Objective To systemically assess impact on postoperative outcomes after red blood cell transfusion(RBCT) in coronary artery bypass graft surgey.Methods A meta-analysis was performed on the comparison and synthesis of findings from included studies published from January 1980 to January 2014.Pooled odds ratio(OR) and 95 ％ confidence interval(CI) were calculated using RevManS.3 software.Sensitivity analysis was conducted and possible publication bias was tested as well.Results Seven retrospective studies including 71 228 patients(33 872 RBCT cases,37 356 control cases) were eligible for inclusion.The pooled analysis revealed difference in the 30-day mortality OR =1.85 (95％ CI:1.35-2.54),1-year mortality OR =2.02 (95 ％ CI:1.44-2.84),shock OR =2.92 (95 ％ CI:1.96-4.35),renal dysfunction OR =7.67 (95 ％ CI:1.44-40.94),mediastinitis OR =2.26 (95 ％ CI:1.72-2.97),and myocardial infarction OR =3.53 (95 ％ CI:2.89-4.29).Conclusion Perioperative RBCT can incresase the risk of postoperative mortality and complications in coronary artery bypass graft surgey.High-quality randomized case cohort studies are still needed for the further proof of the risk.

BACKGROUND: Revascularization is a challenge for the tissue-engineered bone carrying cells after implanted into human body. Previous studies have found that tanshinol can improve the functions of endothelial progenitor cells and exert vascular protective effects.OBJECTIVE: To prepare the β-calcium phosphate (β-TCP) scaffold with tanshinol coating, and to observe its cytocompatibility.METHODS: The β-TCP scaffolds coated with 10-7, 10-6 and 10-5 mol of tanshinol were constructed by negative pressure absorption method. The distribution of tanshinol coating on the scaffold was observed using scanning electron microscopy,and the inner ingredients were analyzed by infrared spectrum. Human endothelial progenitor cells (hEPCs) were cultured in the extracts of β-TCP and β-TCP scaffolds with 10-7, 10-6, 10-5 mol of tanshinol coatings, respectively. The cell proliferation was detected at 2, 4, 6, 8 and 10 days of culture; the levels of nitric oxide and vascular endothelial growth factor in the supernatants were detected at 1, 7 and 14 days of culture; the lumen formation on the matrigel was observed after 14-day culture. hEPCs were respectively seeded onto the β-TCP and β-TCP scaffolds with different dosages of tanshinol coating,and then the cell growth was observed under scanning electron microscope at 7 days.RESULTS AND CONCLUSION: The tanshinol coating evenly distributed on the inner surface of the pores, and its crystalline structure became dense with dosage increasing. Infrared spectrum analysis revealed no changes in the characteristic absorption peak of tanshinol and TCP in the scaffold. The β-TCP scaffolds with tanshinol coating could promote the proliferation of hEPCs, especially the scaffolds with 10-6 and 10-5 mol tanshinol coating. Compared with the β-TCP scaffold, the scaffolds with 10-6 and 10-5 mol tanshinol coating significantly upregulated the nitric oxide level at 14 days of culture, and significantly increased the level of vascular endothelial growth factor at 7 and 14 days of culture (P <0.05). Although it could be found in all β-TCP scaffolds with tanshinol coating, the lumen formation was the maturest in the scaffold with 10-5 mol tanshinol coating. These results suggest the β-TCP scaffolds with tanshinol coating can promote the proliferation and endothelial differentiation of hEPCs, and hold a good cytocompatibility.

Objective To observe the efficacy of the treatment of mycophenolate mofetil (MMF) combined with prednisone on steroid-resistant idiopathic membranoproliferative glomerulonephrifis (IMPGN) patients with moderate to severe proteinufia. Methods Thirteen cases were diagnosed as IMPGN by renal biopsy after excluding secondary factors. Among 13 patients, 9 had severe proteinuria and another 4 had moderate proteinuria, 9 with hypertension and 11 with decreased renal function. Before MMF therapy, all of the cases were resistant to the treatment of glucocorticoid (prednisone 1 mg·kg-1·d-1) for 8 weeks or more. The dose of MMF was 1.5 g/d. Patients were followed up every month for blood pressure, urinary protein excretion, liver and kidney function, complete blood count, and adverse effects. Results At the initiation, the 24 h urinary protein excretion was (4.1±1.4) g, Scr (131.0±44.9) μmol/L, and estimated glomerular filtration rate (eGFR) (63.3±26.8) ml·min-1·(1.73 m2)-1. After prednisene therapy for at least 2 months, the 24 h urinary protein excretion (4.2±1.5) g, Ser (133.2±52.8)μmol/L and eGYR (63.3±27.1) ml·min-1·(1.73 m2)-1did not change significantly. After 3 months of the addition of MMF, 24 h urinary protein excretion declined slightly [(3.8±1.2) g, P>0.05]. After 6 months, 24 h urinary protein excretion declined significantly [(2.5±0.9) g, P<0.05], with decrease in Set and eGFR[(97.2±27.3) μmol/L and (81.3±24.2) ml·min-1·(1.73 m2)-1, P<0.05)]. At the end of 1 year, 24 h urinary protein excretion was only (1.5±0.6) g(P<0.01 ), Ser and eGFR were (95.9±22.5)μmol/L and (81.2±23.8) ml·min-1·(1.73 m2)-1(P<0.01). All the patients experienced a partial remission of proteinuria (urinary protein excretion decreased by 50% or more). Adverse event including stomach upset was found in 1 patient. Conclusion MMF combined with glucosteroids can effectively decrease proteinuria and improve renal function without obvious side effect in steroid-resistant IMPGN.

Objective To investigate the effects of repeated low dose intravenous infusion of low molecular weight iron dextran and iron sucrose on oxidative stress in chronic renal failure (CRF) rats. Methods CRF model was established by 5/6 subtotal nephrectomy (5/6 Nx). Four weeks after removing the right kidney, successful rats were randomly divided into low molecular weight iron dextran group, sucrose iron group and CRF control group. The sham group was established simultaneously. The dose of iron administrated in each rat was similar in iron dextran group and sucrose iron group. There were 6 rats in each group. Animals were observed for 6weeks, then the blood, urine and renal tissue samples were collected, and indexes of renal function,anemia, iron status and oxidative stress were investigated. Results The hemoglobulin (Hb) level in iron groups was significantly higher as compared to control group (P＜0.05) but was not significantly different between two iron groups. The levels of serum iron, ferritin and saturation rate of transferring (TS) were obviously lower in control group as compared to sham group (P＜0.05).Levels of above 3 indexes were significantly higher in two iron groups as compared to control group (P＜0.05), but were not significantly different between two iron groups. Concentration of plasma advanced oxidation protein products (AOPP) was obviously higher in two iron groups than that in control group [(127.84±21.19) μmol/L, (134.21±29.38) μmol/L vs (81.83±19.93) μmol/L, P＜0.05]. Plasma malonaldehyde (MDA) was significantly higher in iron sucrose group than that in iron dextran group [(6.06±0.73) nmol/L vs (4.99i0.80) nmol/L, P＜0.05]. Serum levels of superoxide dismutase (SOD) and total anti-oxidant capacity (TAOC) had no significant differences among three CRF groups. Concentration of plasma glutathione peroxidase (GSH-Px) was significantly decreased in three CRF groups as compared to sham group (P＜0.05), while plasma GSH-Px was significantly lower in sucrose iron group than that in iron dextran group and control group [(2123.11±74.78)nmol ·ml-1 ·min-1 vs (2352.84±163.90) nmol· ml-1 ·min-1, (2310.23±125.99) nmol ·ml-1 ·min-1, P＜0.05]. Conclusions Injection of intravenous iron can partially improve the anemia and the iron status indexes in 5/6 Nx CRF rats. Repeated low dose intravenous infusion of iron dextran and iron sucrose can aggravate the oxidative stress state in CRF rats, and the iron sucrose is worst.

Objective To investigate the correlation between plasma pentraxin 3 (PTX3)and cardiovascular disease(CVD) in maintenance hemodialysis(MHD) patients.Methods Plasma was obtained from 98 MHD patients before and after a session of HD and 50 age-matched healthy subjects.Plasma PTX3 was measured by enzyme-linked immunosorbant assay (ELISA).Spearman correlation and linear regression were used to examine the correlation between plasma PTX3 level and other laboratory parameters.Binary Logistic regression was used to assess the correlation between plasma PTX3 level and CVD.Receiver operator characteristic (ROC) curve was used to analyze the correlation among PTX3, high sensitive C-reactive protein(hsCRP) and CVD.Results Plasma PTX3 level was significantly higher in MHD patients compared to healthy controls [1.87 (1.34-2.50) μg/L vs 1.11(0.86-1.51) μg/L, P＜0.01], and increased after a single HD session[post-HD 2.18(1.80-3.14) μg/L vs pre-HD 1.87(1.34-2.50) μg/L, P＜0.01].Patients with CVD had higher concentrations of PTX3 than those without CVD[2.18 (1.48-2.74) μg/L vs 1.76 (1.25-2.26) μg/L, P＜0.05].High plasma PTX3 (＞1.87 μg/L) was positively and independently associated with CVD[OR=3.15, 95％CI(1.17-8.50), P＜0.05].ROC curve analysis showed the PTX3 was more closely correlated to CVD than hsCRP in MHD patients with hsCRP ＞3 mg/L, and the area under the curve of PTX3 and hsCRP was 0.655 ±0.083(P＜0.05) and 0.562±0.083(P＞0.05) respectively.Plasma PTX3 level was negatively correlated with body mass index (ρ=-0.248,P＜0.05), pre-albumin(ρ=-0.218, P＜0.05), total cholesterol(ρ=-0.265, P＜0.01), triglyceride (ρ=-0.246, P＜0.05), LDL-cholesterol (ρ=-0.254, P＜0.05), hemoglobin (ρ=-0.212, P＜0.05), and positively with erythropoietin dose per week(ρ=0.184, P＜0.01), cardiac troponin T (ρ=0.287,P＜0.01), carotid artery intima-media thickness (ρ=0.294, P＜0.05).Conclusions PTX3 level ismarkedly elevated in HD patients.HD procedure induces PTX3 elevation.Plasma PTX3 could be auseful marker of CVD risk factors in MHD patients.

Objective To assess the risk factors of intradialytic-hypotension (IDH) among maintaining hemodialysis (MHD) patients and to explore the relation between NT-proBNP and IDH,thus to provide clinical evidence for the prevention and treatment of IDH.Methods A total of 202 MHD patients during March 2009 to May 2009 in our dialysis center were enrolled in the study.Intradialytic blood pressure (BP) was measured during a 3-month period.IDH was defined as an event characterized by a sudden drop in systolic BP more than 20 mm Hg or in mean artery pressure (MAP) more than l0 mm Hg.Logistic regression analysis was used to assess the risk factors of IDH.ROC curve was used to evaluate the diagnostic efficacy of serum NT-proBNP.Results The incidence of IDH was 42.1％.One hundred and seventeen patients with no-IDH (＜1/10 hypotensive events per 3 months) were served as controls.Fifty-five patients with o-IDH (≥ 1/ 10 but ≤1/3 hypotensive events per 3 months) and 30 patients with f-IDH (＞1/3 hypotensive events per 3 months) were identified among 202 patients.Multivariate regression analysis showed that age,gender,ultrafiltration rate,serum NT-proBNP,serum albumin,aortic root dimension (AoRD) were associated with IDH among MHD patients.Serum NT-proBNP was positively correlated with IDH.The area under the ROC curve (AUC) of NT-proBNP was 0.76 (95％ CI 0.69 to 0.83,P＜0.01).The cut-off value of serum NT-proBNP for IDH was 1746.5 ng/L,with a sensitivity of 88.61％ and a specificity of 51.10％.Furthermore,the AUC of NT-proBNP for f-IDH was 0.65 (95％ CI 0.53 to 0.763,P＜0.01).The cut-off value of serum NT-proBNP for f-IDH was 8208.0 ng/L,with a sensitivity of 33.33％ and a specificity of 91.30％.Conclusions Elderly,female,high ultrafiltration rate,high level of serum NT-proBNP,hypoalbuminemia,shorter AoRD are independent risk factors of IDH among MHD patients.Serum NT-proBNP can be used as a predictor of IDH.

Objective To explore the effects of Dimethyloxalyl Glycine(DMOG)on isehemic acute renal failure(iARF)in mice and its relationship with activation of hypoxia inducible factor 1α(HIF-1α).Method Twenty five C57/BL male mice were divided into 5 groups randomly:control group,DMOG group,sham operation group,ischemia/reperfusion(I/R)group and DMOG pretreated group(DMOG+I/R).Ischemia/reperfusion injury was induced in mice by clamping both renal pedicles for 30 minutes.The expression of HIF-1α was determined by Western blot.Renal function was reflected by blood urea nitrogen(BUN)and serum creatinine(Scr).Morphologic changes were evaluated under light microscopy.Apoptosis in the kidney was detected by TUNEL staining.Expression of Vimentin,a marker of tubulointerstitial damage was detected by immunohistochemistry.Results The elvated levels of of BUN((65.8±2.6) vs (13.6±0.7),P＜0.01],and Scr[(229.5±11.2) vs (6.5±0.8),P＜0.01]andwere found morphological injury were induced by the ischemic insult in I/R group.Administration of DMOG dramatically improved renal function[BUN,(26.3±6.5)vs(65.8±2.6);Scr,(27.0±14.1)vs(229.5±11.2),P＜0.01]associated with amelioration of tubulointerstital damage.In the DMOG treated group,the protein level of HIF-1α in the kidney of mile was also up-regulated significantly.Conclusions The protection against iARF in mice by DMOG administration is mediated by activation of HIF-1α.

Objective To study the urea rebound after hemodialysis in maintenance hemodialysis (MHD) patients and its impact factors. Methods From 124 stable MHD patients, blood samples were collected at the beginning, immediate post-hemodialysis, 15 minutes and 30 minutes after hemodialysis. The urea rebound was quantified, and its effect on URR and spKt/V was investigated. The impact factors on urea rebound were analyzed. Results In this group of patients, average post-hemodialytic urea rebound was 13.6%, leading to over-estimation of URR and spKt/V of 0.04 and 0.14, respectively. Hemodialysis efficiency expressed as K/V determined urea rebound most significantly. Other impact factors included higher hemoglobin, higher relative ultrafiltration, arteriovenous access, and male patients. Conclusions Urea rebound is common after the hemodialysis. For specific patients and hemodialysis sessions, ignoring it would result in significant over-estimation of delivered hemodialysis dose.

Objective To examine the association between residual renal function at initiation of dialysis and prognosis in maintenance dialysis patients.Methods Incident patients with end-stage renal diseases initiating dialysis between 1 January 2005 and 30 September 2009,followed up to 31 March 2010 were enrolled in this study.Residual renal function was evaluated using eGFR estimated by the abbreviated MDRD equation.Patients were classified into four groups according to eGFR of ≥10.5,8 to ＜10.5,6 to ＜8,＜6 ml·min-1·(1.73 m2)-1.The outcome was all-cause and cardiocerebral vascular mortality.Results (1) A total of 562 patients were included.The median eGFR at initiation of dialysis was 5.60 (2.26-12.62) ml·min-1·(1.73 m2)-1.The median follow-up time was 17 (0-58) months from initiation of dialysis and 141 patients died within this period.The median survival time was 45.48 (43.05-47.90) months.With eGFR declined,Scr,BUN,serum uric acid,serum prealbumin,phosphorus,calcium and phosphate product,iPTH,mean arterial pressure (MAP) at initiation of dialysis increased (P＜0.05),and hemoglobin,proportion of male,proportion of diabetes comorbidity,proportion of the Charlson comorbidity index ≥5 decreased (P＜0.05).Though there was no significant difference among the four groups,the proportion of left ventricular hypertrophy comorbidity increased when eGFR declined.(2) There was no significant difference of all-cause mortality among four groups using Kaplan-Meire survival curve.Cox regression model indicated no significant difference of all-cause mortality in levels of eGFR (HR=1.012,95％CI 0.961-1.065,P=0.654).Without patients died in the first 3 months,the multivariate Cox regression model indicated eGFR at initiation of dialysis was the protective factor to 1 year survival (HR=0.791,95％CI 0.669-0.935,P＜0.01).(3) The multivariate Cox regression model indicated the risk of overall and 1 year cardiocerebral vascular death decreased with eGFR at initiation of dialysis increased (HR=0.868,95％CI 0.777-0.971,P＜0.05; HR=0.937,95％CI 0.851-0.992,P＜0.05,respectively).(4) The multivariate Cox regression model indicated eGFR at initiation of dialysis was benefit to survival of patients treated by peritoneal dialysis,with all-cause death risk decreased by 10％ when eGFR increased by 1 ml·min-1·(1.73 m2)-1 (HR=0.90,95％CI 0.81-0.99,P＜0.05).In hemodialysis patients,Kaplan-Meire survival curve was significantly different among the four groups (Log-rank test,P=0.047); the survival of the group of 8 to ＜10.5 ml·min-1·(1.73 m2)-1 was lower as compared to the groups of 6 to ＜8 (Log-rank test,P=0.033) and ＜6 ml·min-1(1.73 m2)-1 (Log-rank test,P=0.005); but the multivariate Cox regression model indicated no relationship between survival and eGFR.In the subgroup of chronic glomerulonephritis as primary renal disease,the eGFR at initiation of dialysis was the benefit factor,with all-cause death risk decreased by 16.6％ (HR=0.834,95％CI 0.736-0.946,P＜0.01) and cardiocerebral vascular death risk decreased by 18.2％ (HR=0.818,95％CI 0.669-0.999,P＜0.05) when eGFR increased by 1 ml ·min-1 ·(1.73 m2)-1.In the subgroup of chronic glomerulonephritis treated by peritoneal dialysis,the all-cause death risk decreased by 32.1％ with eGFR increased by 1 ml·min 1·(1.73 m2)-1 (HR=0.679,95％CI 0.535-0.862,P＜0.01).Conclusions Early initiation of dialysis may not be associated with improved overall survival,but may reduce cardiocerebral vascular and 1 year all-cause mortality,improve the survival of chronic glomerulonephritis patients and peritoneal dialysis patients.

BACKGROUND: There are various methods to observe and detect early angiogenesis in the process of entochondrostosis, but each holds certain deficiencies.OBJECTIVE: To explore the possibility of tetracycline and alizarin complexone as an indirect marker ofangiogenesis in the process of entochondrostosis.METHODS: New Zealand white rabbit models of bilateral radial bone defects were prepared, followed by β-tricalcium phosphate implantation, and then given the injection of tetracycline and alizarin complexone at 1 and 15 days,respectively. Samples were collected at 28 days, some of which were observed using fluorescence/light microscope after ink perfusion and hard tissue slicing, and the others were decalcified and observed using immunohistochemistry. The uniformity between lumen structures labeled with bone affinity fluorescein and vascular structures marked by immunohistochemistry and ink perfusion was compared.RESULTS AND CONCLUSION: The lumen structure labeled with bone affinity fluorescein was confirmed to be a CD34 positive vascular structure. Under the fluorescence microscope, the bone affinity fluorescein labeled vascular morphology was consistent with ink perfusion-labeled, and black ink lines could be observed in the lumen structures labeled with bone affinity fluorescein after ink perfusion. In addition, the color of the lumen labeled with fluorescein was more gorgeous,three-dimensional structure more vivid, and the vascular evolution process distinguished more easily by different fluorescein colors, exhibiting unique advantages. Therefore, it is available to detect the early angiogenesis in the process of entochondrostosis.