Objective To investigate the changes in the concentration of myocardin in children with lupus nephritis (LN) under different degree of vessel damage.Methods Forty-nine children diagnosed with LN by routine tissue immunolfuorescence, light microscope, and electron microscope were included, and 30 healthy children were included as control group. The pathological classiifcations were performed according to the ISN/RPS 2003 LN pathological classiifcation criterion. According to the Katafuchi evaluation method, the semi quantitative assessment of glomerular and kidney tubule damage was carried out, and the degree of vascular damage was evaluated at the same time. Double antibody sandwich method was used to detect the concentration of serum myocardin.Results The glomerular and kidney tubules damage in children with LN were signiifcantly aggravated with higher pathological classification (P<0.05). Glomerular damage was positively correlated with renal interstitial damage (r=0.96, P<0.01). The degree of vascular damage was related to the degree of glomerular injury and renal interstitial injury, while it was no related with the results of clinical tests. There were different concentrations of myocardin among mild-, moderate-, severe-vessel damage and control groups (F=378.61,P<0.001), and the concentration of myocardin in moderate- and severe-vessel damage groups were obviously lower than those in control group and mild-vessel damage group (P<0.01) while there was no difference between control group and mild-vessel damage group (P>0.05). According to pathological type, there were signiifcant differences in the concentration of myocardial between control group and different pathological types (F=626.793,P<0.01). FromⅡ,Ⅲ,Ⅲ+Ⅴ,Ⅳ toⅣ+Ⅴ, the concentrations of myocardial were decreased systematically, and there were statistic differences between groups (P all<0.05).Conclusion The concentration of myocardin in children with LN can relfect the renal vascular damage to a certain extent. Elevation of myocardin concentration may be helpful for the repair of vascular damage.

Objective To explore the role of nuclear translational factor homeobox A13(HOXA13)gene in epithelial - to - mesenchymal transition(EMT)induced by human serum albumin(HSA)overload in human renal tu-bular epithelial(HKC)cells. Methods HKC cells were treated with different concentrations of HSA(ranging from 0 - 30 g/ L)for 48 h or 20 g/ L HSA for different times(ranging from 0 - 72 h)in vitro. The protein expressions of cy-tokeratin(CK),Vimentin,and HOXA13 protein in HKC cells were detected by using Western blot respectively. Mean-while,liposome - mediated DNA transfection was used to transfect the HOXA13 gene into HKC cells before HSA treat-ment,and the expressions of CK,Vimentin and HOXA13 protein in HKC cells were also detected by using Western blot. Results (1)The protein expression of CK decreased but Vimentin increased after HKC cells were exposed to HSA,which was in a concentration - and time - dependent manner.(2)Expression of HOXA13 was down - regulated by HSA in a dose - and time - dependent manner,and the expressions of HOXA13 protein in HKC in 5 g/ L,10 g/ L, 20 g/ L,30 g/ L group were 58. 24%(P = 0. 005),44. 73%(P = 0. 003),38. 40%(P = 0. 033)and 24. 83%(P =0. 011)respectively as compared with 0 g/ L group. Likewise,the protein expressions of HOXA13 in 24 h,48 h,72 h group were 52. 00%(P = 0. 023),46. 83%(P = 0. 008)and 35. 10%(P = 0. 034)respectively as compared with 0 h group.(3)There was a positive correlation between the levels of HOXA13 protein expression and CK protein expression (r = 0. 86,P = 0. 005),while the relationship between the levels of HOXA13 protein expression and Vimentin protein expression was negative(r = - 0. 94,P = 0. 002).(4)Up - regulated expression of HOXA13 in HKC cells by lipo-fectamine transfection alleviated the degree of EMT induced by HSA significantly. The expression of Vimentin decreased by 35. 34%(P = 0. 005)while the expression of CK increased 360. 00% - fold(P = 0. 005),compared with that of untransfected HKC cells. Conclusion EMT induced by HSA in HKC cells may play a role through HOXA13.

Objective To discuss the role of EB virus (EBV)in the pathogenesis of systemic lupus erythematosus(SLE) in children through investigating the copies of EBV DNA and expression of EBV genes in peripheral blood mononuclear cells(PBMCs).Methods (1)PBMCs were isolated from 30 patients with SLE and 12 healthy normal controls respectively and DNA was extracted from PBMCs.(2) PBMCs were co-cultured with EBV for 12 days and RNA was extracted from PBMCs.(3)Real-time fluorescence quantitative PCR(Real-time PCR) was applied to detect the copies of EBV DNA in PBMCs.(4)Reverse transcription PCR was applied to detect expression of EBV genes.Results (1) Compared with the healthy control group [(40.1 ± 11.6) copies/μg],a significant increase of EBV DNA copies was observed in SLE group[(658.6 ± 183.6) copies/μg] (P ＜0.05).The EBV DNA copies in the active SLE group [(785.2 ± 179.2) copies/μg] were significantly higher than those in the non-active SLE group [(586.0 ± 193.1) copies/μg] (P ＜ 0.05).(2)There was no correlation between EBV DNA copies and systemic lupus erythematosus disease activity index (r =0.03,P ＞ 0.05).(3) After PBMCs got co-cultured with EBV,expression of latent EBV genes and lytic genes were both increased in the patients and healthy controls.The latent EBV genes including latent membrane protein 1 (LMP1),LMP2,EBV nuclear antigen 1 and the lytic genes including BCRF1,BLLF1 were all increased significantly in the patients compared with the healthy controls (all P ＜ 0.05).Conclusions There is a significant increase of EBV DNA copies and aberrant expression of EBV genes in SLE patients,which suggests that EBV may contribute to the pathogenesis of SLE.

Objective To investigate the expression and significance of Epstein-Barr virus (EBV) genes in children with systemic lupus erythematosus (SLE).Methods Peripheral blood mononuclear cells (PBMCs) were isolated from 20 children with SLE and 12 healthy human controls.Enzyme-linked immunosorbent assay (ELISA) was conducted to detect anti-EBV viral capsid antigen (VCA) IgG/IgM antibodies.The culture supernatants of cells from patients with anti-EBV VCA IgG/IgM antibodies were collected,and PBMCs from the patients and controls were co-cultured with the supernatants respectively for 12 days.RNA was extracted from PBMCs before and after the coculture,and reverse transcription-PCR was performed to detect the expression of EBV genes,including LMP1,LMP2,EBNA1,BCRF1,BLLF1 and BILF1 genes.Results LMP1 gene was detected in fresh PBMCs from 10 out of 20 patients and 1 out of 12 controls (P ＜ 0.05).No significant differences were observed between the patients and controls in the detection rate of LMP2 gene (4/20 vs.1/12),EBNA1 gene (13/20 vs.3/12),BCRF1 gene (3/20 vs.1/12) or BLLF1 gene (5/20 vs.2/12) in fresh PBMCs.After co-culture with the supernatants of cells from patients with anti-EBV VCA IgG/IgM antibodies,the expressions of EBV genes in these PBMCs were increased to different degrees,and there was a significant difference in the expressions of EBV latent genes LMP1,LMP2 and EBNA-1 as well as EBV replicative genes BCRF1 and BLLF1 between the patient-derived and control-derived PBMCs (all P ＜ 0.05).Conclusions There is an aberrant expression of EBV genes in children with SLE,and EBV genes may contribute to the development of SLE.

This paper describes the clinical epidemiologic features, main pathogenesis, early diagnostic biomarkers and managements of septic acute kidney injury in children. It is suggested that pediatric clinicians should increase awareness of the treatment of septic acute kidney injury in children.

Objective To research Henoch-Schonlein purpura purpura (HSP) and renal pathology in children.Methods 31 hospitalized HSP children that with normal urine routine and accepted renal biopsy in our hospital.Results There were different levels of kidney pathological damage in this group of 31 cases,the results of light microscope were from grade Ⅱ to grade Ⅵ The proportion was grade Ⅱ(35.48％,11 of 31),grade Ⅲ (54.83％,17 of 31),and grade Ⅳ,Ⅴ and Ⅵ (each 1 case of 31,3.23％ ).lmmunofluorescence pathology results were showed as following:merely IgA depositional (48.38％,15 of 31 ),IgA + IgG depositional ( 19.36％,6 of 31 ),IgA + IgM depositional ( 19.36％,6of 31 ),IgA + igG + IgM depositional ( 12.90％,4 of 31 ).Microalbuminuria had been founded in 14 cases,and the microalbuminuria level of 10 cases were higher than normal value( 10 of 14,71.43％ ).Conclusions HSP children had renal pathologic dysfunction,even the urine routine were normal,and the detection of urine microalbumin was a significant marker in the early stage.

ObjectiveStudy the relationship among CaSR expression, tubulointerstitial damage,metabolic disturbance of calcium and phosphorus and microvascular density around the tubulointerstitium in children with steroid-resistant nephrotic syndrome.Methods36 cases of children with primary nephrotic syndrome were divided into hormone-sensitive group and steroid-resistant group.Semi-quantitative scores for tubulointerstitial pathological evaluation of the extent of damage, automatic biochemical analyzer for the determination of serum calcium (Ca), phosphorus (P) concentration of renal tubular epithelial CaSR expression and microvessel microvascular density around the tubulointerstitium were determined by immunohistochemical assay.ResultsMore severe the tubulointerstitial damage, lower level of serum Ca and higher level of serum P were observed [(2.26 ± 0.15) mmol/L]in children of the steroid-resistant group and the steroid-sensitive group [(1.90 + 0.12) mmol/L, P ＜ 0.05].CaSR expression (4.63 + 0.78) of renal tubular epithelial cells in the steroid- sensitive group was significantly lower than that in the steroid-resistant group (6.56 + 1.22, P ＜ 0.05), but microvascular density was significantly higher in the steroid- sensitive group(2.98 +0.35 vs 2.02 +0.24, P ＜0.05).When the tubulointerstitial damage was mild, CaSR expression (4.15 +0.58) in renal tubular epithelial cells in the steroid- sensitive group (4.26 ±0.61) was lower than the steroid-resistant group(3.12 ± 0.33; 3.01 ± 0.21), and microvascular density was higher,but the difference was not significant(P ＞0.05).In the moderate tubulointerstitial damage, CaSR expression in renal tubular epithelial cells in the steroid- sensitive group (5.35 ± 0.64) was significantly lower than the resistant group (7.37 +0.81, P ＜0.01), and microvascular density was significantly higher than the resistant group (2.81 ±0.16, 2.02 ±0.14, P ＜0.05).Compared by mild and moderate tubulointerstitial damage in children with the steroid-resistant, CaSR expression (11.46 ± 1.38) in children with severe tubulointerstitial damage was significantly increased, and microvascular density (1.15 ± 0.11) was significantly decreased (all P ＜ 0.01).ConclusionsCaSR expression was increased and microvascular density around the tubulointerstitium was decreased in children with steroid-resistant nephrotic syndrome.Dut to steroid resistance, the cytotoxic of steroid damaged the renal tubular epithelial cells, the metabolic disturbance of calcium and phosphorus and the damage of blood vessel endothelium finally resulted in severe tubulointerstitial damage.

Objective This study investigated high fat diet influence on the changes of vitamin D receptor (VDR) expression and endothelial nitric oxide synthase (eNOS) in apolipoprotein E-deficient(apoE-/-) mice.MethodsApoE-/- mice and C57BLP6J mice were divide into two groups (normal control and high fat diet),high fat diet group were feed high fat feedstuff.Plasma 25-(OH)D levels were determined by competitive protein binding radioimmunity,VDR expression were determined by immunofluorescence and reverse transcription-polymerase chain reaction.The levels of NO and eNOS were determined by nitrate reductase.ResultsCompared with normal control group,high fat diet caused more severe dam-age of atherosclerosis in wild type mice and apoE-/- mice.In apoE-/- mice,the levels of plasma 25-(OH)D were significantly decreased [(26.44±1.28) ng/mL,(22.68±2.07)ng/mL,(17.46±2.22)ng/mL,(15.88±0.97)ng/mL,P＜0.01],the expression of VDR protein and mRNA were significantly increased[VDR :0.244±0.088,0.346±0.132,0.547±0.128,0.768±0.162;VDRmRNA:0.228±0.083,0.375±0.103,0.451±0.117,0.597±0.131,P＜0.01],and the levels of NO and eNOS were significantly increased[NO:(39.74±4.81)μmol/L,(48.1±5.24 )μmol/L,(67.34±6.14 )μmol/L,(86.74±8.05)μmol/L;eNOS:(8.6±0.77 )U/L,(12.28±1.42)U/L,(15.96±0.92)U/L,(18.68±1.15)U/L,P＜0.01].These changes were more significantly in high fat diet group(P＜0.01).ConclusionsThere were abnormalities of plasma 25-(OH)D level,VDR expression and the level of NO and eNOS in apoE-/- mice.These changes were more significantly in high fat diet group.

OBJECTIVE: To explore the change in ambulatory blood pressure monitoring (ABPM) value and the sympathetic nervous system (SNS) level in children with primary nephrotic syndrome(PNS) and their relationship. METHODS: ABPM and casual blood pressure(CBP) were tested in 114 children with PNS and 12 normal children as a control group. The 24-h urine noradrenaline(NA), adrenaline(A) and dopamine(DA) content were detected through high-performance liquid chromatography with electrochemical luminescence and the correlation with ABP was analyzed. RESULTS: Among 114 children with PNS, 101 had elevated blood pressure (88.6%), 45 showed high incidence of masked hypertension (39.5%), and 80 non-dipper blood pressure (70.2%). Systolic blood pressure level and blood pressure load were greater than diastolic blood pressure. NA, A, and DA levels of the PNS group were significantly higher than those of the control group, while those of the elevated blood pressure group were significantly higher than those of the normal blood pressure group in PNS children. SNS levels were positively correlated with blood pressure levels and blood pressure load, and negatively correlated with night BP decreasing rates. CONCLUSION Children with PNS have high incidence of hypertension with large proportion of masked hypertension and non-dipper blood pressure. Severe masked hypertension classification should be set up. In PNS children, SNS activity is elevated that might evaluate the blood pressure level and decrease blood pressure circadian rhythm.
Adolescent ; Blood Pressure ; physiology ; Blood Pressure Monitoring, Ambulatory ; Case-Control Studies ; Child ; Child, Preschool ; Female ; Humans ; Hypertension ; diagnosis ; etiology ; Male ; Nephrotic Syndrome ; complications ; physiopathology ; Sympathetic Nervous System ; physiopathology

Objective To explore the relationship between vascular endothelial growth factor (VEGF) concentration in urine and renal vascular damage in children with Henoch Schonlein purpura nephritis (HSPN).Methods The kidney pathological lesion of 78 biopsy-proven HSPN children was assessed with renal vascular damage, glomerular pathological damage, and tubulointerstitial pathological damage semi-quantitative points. The children were divided into 3 groups (light, medium, and heavy group) according to the renal vascular, glomerular, tubulointerstitial, glomerular and tubulointerstitial total pathological points. Blood and urine vascular endothelial growth factor concentration was detected by enzyme linked immunosorbent assay;the localized renal VEGF expression and microvessel density were detected by immunohistochemistry assay in the kidneys. Results The semi-quantitative points of glomerular, tubulointerstitial, renal vascular, and glomerular and tubulointerstitial total points in different groups had significant difference (all P＜0.01);the minor renal vascular damage, the higher light microvessel density, blood and kidney concentration of VEGF, and the VEGF excretion in the urine were also lower in different groups, and there were significant differences (all P＜0.01). Glomerular points were positively related with tubular points, vascular points, kidney total score (r=0.596,0.612, and 0.728;P＜0.05, 0.05, and 0.01 respectively). Microvessel density was highly positively related with blood VEGF and renal VEGF, and negatively rela-ted with urine VEGF (r=0.601, 0.696, and -0.639,all P＜0.01). Conclusion The urinary excretion of VEGF leads to the decrease of local kidney VEGF concentration resulting in the renal vascular injury, which may be the important reason for renal vascular damage and pathology chronic progress in HSPN children.