INTRODUCTION Some patients with idiopathic membranous nephropathy (iMN) do not respond to cyclophosphamide plus steroids treatment, and we define them as non-responsive iMN. The combined regimen of rituximab (RTX) and tacrolimus (TAC) has an excellent effect on this kind of non-responsive iMN patients; however, the optimal dose is still unclear. In this retrospective study, we comapred the efficacy and safety of ultra-low dose RTX plus low-dose TAC therapy versus standard TAC monotherapy in patients with non-responsive iMN. MATERIALS AND METHODS Sixty-seven Chinese non-responsive iMN patients were included. There were 41 patients received standard tacrolimus monotherapy (TAC) and 26 patients received ultra-low dose rituximab plus low dose tacrolimus (RTX/TAC) combination therapy. All patients were observed for 12 months. RESULTS 18 patients (18/26, 69.2%) in the RTX/TAC group and 17 patients (17/41, 41.5%) in the TAC group achieved clinical response after 12-month follow-up (P=0.044). The median time for achieving response in the two groups was 3.0 months. As indicated by Kaplan-Meier curve, the response rate in the RTX/TAC group was higher than that in the TAC group (P=0.015). 24-hour proteinuria, serum albumin, estimated glomerular filtration rate (eGFR) and serum creatinine in the two groups were comparable at baseline; howerver, after 12-month follow up, they were significantly improved in the RTX/TAC group compared with the TAC group (P<0.05). B-cell depletion was achieved in all patients in the RTX/TAC group during the whole follow-up period. Pneumonia, urinary tract infections and glucose intolerance were the major side effects observed in this study. All adverse events were mild, and the cumulative incidence was lower in the RTX/TAC group compared with that in the TAC group (9 (34.6%) vs 27 (65.9%), P=0.023). CONCLUSION The combination of ultra-low dose rituximab and low dose tacrolimus is more effective in inducing proteinuria response, improving eGFR and serum albumin in non-responsive iMN patients than standard tacrolimus monotherapy. The combined treatment also has higher safty.

The purpose of this study is to investigate the changing spectrum and clinicopathologic correlation of biopsy-proven renal diseases in central China. We retrospectively analyzed data of 4931 patients who underwent renal biopsy in ten hospitals between September 1994 and December 2014. Among them, 81.55% were primary glomerular diseases (GD), and 13.02% were secondary GD. IgA nephropathy (IgAN) was the most common primary GD (43.45%), followed by focal glomerulonephritis (16.79%), mesangial proliferative glomerulonephritis (MsPGN, 14.35%), and membranous nephropathy (MN, 13.28%). IgAN was leading primary GD in patients under 60 years old, while MN was the leading one over 60 years old. The most frequent secondary GD was lupus nephritis (LN) (47.35%). The prevalence of IgAN, MN and minimal change disease was found to increase significantly (p < 0.001, p < 0.001, and p < 0.01, respectively), while that of MsPGN, membranoproliferative glomerulonephritis and LN decreased significantly (p < 0.001, p < 0.001, and p < 0.05, respectively). The main indication for renal biopsy was proteinuria and hematuria (49.03%), followed by nephrotic syndrome (NS, 20.36%). IgAN was the most common cause in patients with proteinuria and hematuria, chronic-progressive kidney injury, hematuria and acute kidney injury; and MN was the leading cause of NS. Primary GD remained the predominant renal disease in central China. IgAN and LN were the most prevalent histopathologic lesions of primary and secondary GD, respectively. The spectrum of biopsy-proven renal disease had a great change in the past two decades. Proteinuria and hematuria was the main indication for renal biopsy.

A 5/6 nephrectomized (Nx) rat model was employed to address the impact of telmisartan on CKD related renal injury and the underlying molecular mechanisms. It was noted that telmisartan provided protection for rats against 5/6 Nx induced lethality. Telmisartan treated 5/6 Nx rats manifested improved renal function as characterized by the higher GFR but lower urinary albumin, BUN and Scr as compared with that of control rats. Telmisartan treatment also significantly decreased systolic blood pressure and alleviated glomerulosclerosis and interstitial fibrosis. Mechanistic studies revealed that telmisartan possesses the capability to increase NO generation in the kidney. Further studies demonstrated that telmisartan promotes PPARγ expression, by which it specifically enhances nNOS expression in the kidneys after 5/6 Nx insult. Particularly, blockade of PPARγ signaling by GW9662 abolished the protective effect conferred by telmisartan, indicating that telmisartan induction of renal nNOS expression along with NO generation is dependent on PPARγ signaling. Together, our data support that telmisartan could be a promising drug for treatment of chronic kidney diseases in diverse clinical settings.

Curcumin, as a main pharmacological component in the traditional Chinese medicine—turmeric, has shown anti-inflammatory, anti-oxidation, anti-tumor and anti-fibrotic effects. This study aimed to investigate the possible underlying signaling pathway which was involved in the inhibition of LDL-induced proliferation of mesangial cells and matrix by curcumin. Rat mesangial cells in vitro were incubated with low-density lipoprotein (LDL) and different concentrations of curcumin (0, 6.25, 12.5, 25.0 μmol/L) or p38 MAPK inhibitor, SB203580 (10 μmol/L). Under LDL incubation, mesangial cells proliferated, the expression of MMP-2 mRNA and protein was decreased, the expression of COX-2 mRNA and protein was increased, reactive oxygen species (ROS) generation was increased and p38 MAPK was activated significantly (P<0.05). When LDL-induced cells were treated with curcumin in the concentration of 12.5 or 25.0 μmol/L, LDL-induced proliferation of mesangial cells was suppressed, the expression of MMP-2 mRNA and protein increased, the expression of COX-2 mRNA and protein downregulated, the production of ROS inhibited and p38 MAPK inactivated (P<0.05). In conclusion, curcumin can inhibit the LDL-induced proliferation of mesangial cells and up-regulate the expression of MMP-2, which may be related with the inhibitory effect of curcumin on COX-2 expression, ROS production and p38 MAPK.

OBJECTIVES:This study aims to analyze the relationship between nutcracker syndrome (NCS) and nutcracker phenomenon (NCP) in glomerular nephritis (GN) of patients with symptom of isolated hematuria. Our observations reveal that patients with combined GN and NCP/NCS have dysmorphic urine red blood cells or mixed-morphological urine red blood cells while patients with NCS only (without GN) contain isomorphic urine red blood cells.PATIENTS AND METHODS:Clinical and pathological data of 32 patients with NCP and complicating GN were analyzed. A different group of 17 patients with NCS served as the control. All patients underwent color Doppler ultrasonography. Routine urine examination, red blood cell counts, and phase observations of urinary sediments were performed both before and after exercise. twenty four hour urinary protein and albumin quantities were determined. Twenty-nine patients underwent renal needle biopsy.RESULTS:All 32 patients were diagnosed with NCP. Results of urinary sediment examination of patients were either normal or showed isomorphic hematuria before exercise. Most patients exhibited mixed-morphological or dysmorphic hematuria at different degrees after exercise. Renal pathological findings in 29 patients included multiple types and showed no relevance to urinary examination results. All patients diagnosed with GN complicated by NCP were identified through clinical and laboratory examinations and renal biopsy.CONCLUSIONS:NCP may coexist with a glomerular disease. NCS patients with urine red blood cells of mixed morphology or showing dysmorphism after exercise should be noted, with or without the coexistence of GN. Renal needle biopsy must be performed when necessary to avoid adverse effects on the patient's condition.

Background and objectives Previous studies have identified inflammatory features that enable the prediction of renal outcome of IgA nephropathy (IgAN); however, validation of these findings is still needed. This prospective study was performed to determine the characteristics of renal interstitial infiltration and tertiary lymphoid organ (TLO) neogenesis in a cohort of Chinese patients with IgAN. Design, setting, participants, & measurements Adult patients with IgAN were recruited into this study from June 2009 to June 2010. Inflammatory cells in renal biopsy tissues were detected by immunohistochemistry and immunofluorescence. Correlations between the density of interstitial inflammatory cells, grades of TLOs, and clinicopathologic features were evaluated. Of 152 eligible patients, 72 (47%) were successfully followed-up by telephone at 30 months after renal biopsy. Twelve patients were classified as the severe group and 60 patients were classified as the stable group, according to the progression of serum creatinine levels during the follow-up period. A comparison of the severity of interstitial infiltration and the frequency of TLO neogenesis between the two groups was performed. Results The accumulation of interstitial inflammatory cells was correlated with decreased renal function, heavy proteinuria, and severe glomerular, interstitial, and arterial lesions in patients with IgAN. TLOs, identified as nodular inflammatory infiltrates containing organized DC-SIGN(+), CD4(+), CD8(+), and CD20(+) cells, were observed in 37.5% of patients. Patients with high-grade TLOs exhibited a high percentage of mesangial hypercellularity and crescents as well as severe interstitial and arterial lesions. Patients in the severe group exhibited more severe interstitial infiltration and a higher percentage of TLO neogenesis (83.3% versus 33.3%; P=0.001) compared with patients in the stable group. Conclusions As contributors to an active local inflammatory response, the severity of interstitial infiltration and the frequency of TLO neogenesis are correlated with glomerular, interstitial, and arterial lesions as well as IgAN progression.

The present study investigated the protective role of growth hormone (GH) against hyperhomocysteinemia (hHcys)-induced activations of reactive oxygen species/hypoxia-inducible factor (HIF)-1α, epithelial–mesenchymal transition (EMT), and consequent glomerular injury. A hHcys model was induced by folate free diet in mice. The urine protein excretion significantly increased while plasma GH levels dramatically decreased in hHcys. Real-time reverse transcription polymerase chain reaction showed that GH receptor (GHR) level increased in the cortex of hHcys mice, which mainly occurred in podocytes as shown by confocal microscopy. Recombinant mouse growth hormone (rmGH) treatment (0.02 mg/kg, once a day for 6 weeks) significantly restored the plasma GH, inhibited GHR upregulation and attenuated proteinuria. Correspondingly, rmGH treatment also blocked hHcys-induced decrease in the expression of podocin, a podocyte slit diaphragm molecule, and inhibited the increases in the expression of desmin, a podocyte injury marker. It was also demonstrated that in hHcys the expression of epithelial markers, p-cadherin and ZO-1, decreased, while the expression of mesenchymal markers, antifibroblast-specific protein 1 (FSP-1) and α-SMA, increased in podocytes, which together suggest the activation of EMT in podocytes. Nicotinamide adenine dinucleotide phosphate oxidase (Nox)-dependent superoxide anion (O2 .−) and hypoxia-inducible factor-1α (HIF-1α) level in the hHcys mice cortex was markedly enhanced. These hHcys-induced EMT enhancement and Nox-dependent O2 .−/HIF-1α activation were significantly attenuated by rmGH treatment. HIF-1α level increased in Hcys-treated cultured podocytes, which were blocked by rmGH treatment. Meanwhile, homocysteine (Hcys)-induced EMT in cultured podocytes was significantly reversed by HIF-1α siRNA. All these results support the view that GH ameliorates hHcys-induced glomerular injury by reducing Nox-dependent O2 .−/HIF-1α signal pathway and EMT.

Objective To investigate the correlation between inflammation status and uremic pruritus in maintenance hemodialysis (MHD) patients. Methods Thirty-nine MHD patients and twelve healthy controls were recruited to the study. We inquired of MHD patients about the severity of their pruritus by visual analog scale (VAS). Blood samples were taken before and after hemodialysis during the inquiry day. Inflammatory factors including interleukin (IL) -2, IL-6, IL-10, tumor necrosis factor (TNF) were measured by Cytometric Bead Array. Results Preand after-dialysis levels of IL-2, IL-6, IL-10 and TNF and pre-dialysis level of hsCRP were significantly higher in MHD patients than in healthy controls, and these levels had no significant correlation with age or sex. Spearman rank correlation analysis and linear regression analysis showed that pre-dialysis IL-2 level was positively correlated with VAS score (β=0.586, t=4.399, F=19.354, P< 0.01). Based on VAS score, MHD patients could be divided into 3 groups, no pruritus group (VAS=0.38%), mild to moderate pruritus group [VAS=1～5(41%)], and severe pruritus group [(VAS> 5(21%)]. Preand after-dialysis IL-2 levels were significantly higher in severe pruritus group than in no pruritus group. Conclusion A higher prevalence of uremic pruritus was found in MHD patients. Inflammation plays an important role in the pathogenesis of uremic pruritus. IL-2 closely relates to uremic pruritus in MHD patients.

Cdc42-interacting protein-4 (CIP4) is an F-BAR (Fer/CIP4 and Bin, amphiphysin, Rvs) family member that regulates membrane deformation and endocytosis, playing a key role in extracellular matrix (ECM) deposition and invasion of cancer cells. These processes are analogous to those observed during the initial epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells. The role of CIP4 in renal tubular EMT and renal tubulointerstitial fibrosis was investigated over the course of the current study, demonstrating that the expression of CIP4 increased in the tubular epithelia of 5/6-nephrectomized rats and TGF-β1 treated HK-2 cells. Endogenous CIP4 evidenced punctate localization throughout the cytosol, with elevated levels observed in the perinuclear region of HK-2 cells. Subsequent to TGF-β1 treatment, CIP4 expression increased, forming clusters at the cell periphery that gradually redistributed into the cytoplasm. Simultaneously, EMT induction in cells was confirmed by the prevalence of morphological changes, loss of E-cadherin, increase in α-SMA expression, and secretion of fibronectin. Overexpression of CIP4 promoted characteristics similar to those commonly observed in EMT, and small interfering RNA (siRNA) molecules capable of CIP4 knockdown were used to demonstrate reversed EMT. Cumulatively, results of the current study suggest that CIP4 promotes TGF-β1-induced EMT in tubular epithelial cells. Through this mechanism, CIP4 is capable of inducing ECM deposition and exacerbating progressive fibrosis in chronic renal failure.

Objective To observe the effect of CIP4(Cdc42 interacting protein 4)on human renal tubular epithelial to mesenchymal transition(EMT)induced by transforming growth factor β1(TGF-β1)and to study the associated mechanism. Methods Human proximal tubular epithelial cells (HK-2 cell line) were cultured with TGF-β1 (10μg/L) for 72 hours. The protein expressions of E-cadherin and α-SMA were measured by Western blotting. One set of siRNA oligos specific for CIP4 and CIP4 construction of the entire coding sequence were designed based on the full CIP4 sequence in GenBank. Then HK-2 cells were transfected with CIP4-siRNA or pcDNA3.1-hCIP4 via lipofactamine 2000. The protein expressions of CIP4, E-cadherin and α-SMA were evaluated respectively in control cells, TGF-β1 treated cells, siRNA transfected cells, pcDNA3.1-hCIP4-transfected cells by Western blotting. The distribution of E-cadherin and α-SMA was observed by confocal microscope. After TGF-β1-treated HK-2 cells were interferenced with specific inhibitor of PI3K-Akt (wortmannin) 1μmol/L for 48 hours, Western blotting was used to detect the CIP4 protein in control cells and interferenced cells. Results With TGF-β1 stimulation, the expression of E-cadherin protein was decreased markedly (P＜0.05), and in contract, the expression of α-SMA were increased notably (P＜0.05), which revealed that TGF-β1 could induce EMT. After transfected with CIP4-siRNA, the protein expression of E-cadherin was increased (P＜0.05), and the protein expression of α-SMA was decreased (P＜0.05). The EMT induced by TGF-β1 was effectively reversed. After transfected with pcDNA3.1-hCIP4, the expression of E-cadherin protein was down-regnlated (P＜0.05), and the expression of α-SMA protein was up-regulated compared with control group (P＜0.05), leading to EMT. After HK-2 cells were interferenced with wortmannin for 48 hours, the expression of CIP4 was decreased (P＜0.05). Conclusion TGF-β1 upregulates the expression of CIP4 via PI3K-Akt pathway, and CIP4 may participate in EMT induced by TGF-β1.

Background. The p38 mitogen-activated protein kinase (p38 MAPK) is an important intracellular signal transduction pathway involved in TGF-β1-induced epithelial–mesenchymal transition (EMT). Sema4C, a member of the semaphorin family, was found to be essential for the activation of p38 MAPK. However, the role of Sema4C in promoting TGF-β1-induced EMT is unclear. Methods. Renal fibrosis was induced by 5/6 subtotal nephrectomy rat model. In vitro, Sema4C was induced in human proximal tubular epithelial cells (HKC) by treatment with TGF-β1, or was inhibited by siRNA or was over-expressed by Sema4C transfection. The selective p38 MAPK inhibitor, SB203580, was administered to inhibit the p38 pathway. The expression of Sema4C, the markers of EMT, p38 phosphorylation and fibronectin secretion were measured by western blotting, immunohistochemistry, immunocytochemistry or enzyme-linked immunosorbent assay. Results. The expression of Sema4C increased in HKC cells that were treated with TGF-β1. Knockdown of Sema4C potently inhibited phosphorylation of p38 MAPK and reversed TGF-β1-induced EMT. Over-expression of Sema4C via Sema4C transfection elicited p38 MAPK phosphorylation and promoted EMT. The effects of Sema4C during EMT were blocked by a p38-specific inhibitor. In vivo, the expression of Sema4C increased in the tubular epithelia of 5/6-nephrectomized rats and human fibrotic renal tissue, and similar localization of phosphorylated p38 and Sema4C was demonstrated by immunohistochemistry on serial sections. Conclusions. Our findings suggest that Sema4C plays an important role in TGF-β1-induced EMT through activation of p38 MAPK in proximal tubular epithelial cells.

Epithelial-to-Mesenchymal Transition (EMT) is an important pathogenic mechanism mediating glomerular injury or sclerosis in a variety of renal and systemic diseases such as hyperhomocysteinemia (hHcys). The present study was designed to test whether Hcys-induced EMT in podocytes is reversed by growth hormone (GH), a hormone regulating cell differentiation and growth and to explore the cellular and molecular mechanism mediating its action. It was found that Hcys induced significant EMT in podocytes, as shown by marked decreases in slit diaphragm-associated protein P-cadherin and zonula occludens-1 as epithelial markers and by dramatic increases in the expression of mesenchymal markers, fibroblast specific protein-1 and α-smooth muscle actin, which were detected by all examinations via immunocytochemistry, real time RT-PCR and Western blot analysis. When podocytes were treated with GH at 25 ng/mL, however, Hcys failed to induce podocyte EMT. Using electromagnetic spin resonance spectrometry, Hcys-induced superoxide (O2.-) production via NADPH oxidase was found to be significantly inhibited by GH (66%). Functionally, GH was shown to substantially inhibit Hcys-induced increases in the permeability of podocyte monolayers and to block the decrease in podocin expression in these cells. In addition, NADPH oxidase subunit, gp91phox and GH receptors aggregated in membrane raft clusters, which produced O2.- in response to Hcys and could be blocked by GH, membrane raft disruptors filipin and MCD or NADPH oxidase inhibitor, apocynin. It is concluded that Hcys-induced podocyte EMT is associated with transmembrane membrane raft-redox signaling and that GH reverses this Hcys-induced EMT protecting podocytes from functional disturbance.

Objective To observe the expression and localization of CIP4 (Cdc42 interacting protein-4) in the renal fibrosis and the effect of CIP4 on the expression of E-cadherin,vimentin and β-catenin tyrosine phosphorylation. Methods In vitro, the human tubular epithelial cells (HK-2 cell line) were cultured with 10 μg / L TGF-β1 for 72 h. The protein expressions of CIP4, E-cadherin, vimentin and β-catenin tyrosine phosphorylation were measured by Western blotting; the expression of CIP4 mRNA was detected by RT-PCR. The intracellular distribution of CIP4 was observe by confocal microscope. In vivo, Masson staining was used to evaluate the level of renal fibrosis; the expression and distribution of CIP4 in renal tissue were detected by immunohistochemistry. HK-2 cells were transfected with pcDNA3. 1-CIP via lipofectamine 2000. The expressions of E-cadherin, vimentin and β-catenin tyrosine phosphorylation level in the transfected cells were detected by Western blotting. Results The expressions of CIP4 mRNA and protein were up-regulated in renal tubular EMT cells. Most of CIP4 protein localized in cell membrane, and some was in cytoplasm. After stimulation by TGF-β1, the expression of CIP4 protein both in cytoplasm and nucleus was greatly increased (P ＜0.05),especially in cytoplasm. In vivo, CIP4 was expressed in renal tubular epithelia, but little expressed in glomeruli. In renal from 5/6 nephrectomized rats, CIP4 expression was significantly increased. In the CIP4 transfectants, the expression of CIP4, vimentin and β-catenin tyrosine phosphorylation level were up-regulated (P ＜0.05), but E-cadherin expression was suppressed (P ＜0.05).Conclusion The overexpression of CIP4 is likely to take part in the epithelial-to-mesenchymal transition process, thereby promoting the renal fibrosis.

Objective To determine the levels of serum homocysteine(Hcy),arginine vasopressin(AVP) and endothelin in patients with maintenance hemodialysis(MHD) and how hemoperfusion affects these three biomarkers.Methods Sixty patients with MHD were randomized into two groups:hemoperfusion/hemodialysis combination group(HP+HD group,n=30) and simple hemodialysis group(HD group,n=30).The both groups underwent venous blood sampling before and after treatment.Twenty-five healthy subjects were selected as normal controls(control group).And the levels of Hcy,AVP and endothelin in serum were measured.Comparison among groups was performed using oneway ANOVA.Results The levels of Hcy,AVP and endothelin were(13.4±1.0)μmol/L,(354±49)ng/L and(142±16) ng/L in the serum in HP+HD group,and were(14.0±1.3)μmol/L,(348±43)ng/L and(142±14)ng/L in the serum in HD group.Both levels were significantly higher than those of control group [(7.2±0.9)μmol/L,(256±41)ng/L,(115± 10)ng/L,respectively](P<0.05).There was no significance of Hcy,AVP and endothelin in HP+HD group and HD group before treatment.There was a significant decrease in the level of Hcy,AVP and endothelin[(8.7±0.9)μmol/L,(265±39)ng/L,(119±12)ng/L,respectively] in HP+HD group after treatment(P<0.05),whereas there was no significance among each parameter in HD group before and after treatment.Conclusion Compared with the control group,the levels of serum Hcy,AVP and endothelin were significantly increased in the patients with MHD.The hemoperfusion/hemodialysis combination may be an effective approach to reduce the level of Hcy,AVP and endothelin in patients with MHD.

目的 了解乌鲁木齐市天山区35岁以上成人慢性肾脏病(CKD)的流行病学特征及危险因素.方法 以分层多级整群抽样法,对乌鲁木齐市天山区4个社区的2131名35岁以上常住居民进行问卷调查、体格检查和实验室检查.结果 在2131名资料完整的居民中,经年龄、性另校正后,白蛋白尿的患病率为2.63%(95%CI:1.78%～3.48%);血尿的患病率为7.43%(95%CI:6.11%～8.75%);肾功能下降的患病率为1.72%(95%CI:1.08%～2.35%).该人群CKD的患病率为9.99%(95%CI:8.47%～11.55%),知晓率为2.44%.多因素Logistic回归显示,白蛋白尿、血尿、年龄增加10岁、高尿酸血症与肾功能下降独立相关;血尿、肾功能下降与白蛋白尿独立相关;白蛋白尿、肾功能下降、女性与血尿独立相关.结论 作为中国西部大城市,乌鲁木齐市35岁以上成人CKD的患病率为9.99%,知晓率为2.44%;CKD的危险因素与我国大城市及西方发达国家类似.

Evaluating the prevalence of kidney damage according to population-based studies in different communities has been limited in developing countries. We conducted a population-based screening study in Uygur people of Urumqi, aiming to identify the prevalence and associated risk factors of chronic kidney disease (CKD) in Uygur populations. A total of 2576 residents (> 18 years) from four districts of Urumqi were interviewed from June 2007 to January 2009 and tested for haematuria, albuminuria and reduced renal function. Associations between age, gender, smoking, diabetes mellitus, hypertension, hyperuricaemia and kidney damage were examined. There were 2576 subjects enrolled in this study. After age correction, the prevalence of albuminuria, haematuria and reduced estimated glomerular filtration rate (eGFR) was 3.58%, 2.26% and 1.03%, respectively. Approximately 5.65% of the sample population had at least one indicator of kidney damage. Age, diabetes mellitus, hypercholesteremia, hyperuricaemia and hyperlipidaemia were independently associated with CKD. In the general Uygur adult population from Urumqi, 5.65% had either proteinuria, haematuria or reduced eGFR, indicating the presence of kidney damage, with an awareness of only 1.05%. The high prevalence and low awareness of CKD in this population suggest an urgent need for CKD prevention programs in Uygur people.

Objective:To study the role and mechanism of active vitamin D in mesangial proliferative golmerulonephritis.Method: Seventy-two male SD rat were devided into three average groups randomly:saline control rats,nephritis rats and active vitamin D_3 rats. Executed 6 rats of each group randomly and collected the renal tissue samples at day 1,3,7 and 14,respectively.①The pathologic abnormalities of MsPGN was observed by HE dyeing;②The expression of PCNA and Bcl-2 were detected by immune-histochemistry.③The expression of PCNA protein was detected by western blot in each group.Result:Compared to control group,the expression of PCNA and Bcl-2 in glomerulo- nephritis group was significantly increased(P<0.01),respectively;compared to nephritis group,the expression of PCNA and Bcl-2 in active vitamin D_3 group was significantly reduced(P<0.01).The expression of PCNA and Bcl-2 between pathologic classify was positive correlation(P<0.01) Respectively.The expression of PCNA,PCNAmRNA and Bcl-2 were positive correlation with each other(P<0.01).Conclusion:Active vitamin D_3 can suppress the proliferation of mesangial cells by inhibiting the expression of PCNA and PCNAmRNA,promote apoptosis by reducing the expression of Bcl-2,attenuates progression of the mesangial proliferative glomerulonephrisis.

目的 了解乌鲁木齐市天山区成人血糖异常分布情况,探讨血糖异常分布与慢性肾脏病(chronic kidney disease,CKD)的关系.方法 从2007年"乌鲁木齐市天山区35岁以上成人慢性肾脏病流行病学调查及相关因素分析"资料中选取2 131名乌鲁木齐市天山区居民作为研究对象,根据相关疾病诊断标准对资料进行分析.结果 在2131名资料完整的居民中,空腹血糖异常及糖尿病的患病率按年龄、性别标准化后分别为13.01%和14.63%,其患病率随年龄增长而升高(P=0.027,P=0.006).糖尿病组血尿、白蛋白尿、估算肾小球滤过率(estimated glomerular filtration rate,eGFR)下降以及CKD患病率显著高于血糖正常组和异常组(P<0.05).趋势性检验分析显示,糖尿病患者CKD患病率随着其病程的延长而升高(P<0.01).结论 在乌鲁木齐市天山区35岁以上成人中,血糖异常和糖尿病的患病率较高,且随着糖尿病病程的延长,CKD的患病率也逐渐升高.

Objective: To explore the effects of Curcumin on renal lesions and its influence to expression of heme oxygenase-1(HO-1) in the kidneys of diabetic rats.Methods: Diabetic rats were randomly divided into control(n=10) and experimental group(n=10)(treated with Curcumin),blood biochemical parameters and 24 h urinary albumin excretion were compared.The level of HO-1 mRNA was examined by RT-PCR.The site and level of expression of HO-1 protein were examined by immunohistochemistry staining.Results: Compared with that in normal rats respectively,Ccr and urinary albumin excretion increased markedly in diabetic rats,but the expression of HO-1 mRNA and protein were not increased.HO-1 protein was mainly expressed in renal tubular cells,collecting ducts in medulla and Henle's loop.Ccr and urinary albumin excretion were decreased markedly and the expression of mRNA and protein of HO-1 were induced by the treatment of Curcumin.Conclusion: Curcumin has therapeutic effects on diabetic nephropathy.The mechanism is,at least in part,through induction of HO-1.

Objective To investigate the effects of recombinant human growth hormone(rhGH)on serum total cholesterol(TC),triglycerides(TG),high density lipoprotein-cholesterol(HDL),low density lipoprotein-cholesterol(LDL),insulin-like growth factor-1(IGF-1)and insulin-like growth factor binding protein 3(IGFBP-3)in nephrotic patients. Methods One hundred nephrotic patients were randomly divided into conventional group(n=50)and rhGH-treated group(n=50).Ten normal subjects were chosen as normal group.IGF-1 and IGFBP-3 concentrations in serum were measured with RIA.TC,TG,HDL and LDL levels in serum were measured with automatic biochemistry appliance. Results Serum levels of IGF-1 and IGFBP-3 in conventional group and rhGH-treated group decreased compared with normal group.Serum TC,TG,HDL and LDL in two treated groups were higher than those in normal group before and after the treatment.Serum levels of IGF-1 and IGFBP-3 in rhGH-treated group significantly increased after the treatment for 2 weeks,while serum TC and LDL levels decreased significantly.There was no statistical difference between two groups in serum TG and HDL levels before and after the treatment. Conclusion The dyslipidemia in nephrotic patients might be caused by the decrease of IGF-1/IGFBP-3.rhGH could improve the serum lipid by upregulating the expression of IGF-1/IGFBP-3 in serum.