Objective To study the arterial stiffness in non-diabetic pre-dialysis chronic kidney disease (CKD) patients and to explore the associated factors. Methods Automatic pulse wave velocity (PWV) measuring system was used to examine carotid-femoral pulse wave velocity (CFPWV) as the parameters reflecting central elastic large arterial elasticity. Vascular calcification was quantitatively evaluated by plain radiographic film of abdomen, pelvis and hands. Blood pressure, biochemical parameters and intact parathyroid hormone (iPTH) were routinely detected. Stepwise multiple linear regression analysis was used to assess the associated factors of arterial stiffness. Results Ninety-six non-diabetic pre-dialysis CKD patients and 30 healthy people were enrolled in this trial. CFPWV in stage 3, 4 and 5 CKD patients was significantly higher than that in healthy controls [(11.63±2.39) m/s, (11.70±2.80) m/s, (12.88±2.49) m/s vs (9.70±1.66)m/s , all P<0.05]. Stepwise multiple regression analysis demonstrated that age, mean arterial pressure, vascular calcification and iPTH were independent impact factors of CFPWV. Conclusions Arterial stiffness of large artery increases in non-diabetic pre-dialysis CKD patients. Age, mean arterial pressure, vascular calcification and iPTH are independent impact factors of CFPWV.

Objective To investigate the incidence, risk factors and outcome of acute kidney injury (AKI) following cardiac surgeries. Methods Clinical data of 1056 patients undergoing open heart surgery in Renji Hospital from January 2004 to June 2007 were retrospectively analyzed. Univariate and multivariate analyses were used to evaluate possible pre-,intra-, and post-operative parameters associated with AKI according to AKI Network (AKIN). Results Of the 1056 patients, 328 (31.06%) developed AKI. In-hospital mortality was 4.07% in all discharges while 11.59% in AKI patients (P<0.01). Multivariate logistic regression analysis revealed that increased age (OR=1.40), pre-operative hyperurieemia (OR=1.97), pre-operative left ventricular insufficiency (OR=2.53), combined surgery (OR=2.79), prolonged operation time (OR=1.43), post-operative circulation volume insufficiency (OR=11.08) were risk factors of AKI. Conclusions AKI is a common complication and associated with increased mortality following cardiac surgery. Increased age, pre-operative hyperuricemia, pre-operative left ventricular insufficiency, combined surgery, prolonged operation time, post-operative circulation volume insufficiency are useful in stratifying risk factors for the development of AKI.

ObjectiveTo investigate the prevalence and associated risk factors of chronic kidney disease (CKD) in adult population receiving body check from urban area of Hefei, Anhni. MethodsA total of 33 451 subjects who were older than 20 years and received healthy examination in Health Center of Anhui Provincial Hospital from January 2005 to December 2007 were enrolled in this study. CKD was defined as proteinuria, and/or hematuria, and/or using the simplified MDRD equation. ResultsThe prevalence of proteinuria was 2.74% (95%CI: 2.57%-2.92%), hematuria 7.67% (95% CI:7.39%-7.96%), and reduced eGFR 0.80%(95% CI:0.71%-0.90%). 9.92% (95% CI:9.60%-10.25%) subjects had at least one indicator of kidney damage. Age, female, diabetes mellitus, hypertension, and hyperuricemia were independently associated with CKD. ConclusionsThe prevalence of chronic kidney disease is 9.92% in adult population receiving body check from urban area of Hefei, Anhui. Independent risk factors associated with CKD are age, female, diabetes mellitus, hypertension, and hyperoricemia.

ObjectiveTo evaluate the applicability of modified formulas based on plasma creatinine levels in Chinese patients with chronic kidney disease (CKD). MethodsA total of 327 CKD patients were investigated. Glomerular filtration rate (GFR) was estimated with Chinese equations and Ruijin equation. The accuracy of estimated GFR was compared with 99mTc-DTPA-GFR (sGFR) in CKD patients. ResultsBland-Ahman analysis demonstrated that Ruijin equation was more consistent with sGFR than the other equations. But all the equations were not well consistent with sGFR. Linear regression showed that the slopes of Ruijin equation and MDRD-1 equation were closer to the identical line. 15%, 30% and 50% accuracy of Ruijin equation were higher than the other equations. But 30% accuracy of Ruijin equation was still less than 70%. When the accuracy of estimated GFRs was compared with sGFR in different stages of CKD, GFR estimated by Ruijin equation showed good results. ConclusionsWhen plasma creatinine is checked with enzymatic method, modified GFR estimation equations may show great bias in Chinese CKD patients. More clinical trails should be carried out to evaluate and identify the application of modified GFR estimation equations in Chinese patients with CKD.

ObjectiveTo investigate the effects of losartan on angiotensin (Ang)Ⅱ-induced the generation of oxidative stress and expression of transforming growth factor β1(TGF-β1) in rat proximal tubular epithelial cells and to explore its underlying mechanism. MethodsNRK-52E cells, a rat proximal tubular epithelial cell line, were applied to explore the antioxidationand antifibrosis of losartan. The expression of three subunits of nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase, including p47phox, Nox-4, p22phox, and TGF-β1 were determined by real-time RT-PCR and/or Western blot. The generation of reactive oxygen species (ROS) was measured by DCF fluorescence analysis. Superoxide dismutase (SOD) in the supernatant was measured by colorimetric method. Results10-7 mol/L Ang Ⅱ up-regulated p22prox, p47phox and Nox-4 mRNA and protein expression, and the mRNA increased by 5.57-fold, 5.55-fold and 9.41-fold at 24 h (P<0.01, respectively) and the protein increased by 4.53-fold, 4.17-fold and 6.50-fold at 24 h (P<0.01, respectively) as compared with control. Losartan greatly reduced the mRNA elevation of p22prox, p47phox and Nox-4 by 2.71-fold, 2.18-fold and 5.23-fold (P<0.01, respectively) and reduced the protein elevation by 3.20-fold, 2.30-fold and 4.30-fold (P<0.01, respectively) as compared with control. Losartan also inhibited ROS generation induced by Ang Ⅱ in rat proximal tubular epithelial cells. SOD level in the supernatant was markedly decreased after Ang Ⅱ stimulation, while losartan could increase SOD levels (P<0.01). Furthermore, losartan signficantly inhibited Ang Ⅱ-induced TGF-β1 mRNA up-regulation by 64% (P<0.01). ConclusionsLosartan acts as an anti-oxidative and anti-fibrotic agent via the mechanisms of blocking NADPH oxidase-dependent oxidative stress and inhibiting TGF-β1 expression.

ObjectiveTo investigate the effects and molecular mechanism of endoplasmic reticalam stress (ERS) on albumin-induced apoptosis in renal proximal tubular cells (HKCs). MethodsWestern blot was performed to detect the relationship of the expression of glucose-regulated protein 78 (GRF78) and CCAAT/enhancer-binding protein-homologous protein (CHOP) with the action time and concentration of haman serum albumin (HSA). Expression levels of CHPO mRNA and protein in HKCs after CHOP siRNA transfection were examined by real-time fluorescence quantitative PCR and Western blot respectively. Annexin-V-FITC and PI doable staining cytometry was used to detect the apoptosis of HKCs induced by HSA and influenced by CHOP siRNA. Results(1)After HKCs were stimulatde by 0, 5, 10, 20 g/L albumin for 24 hours respectively, the expression of GRP78, CHOP and HKCs apoptosis were increased with the albumin concentration (P<0.01). After HKCs were stimulated by 20 g/L albumin for 0, 6, 12, 24, 36 hours respectively, the expression of GRP78 was up-regulated at 6-hour, while CHOP and HKCs apoptosis were increased at 12-hour, and significant differences were found among groups (P<0.01). (2) CHOP siRNA significantly inhibited albumin-induced HKC CHOP mRNA and protein expression, as well as HKC apoptosis (P<0.01). ConclusionsRenal tubular cells exposed to high protein load result in EBS. ERS may subsequently lead to tubular damage by activation of pro-apoptosis factor CHOP.

ObjectiveTo investigate the clinical application of tacrulimus (TAC, FK506) in children with primary nephrotic syndrome (NS). MethodsSixty-five primary NS children received routine or decreased-dosage glucocorticosteroid according to clinical NS types after hospitalization. At the same time, TAC was given orally with the dosage of 0.1 to 0.15 mg/kg, once every 12 hours, for 6 to 24 months. And the serum concentration of TAC was monitored during the course. ResultsAfter the treatment of TAC for 1 to 2 months, 65 patients were recovered with gradually reduced urinary protein, rapidly increased serum albumin, and improvement of cholesterol and triglycerides. Total remission rate was 83.1% and onset time was 7 to 54 days. Twelve cases experienced recurrence. Increased CD4, as well as 3/3 or 3/1 TAC genotype, indicated higher remission rate. Various pathological types had different remission rates or ratio, which were as follows: minimal change nephropathy (96.4%), mesangial proliferative glomendonephritis (90.0%), membranous nephropathy (2/3), membranous proliferative glomerulonephritis (3/5), focal segmental glomerulosclerosis (4/9). The patients would recover in the course of treatment under the conditions of TAC initial dose as 0.1 to 0.15 mg /kg per 12 hours and controlled serum concentration as 5 to 10 g/L. During the treatment, 12 cases appeared gastrointestinal symptoms, mainly as anorexia, nausea and vomiting, 1 abdominal pain, 2 headache, 1 tremor, 1 paresthesia, 3 insomnia, 4 transient increased Scr, 8 slightly increased NAG, 6 increased C3 and α-2 macroglobulin. The symptoms disappeared within one week or after stopping TAC. ConclusionsTAC is effective in primary NS children, even with abnormal liver function or tuberculosis infection. TAC can also be a substitute to cyclosporine A.

ObjectiveTo investigate the prevalence of chronic kidney diseases (CKD) from inpatients with cerebrovascular diseases in Shanghai district. MethodsInpatients with cerebrovascular diseases from neurology department of five hospitals in Shanghai from Jun. 2007 to Feb. 2008 were recruited . All the patients were respectively diagnosed by brain CT, CTA, MRI, MRA and TCD. Laboratory data included urinary microalbumin-to-creatinine ratio (ACR), routine urinalysis, fasting plasma glucose, 2-hour-postprandial plasma glucose, Scr, uric acid, etc. All the serum creatinine samples were uniformly tested in central laboratory of Shanghai Ruijin Hospital.Glomendar filtration rate (GFR) was estimated by complicated MDRD equation and CKD stage was classified according to K/DOQI guidelines. ResultsA total of 1014 hospitalized patients with cerebrovascular diseases were enrolled during the observation period, with M/F ratio of 559/455 and mean age of (68.56±12.17) years. Cerebrovascular diseases included ischemic stroke (708 cases), hemorrhagic stroke (197 cases) and transient cerebral ischemie attack (TIA) (109 cases). Microalbuminuria (MAU) was detected in 11.2%, while 24.8% patients had proteinuria. The prevalence of CKD was 47.7%. The percentage of these inpatients in CKD stage 1 to 5 was approximately 6.90%, 14.69%, 21.60%, 2.56% and 1.97% respectively. The Logistic regression model showed that the risk factors of short-term (<30 days) prognosis were albuminuria, hyperglycemia (fast glucose) and anemia. ConclusionsThe prevalence of CKD in inpatients with cerebrovascular diseases was 47.7% in Shanghai. It is significant to evaluate CKD among patients with cerebrovascular diseases, especially to use the screening of ACR in the early stage.

Objective To observe the changes in the expression of renal tissue TNF-α , NF-κB and the interrelation to renal cell apoptosis, and their influences of Inula Britannica(an inhibitor of inflammatory signal pathway) in exhausted swimming rats, and to investigate the role of inflammatory signal pathway. Methods Forty-eight male Wistar rats were randomly divided into three groups: control group (CN, n=8), exhaustive swimming group (ES, n=24) and Inula Britannica group (IB, n=16). The rats of CN were quiet without swimming. The rats of ES swam to exhaustion and were sacrificed at immediately (ESI, n=8), 6 hour (ES 6 h, n=8) and 24 hour (ES 24 h, n=8) after exhanstiing swimming. The rats of IB group took orally Inula Britannica at the dose of 25 ml/kg body weight at 24 h before swimming and then swam to exhaustive state. The rats of IB group were sacrificed at 6 hour (IB 6 h, n=8) and 24 hour (IB 24 h, n=8) after exhaustiing swimming. The renal cell apoptosis was measured by the method of terminal-deoxynucleotidyl transferase mediated d-UTP nick end labeling (TUNEL). The expression of TNF-α in renal tissue was examined by immunohistochemistry. The changes of NF-κB in renal tissue were measured by flow cytometry and immunnhistochemistry. The interrelation between TNF-α and NF-κB was analyzed by Pearson method, and the interrelation between TNF-α, NF-κB and renal tissue cell apoptosis was analyzed by Spearman method. Resulls The number of renal tissue apoptotic cells was increased progressively from ESI to ES 24 h rats (P <0.05). Immunohistochemistry staining showed that the positive expressions of renal tissue TNF-α and NF-κB were increased progressively at 0 h (0.136±0.009, 0.129±0.011), 6 h (0.171±0.011, 0.166± 0.009) and 24 h (0.229±0.008, 0.218±0.019) after exhaustiing swimming in ES compared with control group (0.109±0.010, 0.095±0.010) ( all P<0.05). The similar changes of renal tissue NF-κB was also revcalved by flow cytometry. The expression of TNF-α was positively correldted with NF-κB (r=0.955, P<0.01 ), and renal cell apoptosis was also positively correlated with TNF-α and NF-κB (r =0.953, r=0.939, P<0.01) in ES rats. Pretreatment with Inula Britannica, inhibited the up-regulation of expressions of renal tissue TNF-α (6 h:0.142±0.012, 24 h:0.130±0.010) and NF-κB (6 h:0.138±0.010, 24 h:0.136±0.011 ) induced by exhausting swimming. Conclusion Overtraining can induce the up-regulating expressions of renal tissue TNF-α and NF-κB, and Inula Britannica can partly counter the above changes in exhaustied swimming rats, which may be one important mechanisms of overtraining-induced renal tissue cell apoptosis and the anti- apoptosis effect of Inula Britannica.

Objective To investigate the effect of fluvastatin on activation of nuclear factor kappa B (NF-κB)induced by angiotensin Ⅱ (Ang Ⅱ ) in rat kidney tubular epithelial cells (NRK-52E). Methods NRK-52E cells were divided into (1)control group ; (2)Ang Ⅱ groups with different concentration and time; (3)Ang Ⅱ (10-6 mol/L)+SB203580 ( 10 μmol/L)group; (4) Ang Ⅱ (10-6mol/L) +different fluvastatin concentration (10-7, 10-6, 10-5 mol/L)groups;(5)Ang Ⅱ (10-6mol/L) +fluvastatin (10-5 mol/L) +mevalonate (10-4 mol/L)groap. Electrophoretic mobility shift assays (EMSA) was used to detect NF-κB activation. Phosphorylation of cellular p38 mitogen-activated protein kinase (p38MAPK) was determined by Western blot. Monocyte chemoattractant protein (MCP)-1 mRNA was determined by RT-PCR. Results Ang Ⅱ stimulated the DNA-binding activity of NF-κB,phosphorylation of p38MAPK and up-regulated the expression of MCP-1mRNA in cultured NRK-52E cells in a dose-dependent manner (P<0.01). Ang Ⅱ (10-6 mol/L) induced a rapid (5 minutes) elevation of the p38MAPK phosphorylation. NF-κB DNA binding activity was increased at as early as 30 minutes(P<0.01), peaked at 2 hours after AngⅡ treatment (P<0.01). This stimulatory effect of Ang Ⅱ on NF-κB was blocked by SB203580 (a specific inhibitor of p38MAPK) (P<0.01). Incubation of cells with fluvastatin significantly inhibited the Ang Ⅱ-induced NF-κB activation and expression of MCP-1 mRNA in dose-dependent manner (P< 0.05). Exogenous mevalonate (10-4 mol/L) prevented the effect of fluvastatin on NF-κB activation (P <0.05). Conclusions Fluvastatin reduces Ang Ⅱ-induced NF-κB activation via the p38MAPK pathway in NRK-52E cells. Such effect of flurastatin is partly through blocked by mevalonate.