本文报道1例婴幼儿型肾单位肾痨，肾脏病理表现为肾小管萎缩、小管基底膜增厚或变薄、间质纤维化和炎性细胞浸润等典型"三联征"。全外显子组测序发现患儿在第3号常染色体的132405215位置上发生c.3218 T>G(exon23)突变，此突变为新发 Nephrocystin- 3（ NPHP3）基因变异，进一步丰富了 NPHP3基因突变谱。

目的 探讨咪唑立宾(MZR)治疗儿童紫癜性肾炎(HSPN)的疗效与安全性.方法 选择2016年1月至2017年10月东部战区总医院儿科收治的儿童HSPN55例,按照随机数字分组法随机分为2组:强的松(PDN)与MZR联合治疗组(联合组,n=38)和MZR单药治疗组(单药组,n=17).分析2组患儿的随访3个月、6个月、12个月和24个月实验室检查结果、预后和不良反应.结果 联合组6个月、12个月和24个月ALB水平高于基线值(P<0.05);单药组12个月和24个月ALB水平高于基线值(P<0.05);联合组6个月、12个月和24个月尿蛋白定量水平低于基线值(P<0.05,P<0.01);单药组12个月和24个月尿蛋白定量水平低于基线值(P<0.05,P<0.01);联合组3个月、6个月、12个月和24个月尿NAG酶水平低于基线值(P<0.01);单药组6个月、12个月和24个月尿NAG酶水平低于基线值(P<0.05,P<0.01);联合组6个月、12个月和24个月尿RB蛋白水平低于基线值(P<0.05,P<0.01);单药组12个月和24个月尿RB蛋白水平低于基线值(P<0.01).预后分级:A级和总体预后分级联合组高于单药组(97.37％vs 82.35％,P<0.05),B级预后分级联合组低于单药组(2.63％vs 17.65％,P<0.05).联合组尿蛋白消失比例明显高于单药组(P<0.01).联合组血WBC升高比例高于单药组(86.84％vs 58.82％,P<0.05),呼吸道感染次数高于单药组(63.16％vs 23.53％,P<0.05),HSP复发次数低于单药组(2.63％vs 17.65％,P<0.05).结论 MZR治疗儿童HSPN有效性和安全性较高,PDN联合MZR治疗HSPN的临床效果高于单药MZR,且长期预后好于单药MZR.

儿童激素耐药型肾病综合征（steroid-resistant nephrotic syndrome，SRNS）是临床上比较棘手的问题，治疗难度大，并发症多发。中华医学会儿科学分会肾脏学组2016年制定了儿童SRNS诊疗指南，2020年国际儿科肾脏病学会（International Pediatric Nephrology Association，IPNA）发布了儿童SRNS临床实践建议。两者在儿童SRNS的治疗、基因诊断和预防接种方面存在一定的差异，现将两项指南中与临床联系密切的内容进行比较，为SRNS儿童的临床管理提供依据。

Objective To analyze the spectrum of children’s kidney pathology by renal biopsy. Methods The clinical and pathological data of the cases in Jinling Hospital involving patients younger than 18 years old who received renal biopsy from April 1st,2004 to December 31th,2017 were retrospectively collected,and compared with

Objective To observe the long_term efficacy and adverse reactions of Rituximab( RTX)in the treatment of children with frequently relapsing nephrotic syndrome(PRNS),and to explore the feasible treatment plan of RTX in children with PRNS. Methods PRNS children with RTX[375 mg∕(m2·time),2_3 times]from Depart_ment of Dediatrics,Jinling Hospital,Nanjing Clinical School of Southern Medical University between Pebruary 2011 and December 2017 were retrospectively reviewed,and followed up for 12 _36 months. Age,gender,number of relapses, dose of steroids and immunosuppressants,adverse reactions and laboratory indicators(peripheral blood CD20 ﹢B lympho_cyte count,24_hour urine protein quantification,etc)were observed. Results Thirty_four patients(23 males and 11 females)with PRNS were included in the present study,and the median age for the first RTX treatment was 6 years (2_12 years). After the first treatment,there was complete remission in 34 patients(100%,34∕34 cases),and 12 pa_tients(35%,12∕34 cases)relapsed during follow_up. The number of relapse after treatment[(0. 27 ± 0. 45)times] significantly decreased compared with that before treatment[(2. 94 ± 1. 08)times;t﹦11. 9,P〈0. 05]. After the second treatment,3 children relapsed due to ＂infection＂ and no discomfort was found in the first 6 months;5 of 23 cases (21. 7%,5∕23 cases)relapsed once and 11 were unclear in the following 6 months. There was a difference between the 2 treatment intervals 〈12 months(12. 5%,2∕16 cases)and ≥12 months(55. 5%,10∕18 cases). After the third treatment,with an interval of 6 to 15 months,1 of 15 patients(6. 67%)relapsed and the rest were stable. In addition, there was a significant difference in the mean accumulated steroid dose of 20 patients between 6 months before treatment [(2. 50 ± 0. 87)g ]and 6 months after treatment[(1. 30 ± 0. 97)g;t﹦6. 05,P﹦0. 001]. Of the 15 patients after RTX treatment for 6_12 months Tacrolimus was reduced from[(1. 62 ± 0. 77)mg∕24 h ]to[(0. 62 ± 0. 96)mg∕24 h;t﹦6. 80,P﹦0. 000]. Two patients after RTX first infusion had chest tightness,palpitations,nausea,vomiting,dizzi_ness,and headache,3 cases had mild upper respiratory tract infection and 1 case had severe pulmonary infection. Conclusion Long_term follow_up of PRNS children treated with RTX turns out to be safe and effective.

Objective To investigate the renoprotective effect of aspirin-triggered lipoxins(ATL)on kidney of mice with acute kidney injury(AKI).Methods Eighty-eight male specific pathogen-free(SPF)C57BL/6J mice were randomly divided into lipopolysaccharide(LPS)groups(including 2 h group,4 h group,8 h group,12 h group, 24 h group),ATL+LPS(including 2 h group,4 h group,8 h group,12 h group,24 h group)and normal control group according to random numble table,and each group had 8 mice.The mice in LPS groups were given LPS intraperitoneal injection to establish AKI animal models,while the mice in ATL+LPS groups were given ATL intraperitoneal injection 30 minutes before LPS intraperitoneal injection.The enzyme linked immunosorbent assay was used to test the serum creatinine(Scr),serum urea nitrogen(BUN),tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and urine neutrophil gelatinase-associated lipocalin(NGAL),kidney injury molecule-1(KIM-1),cysteine-rich protein-61 (Cyr61)and netrin-1 levels of mice.Results The kidney tissue injury scores of mice of ATL+LPS group[4 h:(22.32 ± 1.04)scores,8 h:(31.11 ± 1.86)scores,12 h:(18.22 ± 0.92)scores,24 h:(20.87 ± 3.18)scores] were lower than those of LPS group at the corresponding time points[4 h:(35.47 ± 2.27)scores,8 h:(52.28 ± 2.82) scores,12 h:(54.99 ± 4.56)scores,24 h:(53.41 ± 4.76)scores],and the differences were statistically significant(all P<0.01).The values of Scr,BUN,TNF-α and IL-1β in ATL+LPS group[Scr 8 h:(143.07 ± 5.02)μmol/L, BUN 12 h:(33.07 ± 3.52)mmol/L,TNF-α 4 h:(196.33 ± 14.181)ng/L and 8 h:(221.77 ± 10.11)ng/L,IL-1β 4 h:(50.25 ± 2.67 ng/L)]were lower than those in LPS group at the corresponding time points[Scr 8 h:(227.43 ± 11.17)μmol/L,BUN 12 h:(59.68 ± 3.84)mmol/L,TNF-α 4 h:(267.87 ± 26.48)ng/L and 8 h:(334.78 ± 21.08)ng/L,IL-1β 4 h:(89.45 ± 5.87)ng/L],and the differences were statistically significant(all P<0.01). The urine NGAL[4 h:(56.76 ± 4.01)μg/L,8 h:(65.44 ± 7.81)μg/L],KIM-1[8 h:(78.19 ± 9.48)μg/L] and netrin-1[8 h:(40.12 ± 2.01)ng/L,12 h:(36.87 ± 2.87)ng/L]of mice in ATL+LPS group were lower than those in LPS group at the corresponding time points[NGAL 4 h:(168.77 ± 10.77)μg/L,8 h:(155.33 ± 8.26) μg/L;KIM-1 8 h:(124.73 ± 13.47)μg/L;netrin-1 8 h:(89.17 ± 2.74)ng/L,12 h:(81.11 ± 3.88)ng/L],and the differences were statistically significant(all P<0.01).Conclusions ATL can treat LPS-induced AKI and play a renoprotective role in the kidney.

MicroRNA‑106b (miR‑106b) is reported to be closely associated with skeletal muscle insulin resistance. The present study further investigated the role of miR‑106b in skeletal muscle insulin sensitivity and glucose homeostasis in vivo. Mice were randomly divided into 4 groups and infected with lentivirus expressing miR‑106b (miR‑106b mice), miR‑106b sponge (miR‑106b inhibition mice) or the corresponding empty vectors. Mitofusion‑2 (Mfn2) protein expression levels and glucose transporter (Glut)‑4 protein translocation were significantly reduced in the muscle of miR‑106b mice, whereas they were unaffected in miR‑106b inhibition mice. miR‑106b mice had significantly increased blood glucose levels following 12 h of fasting and impaired glucose tolerance, whereas miR‑106b inhibition mice had no significant alterations in fasting blood glucose levels and glucose tolerance. In vitro, the suppressive effect of miR‑106b on glucose uptake and Glut4 translocation was completely inhibited in C2C12 myotubes infected with Mfn2 plasmids. Following treatment of C2C12 myotubes with Mfn2 small interfering RNA, miR‑106b inhibition consistently increased Mfn2 protein levels and improved glucose uptake and Glut4 translocation. These results indicated that miR‑106b targeted Mfn2 and regulated skeletal muscle insulin sensitivity and glucose tolerance. Therefore, increased miR‑106b expression may be a potential mechanism underlying insulin resistance and type 2 diabetes.

Anti-neutrophil cytoplasm antibody-associated vasculitis (ANCA) is an autoimmune disease with multi organ involvement characterized by vascular wall inflammation and fibrinoid necrosis, including microscopic polyangitis (MPA), granuloma polyangitis (GPA), and eosinophilic granuloma polyangitis (EGPA). Because its clinical manifestations are complicated and non-speciifc, it is dififcult to make early diagnose. In recent years, some new progress has been made in diagnosis and treatment of this disease. The article will review the related information.

Objective Alport syndrome is one of the diseases that may lead to the end-stage renal disease ( ESRD) in chil-dren, and the methods for its diagnosis and treatment remain quite limited.This study aimed to investigate the clinical and genetic di-agnosis of a Chinese family with hematuria companied by genetic nephritis. Methods We analyzed the renal pathology of 7 patients in a family, performed immunofluorescence staining of type-Ⅳcollagen in the nephridial and skin tissue, conducted gene sequencing i-dentification using the exon sequence method, and examined the blood and urine samples from the patients. Results Renal patholo-gy manifested mesenterium hyperplasia in the index patient, with IgM+under the light microscope, no thickening or thinning under the electromicroscope, and no absence of type-Ⅳcollagen on immunofluorescence analysis.Mutation of c.1365_1373del TCCAGGCCC (p.Pro456_Pro458del3) was observed in exon 21 of the COL4A5 gene.Only 1682 amino acids were found in the mutated protein as compared with 1685 in the wild type. Conclusion This is the first case of Alport syndrome induced by gene deletion mutation ever reported in China and abroad.There are many female patients in this family, all with a high risk of reproduction failure.Antepartal gene diagnosis or genetic diagnosis before embryo transfer may contribute to the prevention of the disease.

Objective To explore the clinical effect of Tacrolimus in pediatric refractory nephrotic syndrome.Methods One hundred and ninety-one children with refractory nephrotic syndrome in Nanjing General Hospital of Nanjing Military Region,People's Liberation Army,were enrolled from January 2010 to December 2013,including 101 cases of steroid-dependent nephrotic syndrome,73 cases of steroid-dependent nephrotic syndrome,and 17 cases of frequently relapsing nephrotic syndrome.Tacrolimus was applied to all the patients.The plasma concentrations of Tacrolimus during the treatment were measured and glucocorticoid tapered or some other immunosuppressants discontinued based on clinical judgment.Relevant clinical changes and laboratory test values were observed before treatment and in weeks 4,8 after treatment.Results The overall remission rate was 86.9％ (166/191 cases) after 8 weeks treatment of Tacrolimus.The minimum effective time was 6 days.Serum albumin and cholesterol significantly improved (all P ＜ 0.01),and proteinuria also diminished markedly(t =20.14,P ＜0.01).One hundred and fifteen patients underwent renal biopsy.The treatment with Tacrolimus did well in minimal change nephropathy(MCN) [remission rate was 90.5％ (18/21 cases)],but mesangial proliferative glomerulonephritis(MsPGS) was inferior in its efficacy(87.7％) (57/65 cases).The use of Tacrolimus in focal segmental glomerulosclerosis (FSGS),membranous nephropathy (MN) and membranoproliferative glomerulonephritis(MPGN) also produced remission to some extent.Thirty-two cases were analyzed by way of Tacrolimus metabolic genotype.The remission rate of 3/3 or 1/3 Tacrolimus metabolic genotype was 75.0％ (21/28 cases),but 4 cases with 1/1 tacrolimus metabolic genotype did not remit after 4 weeks treatment.The adverse reactions of tacrolimus were mild,mainly slight digest tract symptoms,transient kidney injury,dysglycemia,headache,dysphoria etc,which did not influence the treatment.Conclusions Tacrolimus has a gold application prospect,and is a powerfully effective immunosuppressant with clinical efficacy and less side effects for refractory nephritic syndrome in children.

Objective To investigate the clinical and genetic diagnosis of a Chinese family with hematuria, which displayed sex-linked hereditary, so that we can find the virulence gene and sites. MethodWe analyzed the clinical manifestation and the renal pathology of the index patient, the typeⅣ collagen in the nephridial tissue and skin by immunofluorescence, and detected theCOL4A5 gene by the next sequence method.ResultsThere were 7 patients in the family, they all showed gross hematuri, two of them had progressed to end-stage renal disease (ERDS), but none of them were involved in eye or ear damage.There was no special lesion of the glomcrulus;the GBM was normal with a normal thickness; by next sequencing we found a mutation of c.1365_1373del TCCAGGCCC (p.Pro456_Pro458del3) in exon 21 ofCOL4A5.Conclusions The mutation, c.1365_1373del TCCAGGCCC inCOL4A5 gene, was a novel deletion ofCOL4A5 up to now. There are many female patients in this family, antepartum gene diagnosis was necessary for them to avoid the disease reoccurring.

Objective To study the clinical, pathological and genetical manifestation of Gitelman syndrome.MethodThe clinical data, renal biopsy pathology, genetic mutations of patients diagnosed with Gitelman syndrome were analyzed.ResultsAll the patients showed hypopotassemia, hypomagnesemia, alkalipoisoning, hyperaldosteronemia,hyperreninemia.SLC12A3 complicated heterozygotic mutation was observed.Conclusions Gitelman syndrome in children is insidious and the incidence rate ofSLC12A3 complicated heterozygotic mutation is high. Genetic tests can diagnose the disease. Pediatrician must recognize the manifestations to avoid misdiagnosis.

Objective Gitelman Syndrome is a disease caused by the mutation of Na-Cl cotransporter gene(SLC12A3).The article studied the significance of diagnosis and identification by genetic mutation. Methods We collected the clinical data, then we sequenced the SLC12A3 gene by the first sequencing technology and MLPA. Results SLC12A3 complicated heterozygotic mutation was observed.One of them showed c.1964G>A, p.(Arg655His) and exon 8 deletion mutation, the other showed c.2543A>T, p.(Asp848Val) and c.976delG, p.(Val326fs) mutation of SLC12A3 gene in children. Conclusion The final diagnosis depended on gene diagnosis. Pediatrician must recognize the manifestations to advoid misdiagnosis.

Objectives To explore the clinical manifestations, treatment and prognosis of a case of blindness caused by nephrotic syndrome with cerebral venous sinus thrombosis (CVST). Methods The clinical manifestations, diagnosis and treatment of a case of NS with CVST were analyzed. The latest domestic and foreign reseach progresses in treatment for CVST in children were reviewed. Results Epilepsy suddenly appeared with diplopia, binocular vision loss and blindness in anticoagulant therapy for the child with NS. Brain magnetic resonance venography (MRV) suggested CVST. MRV reexam-ined showed that the intracranial thrombosis was completely dissolved after urokinase thrombolysis for one month followed by ineffective heparin anticoagulation. At present, international standards of anticoagulant therapy have been adopted in the treatment for CVST patients. Coagulation function (e.g.APTT) and international standardization ratio were monitored in order to prevent bleeding. Conclusions It is better to perform neural imaging examination early in suspected CVST patients. Anti-coagulation and thrombolytic therapy should be given immediately once the risk of bleeding was excluded and used for 3-6 months.

MicroRNA‑106b (miR‑106b) is reported to correlate closely with skeletal muscle insulin resistance. In the current study the effect of miR‑106b on palmitic acid (PA)‑induced mitochondrial dysfunction and insulin resistance was investigated in C2C12 myotubes via the silencing of miR‑106b. MiR‑106b expression was increased under PA treatment, while miR‑106b loss of function improved insulin sensitivity by upregulating its target mitofusin‑2 (Mfn2) in C2C12 myocytes. Furthermore, miR‑106b loss of function partly improved mitochondrial morphological lesions and increased the levels of mitochondial DNA and intracellular adenosine triphosphate that had been impaired by PA exposure in C2C12 myocytes. MiR‑106b loss of function attenuated the levels of intracellular reactive oxygen species (ROS), and upregulated the expression levels of the estrogen‑related receptor (ERR)‑α/peroxisome proliferative activated receptor γ coactivator (PGC)‑1α/Mfn2 axis under PA exposure. In addition, miR‑106b negatively regulated skeletal muscle mitochondrial function and insulin sensitivity under PA‑induced insulin resistance by targeting Mfn2, which may be associated with reduced ROS and upregulation of the ERR‑α/PGC‑1α/Mfn2 axis.

Objective Mizoribine ( MZR) is a new immunosuppressant , however , little domestic research has been done on MZR for treatment of nephrotic syndrome in children .This study was to investigate curative effect and adverse reaction of MZR in the treatment of children with frequently relapsing nephrotic syndrome , using prospective controlled trials . Methods A total of 59 pa-tients with frequency relapsing nephrotic syndrome were randomly divided into two groups .29 patients of treatment group were treated with MZR +glucocorticoid , while 30 patients of control group were given Tripterygium wilfordii ( TW)+glucocorticoid treatment , and the course of treatment lasted for 12 months.24-hour urine protein, urinary N-acetyl β-glucosidase (NAG), serum albumin, serum cholesterol, serum creatinine, recurrence frequency, and average prednisone dosage were observed . Results At the end of treat-ment, Serum albumin in treatment group was higher than that in control group [(40.95 ±6.12)g/L vs (30.25 ±9.02)g/L], and Se-rum cholesterol ([5.45 ±0.82]mmol/L vs [7.53 ±2.74]mmol/L), urinary protein ([0.89 ±0.52]g/24 h vs [1.63 ±2.02]g/24 h), urinary NAG enzyme ([21.43 ±14.16]U/g· Cr vs [41.67 ±12.35]U/g· Cr) levels were lower compared with control group . There was significant difference between the two groups .In terms of mean recurrence times , no significant difference was found at 6th months of follow-up between the two groups, however, treatment group had lower recurrence rate than control group at 3rd month, 9th month, 12th month of follow-up, which was of significant difference .The average amounts of hormone of treatment group were lower than those of control group ([0.56 ±0.16] mg/kg· d vs [0.72 ± 0.34]mg/kg· d)、([0.64 ±0.35]mg/kg· d vs [0.67 ±0.52]mg/kg· d)、([0.53 ±0.41] mg/kg· d vs [0.83 ±0.37] mg/kg· d)、([0.34 ±0.15] mg/kg· d vs [0.54 ±0.26] mg/kg· d) at 3rd month, 6th month, 9th month, 12th month of follow-up, which was of significant difference . Conclusion Compared to Tripterygium wil-fordii combined with hormone therapy , MZR combined with prednisone therapy in children with recurrent NS frequency can reduce the relapse rate and dosage of corticosteroid to improve the clinical remission rate .

ObjectiveTo measure the level of microRNA(miR)-30a in serum of children with nephrotic syndrome,an alyze its correlation with clinical indicators that are used for diagnosis of nephrotic syndrome,and evaluate its role as a diagnostic marker for frequently relapsing nephrotic syndrome(FRNS).MethodsA cohort of 80 children, diagnozed with nephrotic syndrome hospitalized in Department of Pediatrics of Nanjing General Hospital of Nanjing Military Com mand from October 2011 to October 2012,and 30 healthy children as normal control were enrolled in this study. miR NAs were extracted from the serum after adding synthetic cel-miR-39,as extrinsic parameter was spiked. miR-30a lev el was detected by real-time reverse transcription polymerase chain reactions(PCR)with synthetice cel-miR-39 for normalization and synthetice miR-30a for standard curve,and its correlations with clinical indicators were analyzed. Ac cording to absolute quantification of miRNAs calculated by standard curve,receiveer-oprator characteristic curve(ROC)analysis was applied to evaluate the diagnostic ability of miR-30a for frequently relapsing nephrotic syndrome(FRNS).Results(1)The concentration of serum miRNA-30a level was increased in nephrotic syndrome children compared with healthy controls(P<0.01). miRNA-30a level was significantly higher in the FRNS than non-FRNS(P< 0.01).(2)Serum miR-30a inversely correlated with serum albumin,and positively corelated with proteinuria,urine retinol binding protein,and urine N-acetyl-β-glucosaminidase.(3)The ROC curve based on serum miR-30a level was constructed,the area under the curve was 0.895(95% confidence interval,0.827 to 0.986, P<0.001). WhenYouden′s index reached maximum,the sensitivity and specificity of the serum miR-30a were 90.0% and 77.5% respectively.ConclusionOur findings indicated that se rum miR-30a is significantly increased in the NS chil dren,and it correlates with serum albumin,proteinuria,urine retinol binding protein,and urine N-acetyl-β-glucosaminidase. Serum miR-30a has a better diagnostic efficacy for FRNS.

Objective MicroRNAs,as a kind of small single chain non-coding RNA,widely participate in all kinds of biological process,and play an important role in tumor,diabetes and cardiovascular disease.It has been reported that miR-106b correlated closely with insulin resistance and type 2 diabetes.The expression of miR-106 in the db/db mice′s skeletal muscle was explored and the bioinformatics software and database were applied to predict and analyze target genes of miR-106b in order to lay foundation and to provide theoretical basis for experiments.Methods The level of miR-106b in diabetes mellitus mouse′s skeletal muscle was detected by real-time PCR.The studies of miR-106b were reviewed though Pubmed,and the sequence of miR-106b was got from miRBase database,NCBI,UCSC Browser.Target Sean and starBase were used to predict target genes of miR-106b,and the intersection of the two results as gene set was analyzed by GO annotation and pathway overrepresentation.Results ①MiR-106b was upregulated in the db/db mice′s skeletal muscle.②MiR-106b was highly conserved among species.③The gene set maily existed in regulation of metabolic process and biosynthetic process and apoptosis(GO biology process,P0.001);and protein binding and transcription regulator activity(GO molecular function,P0.01).In KEGG pathway,the gene set mostly existed in Wnt signaling pathway,mTOR signaling pathway,TGF-beta signaling pathway,Insulin signaling pathway(signal trasduction path-way,P0.05);and prostate cancer,chro nicmyeloid leukemia,melanoma,ete(human diseases pathway,P0.05).Conclusion MiR-106b was upregulated in the db/db mice′s skeletal muscle.It was responsible for tumorigenesis and cell cycle modulation.It might be involved in the regulation of metabolism process,and play a crucial role in insulin resistance and type 2 diabete.

Objective To explore the relationship between renal pathology and glomerular podocyte injury in childhood Henoch-Sch(o)nlein purpura nephritis (HSPN).Methods Renal pathological types of 72 children suffering from HSPN were reviewed during the period of Jan.2008 to Jan.2011 from Nanjing General Hospital of Nanjing Command.In those cases,grade in pathology and immunofluorescence types were acquired.Podocyte injury was classified by electron microscope.The relationship between podocyte injury and grade in pathology was analyzed.Results Pathological findings were classified,grade Ⅱ in 34 cases(47.2％) and grade m in 38 cases(52.8％).Glomerular podocyte injury was classified by electron microscope as food processes of podocyte fused extensively in 21 cases;food processes of podocyte fused segmental in 35 cases,food processes of podocyte without fusion in 11 cases.There was without renal glamorous in nephridial tissue by electron microscope in 5 cases.Cases with foot process of podocyte fused extensively were more grade Ⅲ1 than those cases with foot process fused segmental and without fusion.According to renal immunofluorescence pathology,IgA + IgM + IgG type was mostly in cases with foot process of podocyte fused extensively,IgA +IgG type was mostly in cases with food processes of podocyte fused segmental and IgA type was mostly in cases with food processes of podocyte without fusion.Conclusions In childhood HSPN,renal pathology changed not only expressing on mesangial cell hyperplasia but also podocyte injury.The more seriously on the degree of podocyte injury,more obviously in pathologic change.

MicroRNA-106b (miR-106b) is reported to correlate closely with skeletal muscle insulin resistance and type 2 diabetes. The aim of this study was to identify an mRNA targeted by miR-106b which regulates skeletal muscle insulin sensitivity. MiR-106b was found to target the 3' untranslated region (3' UTR) of mitofusin-2 (Mfn2) through miR-106b binding sites and to downregulate Mfn2 protein abundance at the post-transcriptional level by luciferase activity assay combined with mutational analysis and immunoblotting. Overexpression of miR-106b resulted in mitochondrial dysfunction and insulin resistance in C2C12 myotubes. MiR-106b was increased in insulin-resistant cultured C2C12 myotubes induced by TNF-α, and accompanied by increasing Mfn2 level, miR-106b loss of function improved mitochondrial function and insulin sensitivity impaired by TNF-α in C2C12 myotubes. In addition, both overexpression and downregulation of miR-106b upregulated peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α and estrogen-related receptor (ERR)-α expression. MiR-106b targeted Mfn2 and regulated skeletal muscle mitochondrial function and insulin sensitivity. Therefor, Inhibition of miR-106b may be a potential new strategy for treating insulin resistance and type 2 diabetes.