GN was significantly younger and primary GN was more common in the male, but frequency of LN was 4 times higher among female. The prevalence of cANCA 2.9%, Sm 4.2%, dsDNA 5.7%, SSA 7.1%, SSB 1.4% were positive in primary GN group, the prevalence of Sm 16.7%, dsDNA 8.3%, SSA 25%, SSB 16.7% were positive in secondary GN group. A higher frequency of anti Sm 25%, anti-dsDNA 25%, anti-SS-A/Ro 75%, anti-SS-B/La 25% was observed in the lupus nephritis group. Conclusion: Lupus nephritis associated with several auto antibodies (anti Sm, anti-dsDNA, anti-SS-A/ Ro, anti-SS-B/La) and each of which are very useful in distinguishing patients with lupus nephritis from other secondary GN.
ABSTRACT
Background: Smoking is significant risk factor for further kidney failure. Haroun et al. found that current smoking was associated with HR of 2.6 for future RRT and having kidney disease listed on the death certificate compared with the former and never smokers [2]. Regarding smoking and kidney pathophysiology, direct vascular effects are probably a major mechanism [3-5]. Smoking is a particularly associated with atherosclerosis. The purpose of this study was to determine the effects of smoking on renal function and arterial stiffness in the CKD patients. Methods: A cross-sectional study was conducted in which adolescents aged 20 to 60 years with CKD total 125 patients with non diabetic CKD (mean age 40.30±10.82) were recruited. CKD was evaluated by the eGFR using the Cockcroft-Gault formula. Cardio-Ankle vascular index (CAVI) was determined as an index of arterial stiffness.Results: Even though there wasn’t an age difference between the smoking and non smoking groups, the renal function (38.1±22.6 vs. 90.5±59.9, p<0.0001) among smokers decreased comparing to the non smokers. The Pearson’s correlation analysis indicated that the smoking index was significantly correlated with the renal function (r=-0.392, p=0.02) and the arterial stiffness (r=0.573, p<0.0001).Conclusion: We found that smoking influenced on renal, it is a significant risk factor of CKD.