The renin-angiotensin system plays an important role in the progression of chronic renal diesases. At present, the main approach for treating the chronic progressive renal disease is to block the role of renin-angiotensin system. Recently, angiotensin receptor blockers have being realized in width with its few side effect and good safety. A number of experimental and clinical resultsin recent 10 years have indicated that ARB can prevent or even reverse the progression of chronic renal diseases in many ways effectively and provided great evidences for current therapy of CPRD.

Objective To study the clinical and pathological features of idiopathic membranous nephropathy(IMN),which has not been able to diagnose only by light microscopy.Methods Nine cases which has not been diagnosed as IMN only by light microscopy from January 1998 to March 2005 were selected.We analyzed their clinical manifestation and pathological findings.Results One case was 6-year old child,who had nephrotic syndrome(NS).The other 8 cases were 45~70 year old adult,their clinical diagnoses being chronic glomerulonephritis or asymptomatic hematuria and /or proteinuria.Light microscopic diagnoses were minor glomerular abnormalities and focal proliferative glomerulonephritis.Immunofluorescence demonstrated scattered granular deposits of IgG along the capillary walls.Under the electron microscopy,small high density deposits were observed along the basement membrane,mainly stage Ⅰand Ⅱ.2 cases were complicated with thin membrane disease.Conclusion Chronic glomerulonephritis or asymptomatic hematuria and /or proteinuria often mixes slightly with IMN which is difficult to be diagnosed clearly depending on simple light microscopy.Therefore,it is very important to diagnosis to perform immunofluorescence and electron microscopy further.

Antibody arrays, as a specific subset of protein arrays,are now used in a wide variety of applications. Although having evolved into indispensable tools for proteomic studies, they seems to be still at the middle point on the way to the final destination to have the antibody arrays with high sensitivity, minimized size and wide dynamic detection range to meet the needs for the detection of different samples. This article reviewed the recent development regarding how to improve the detection sensitivity of the antibody arrays.

Objective To evaluate the therapeutic effect of 89 Sr internal radiotherapy on multiple-bone metastasis of cancer. Methods Forty-nine cancer patients with multiple-bone metastasis received 89 Sr internal radiotherapy. The pain control effect, life quality improvement, change in levels of blood calcium and serum alkaline phosphatase (ALP), and side effects were analyzed respectively. Results The total effective rate of pain control was 77.6 %. The life quality was improved obviously. The levels of blood calcium and ALP were decreased. No obvious side effects were found during the treatment. Conclusion 89 Sr internal radiotherapy had a good therapeutic effect on multiple-bone metastasis of cancer.

Objective To investigate the effects of nephroblastoma over-expressed protein (CCN3) on the formation of extracellular matrix (ECM) induced by transforming growth factor-β1 (TGF-β1) in human mesangial cells (HMCs) and its underlying signal transduction mechanism related with microRNA-29(miRNA-29).Methods HMCs were pretreated with different doses of exogenous CCN3 (5 μg/L,50 μg/L and 500 μg/L) or transfected with pcDNA3.1(+)-CCN3 before exposed to TGF-β1(2 μg/L),to observe the expression of fibronectin (FN),type I collagen (COL I) and miRNA-29a,b and c.The mimics or inhibitor of the miRNA-29a were transfected into HMCs to analyze whether miRNA-29a affect CCN3.The expressions of FN mRNA,COL I mRNA and miRNA-29 family were detected by real time PCR.The protein expressions of FN and COL I were detected by Western blotting and cell immunofluorescence.Results (1) Compared with the normal control group,the expressions of FN and COL I were up-regulated in TGF-β1 group,while the expressions of miRNA-29a,b,c were down-regulated in TGF-β1 group (all P ＜ 0.05).(2) Compared with the TGF-β1 group,the expressions of FN and COL I were decreased when pretreated with the different doses of exogenous of CCN3 or transfected with pcDNA3.1(+)-CCN3 (all P ＜ 0.05).Meanwhile,the expression of miRNA-29a was significantly increased when pretreated with 50 μg/L and 500 μg/L CCN3 or transfected with pcDNA3.1(+)-CCN3 (all P ＜ 0.05);whereas miRNA-29b and c had no statistical difference (all P ＞ 0.05).(3) Compared with TGF-β1+CCN3 group,the expressions of FN and COL I were decreased in CCN3+TGF-β1+miRNA-29a mimics group (all P ＜ 0.05),whereas the expressions of FN and COL I in CCN3+TGF-β1+miRNA-29a inhibitors group were increased (all P ＜ 0.05).Conclusions CCN3 reduces the TGF-β1-induced production of ECM by the up-regulation of miRNA-29a.

Objective To observe NLRP3 inflammasome expression and inflammatory cells infiltration in the BSA-overloaded rats kidney,and to investigate the potential mechanism of renal injury induced by proteinuria.Methods After unilateral right nephrectomy,eighteen healthy male Wistar rats were randomly divided into two groups:protein overload nephropathy model group (n=10),treated with intraperitoneal injections of bovine serum albumin (BSA); control group (n=8),treated with intraperitoneal injections of 0.9％ saline for 9 weeks.Body weigh were measured every week and 24 h urine were collected in 0,2,5,7,9 week.The plasma levels of blood total protein (TP),albumin (Alb),serum creatinine (Scr) and blood urea nitrogen (BUN) were determined by automatic analyzers.Renal pathological changes were evaluated by PAS and Masson stains.Immunohistochemical staining was used to detect the expression of NLRP3,caspase-1,IL-1β,and IL-18,as well as the types of inflammatory cells.The NLRP3,caspase-1,IL-1β,and IL-18 protein and mRNA levels were also analyzed by Western blot and real-time PCR in two groups.Results It was found that there was a significant increase of proteinuria and BUN in model group compare to that in control group (all P ＜ 0.05).However,there were no significant changes in body weight,TP,Alb and Scr between the two groups.Morphological study demonstrated that renal tubular epithelial cell injury,proteinaceous casts in tubular lumen,accompanying with the dominant macrophages and lymphocytes infiltration in interstitium in model group.The immunohistochemistry showed that there were more T (CD3+),B cells (CD20+) and macrophages (CD68+) in renal interstitium in model group than that in control group (P ＜ 0.05).Tubulointerstitial injury score was higher than that of the control group (P＜0.05).Immunohistochemistry,Western blot and real-time PCR all showed that the expression of NLRP3,caspase-1,IL-18 and IL-1 β were significantly increased compared to those in control group (P ＜ 0.05).Furthermore,there were significant correlations between proteinuria and IL-lβ/IL-18 expression (P ＜ 0.05).Conclusion NLRP3 inflammasome activation is involved in tubulointerstitial inflammation caused by proteinuria.

AIM: To investigate the effect of L-arginine(L-arg) on the production of collagens of human mesangial cells. METHODS: Radioimmunoassay, hydroxyproline colorimetric assay and reverse transcription polymerase chain reaction (RT-PCR) were used to determine procollagen Ⅲ, total collagen level in the supernatant and expression of collagen Ⅳ mRNA in human mesangial cells. RESULTS: L-arg significantly inhibited the production of procollagenⅢ, total collagen in the supernatants ( P

The effect of rosiglitazone and advanced glycation end products (AGEs) on the expression of fractalkine in cultured human renal mesangial cells (HRMC) were investigated. Rosiglitazone inhibits the upregulation of fractalkine induced by AGEs in HRMC.

Objective To investigate the effect of albumin on expression of NLRP3 inflammasome and its downstream cytokines IL-1β and IL-18 in tubular epithelial cells.Methods Thirty mesangioproliferative glomerulonephritis (MsPGN) patients with different levels of proteinuria were selected, and their renal biopsy samples were stained by PAS and Masson to observe tubular epithelial cells injury and inflammatory cells infiltration.NLRP3, caspase-1, IL-1β and IL-18, as well as different inflammatory cells, were detected by immunohistostaining.In vitro, Western blotting and real-time PCR were employed to detect NLRP3, caspase-1, IL-1β and IL-18 protein and mRNA in HK-2 cells stimulated by bovine serum albumin (BSA) (20 g/L).Results In MsPGN patients with high levels of proteinuria, there were obvious renal tubular epithelial cell injury and inflammatory cells infiltration (all P ＜ 0.05), and the expressions of NLRP3, caspase-1, IL-1β and IL-18 were up-regulated compared to patients with low levels of proteinuria (all P ＜ 0.05).Furthermore, IL-1β and IL-18expressions were positively correlated with the degree of proteinuria (r=0.836, P ＜ 0.05;r=0.901, P ＜0.05).NLRP3, caspase-1, IL-1β and IL-18 protein and mRNA were significantly increased in HK-2cells stimulated by BSA compared to the control group (all P ＜ 0.05).Conclusions Albumin is able to induce NLRP3 inflammasome activation in tubular epithelial cells, which may be the mechanism of tubulointerstitial injury and inflammation caused by proteinuria.

Objective To evaluate the role of acute kidney injury (AKI) in predicting the early (30-day) and late (30-day to 5-year) mortality of acute myocardial infarction (AMI) patients during hospitalization.Methods A total of 1371 adult patients diagnosed with AMI in the First People's Hospital of Changzhou from January 2008 to December 2012 were analyzed retrospectively with collecting their relevant clinical data from the hospital's database.AKI was categorized according to the 2012 KDIGO AKI criteria.To compare between death group and non-death group in AMI patients during 30-day and 30-day to 5-year.Different AKI stages of patients were compared,and their all-cause mortality were analyzed by Kaplan-Meier.Using multivariate COX regression analysis with two models to assess the factors for AMI patients in 30-day to 5-year.Results The prevalence of AKI after AMI in death group was higher than that in non-death group (the 30-day prevalence was 72.7％ vs 27.4％,P ＜ 0.001;the 5-year prevalence was 36.3％ vs 26.2％,P=0.013).In both early (30-day) and late (30-day to 5-year) follow up,the KDIGO grading distribution of AKI was different between death group and non-death group (P ＜ 0.001 in 30-day follow up and P=0.002 in 30-day to 5-year follow up).Among the 1371 AMI patients,410 (29.9％) developed AKI during the hospital stay.The 30-day and 30-day to 5-year mortality rates were 5.6％ (77/1371) and 11.3％ (146/1294) respectively.All-cause mortality and cardiovascular mortality were significantly higher in patients with AKI-Ⅰ stage,AKI-Ⅱ stage and AKI-Ⅲ stage than those with non-AKI (all P ＜ 0.001),especially in patients with AKI-Ⅲ stage.Further stroke history (HR=3.122,P=0.012),AKI severity (AKI-Ⅰ stage HR=3.034,P=0.028;AKI-Ⅱ stage HR=7.832,P＜0.001;AKI-Ⅲ stage HR=9.919,P＜0.001),and β-blocker therapy (HR=0.591,P=0.040) were independent predictors of 30-day mortality,while aging (HR=1.061,P ＜ 0.001),albumin (HR=0.943,P=0.023),AKI-Ⅲ stage (HR=3.944,P=0.007),β-blocker therapy (HR=0.660,P=0.041) and percutaneous coronary intervention (HR=0.256,P ＜ 0.001) were independent predictors of 30-day to 5-year mortality.Both at early (30-day) and late (30-day to 5-year) follow-up,AKI with or without baseline renal dysfunction were independent predictors of death in patients with AMI (all P ＜ 0.05).Conclusions AKI strongly correlated with short-and long-term allcause mortality of AMI patients,regardless of the baseline renal impairment.Specifically,the more severe AKI,the higher short-term mortality AMI patients have.