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Objective To investigate the related factors and prognosis of pulmonary hypertension (PAH) in hemodialysis (HD) patients for early diagnosis and intervention of PAH.Methods A retrospective cohort study was conducted in 183 long-term hemodialysis patients with complete follow-up data from January 1,2010 to December 30,2015 from the blood purification center of the Third Affiliated Hospital of Sun Yat-sen University.The follow-up deadline was December 30,2017,and the endpoints were death and cardiovascular events.The clinical data,laboratory examinations,cardiac color Doppler ultrasound parameters and prognosis of patients with and without PAH were compared.Multivariate logistic regression was used to analyze the risk factors for PAH in HD patients.The survival rates were calculated by Kaplan-Meier method,and the survival curves were compared by Log-rank test between the two groups.A multivariate Cox proportional hazard regression model was used to examine the association between PAH and all-cause mortality in HD patients.Results Of the 183 hemodialysis patients,79(43.2％) were female,104(56.8％) were male,and the age was (56.1±16.9) years,of which 72(39.3％) were complicated with PAH.Compared with the non-PAH group,patients in the PAH group was older and had a longer duration of dialysis (both P ＜ 0.05).The left atrial diameter (P=0.002) and the proportion of valvular calcification (P=0.004) were significantly higher in the PAH group than that in the non-PAH group.Logistic regression analysis showed increased age (OR=1.027,95％ CI 1.001-1.053,P=0.041) and increased duration of dialysis (OR=1.129,95％ CI 1.004-1.269,P=0.042) were risk factors for PAH in HD patients.After a median follow-up of 27.8 months,Kaplan-Meier survival analysis showed that all-cause mortality was higher in the PAH group than that in the non-PAH group ~x2=5.636,P=0.018).The main cause of death in two groups was cardiovascular event.Afteradjusting for age,diabetes mellitus,duration of dialysis,valvular calcification,and hypertension,Cox regression showed that PAH increased the risk of all-cause mortality in HD patients (HR=1.894,95％ CI 1.083-3.313,P=0.025).Conclusions HD patients complicated with PAH are more common and the prognosis is poor.Increased age and increased duration of dialysis may be risk factors for PAH in HD patients.Regular color Doppler echocardiography is helpful for early detection and diagnosis of PAH.
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Objective@#To analyze the relationship between serum uric acid (SUA) level and clinical indicators in maintenance hemodialysis (MHD) patients, and explore its influence on all-cause mortality and cardiovascular mortality.@*Methods@#This study was a retrospective cohort study. Patients who received MHD from the blood purification center of the Third Affiliated Hospital of Sun Yat-sen University from January 1, 2011 to December 30, 2015 were enrolled in the queue. They were divided into 3 groups according to the first and third quantile of the SUA level quartiles, and the baseline data of clinical and laboratory examinations were compared. The correlation between SUA level and clinical indicators was analyzed by Pearson correlation coefficient. Kaplan-Meier method and Cox proportional hazard regression model were used to examine the association between SUA and all-cause mortality and cardiovascular mortality in MHD patients.@*Results@#A total of 201 patients were enrolled in the study. The age of the patients was (56.9±16.7) years and the baseline SUA level was (531.1±137.9) μmol/L. Patients were divided into 3 groups with the first quantile (442 μmol/L) and the third quantile (620 μmol/L) of the SUA quartiles as the boundary points: group 1 (SUA<442 μmol/L, n=52), group 2 (SUA 442-620 μmol/L, n=101) and group 3 (SUA>620 μmol/L, n=48). The results showed that the patients in group 1 were older and had more proportion of patients with diabetes mellitus and cardiovascular diseases than those in group 3 (all P<0.05). Compared to group 3, the serum albumin, serum phosphorus and serum creatinine were lower in group 1, while the hypersensitive C-reactive protein was higher (all P<0.05). Pearson correlation analysis showed that SUA level was positively correlated with albumin (r=0.135, P=0.047), blood phosphorus (r=0.269, P<0.001) and serum creatinine (r=0.333, P<0.001), and negatively correlated with hypersensitive C-reactive protein (r=-0.216, P=0.002). After a median follow-up of 49.8 months, 66(32.8%) all-cause deaths and 32(15.9%) cardiovascular deaths were recorded. Kaplan-Meier method showed that with the decrease of SUA, all-cause mortality (Log-rank χ2=18.27, P<0.001) and cardiovascular mortality (Log-rank χ2=15.04, P=0.001) increased. After adjusting for age, gender, comorbidity and other factors using the Cox proportional hazards model, the all-cause mortality and cardiovascular mortality decreased by 20.1% (HR=0.799, 95% CI 0.651-0.980, P=0.031) and 29.6% (HR=0.704, 95% CI 0.524-0.946, P=0.020) for each 100 μmol/L increase in baseline SUA. Compared to group 1, all-cause mortality (HR=0.332, 95%CI 0.142-0.774, P=0.011) and cardiovascular mortality (HR=0.140, 95%CI 0.030-0.657, P=0.013) were lower in the group 3.@*Conclusion@#Low SUA level increases the risk of all-cause mortality and cardiovascular mortality in MHD patients.
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Objective To analyze the relationship between serum uric acid (SUA) level and clinical indicators in maintenance hemodialysis (MHD) patients, and explore its influence on all-cause mortality and cardiovascular mortality. Methods This study was a retrospective cohort study. Patients who received MHD from the blood purification center of the Third Affiliated Hospital of SunYat-sen University from January 1, 2011 to December 30, 2015 were enrolled in the queue. They were divided into 3 groups according to the first and third quantile of the SUA level quartiles, and the baseline data of clinical and laboratory examinations were compared. The correlation between SUA level and clinical indicators was analyzed by Pearson correlation coefficient. Kaplan-Meier method and Cox proportional hazard regression model were used to examine the association between SUA and all-cause mortality and cardiovascular mortality in MHD patients. Results A total of 201 patients were enrolled in the study. The age of the patients was (56.9 ± 16.7) years and the baseline SUA level was (531.1±137.9)μmol/L. Patients were divided into 3 groups with the first quantile (442μmol/L) and the third quantile (620 μmol/L) of the SUA quartiles as the boundary points: group 1 (SUA<442 μmol/L, n=52), group 2 (SUA 442-620 μmol/L, n=101) and group 3 (SUA>620 μmol/L, n=48). The results showed that the patients in group 1 were older and had more proportion of patients with diabetes mellitus and cardiovascular diseases than those in group 3 (all P<0.05). Compared to group 3, the serum albumin, serum phosphorus and serum creatinine were lower in group 1, while the hypersensitive C-reactive protein was higher (all P<0.05). Pearson correlation analysis showed that SUA level was positively correlated with albumin (r=0.135, P=0.047), blood phosphorus (r=0.269, P<0.001) and serum creatinine (r=0.333, P<0.001), and negatively correlated with hypersensitive C-reactive protein (r=-0.216, P=0.002). After a median follow-up of 49.8 months, 66(32.8％) all-cause deaths and 32 (15.9％) cardiovascular deaths were recorded. Kaplan-Meier method showed that with the decrease of SUA, all-cause mortality (Log-rank χ2=18.27, P<0.001) and cardiovascular mortality (Log-rank χ2=15.04, P=0.001) increased. After adjusting for age, gender, comorbidity and other factors using the Cox proportional hazards model, the all-cause mortality and cardiovascular mortality decreased by 20.1％(HR=0.799, 95％CI 0.651-0.980, P=0.031) and 29.6％(HR=0.704, 95％CI 0.524-0.946, P=0.020) for each 100μmol/L increase in baseline SUA. Compared to group 1, all-cause mortality (HR=0.332, 95％CI 0.142-0.774, P=0.011) and cardiovascular mortality (HR=0.140, 95％CI 0.030-0.657, P=0.013) were lower in the group 3. Conclusion Low SUA level increases the risk of all-cause mortality and cardiovascular mortality in MHD patients.
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Objective To summarize the experience in diagnosis and treatment of donor bile leakage after living donor liver transplantation. Methods Clinical data of 95 donors underwent living donor liver transplantation were retrospectively analyzed.Postoperative complications of bile leakage were observed,and clinical performance,treatment methods and therapeutic effects were analyzed. Results Bile leakage occurred in 9 donors of 95 donors with liver transplantation,and the incidence was 9%.The location of donor liver was left lateral lobe in 9 cases with bile leakage,all of which were delayed bile leakage of liver section.The clinical performance showed no typical bile peritonitis with increased serum bilirubin.All patients were cured after treatment of percutaneous puncture drainage or drainage tube retention,and there were no cases underwent second operation and death cases. Conclusions Changes in donor liver function and hepatic artery hemodynamics shall be monitored after living donor liver transplantation,and the donors with bile leakage shall be treated actively and will achieve favorable prognosis.
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Objective To investigate whether high glucose can induce endothelial-mesenchymal transition (EndMT) in glomerular endothelial cells and the role of TGF-β in the process.Methods Rat glomerular endothelial cells were divided into five groups:normal glucose (NG,5.5mmol/L),high glucose (HG,15,30 mmol/L),TGF-β inhibition (HG+ LY36,30 mmol/L glucose + 10 μmol/L LY364947),hyperosmotic control (M,5.5 mmol/L glucose+25.5 mmol/L mannitol) and solvent control (D,5.5 mmol/L glucose + 1 ml/L DMSO).Western blotting was performed to detect relative protein quantities of endothelial marker claudin 5 and mesenchymal marker α-smooth muscle actin (α-SMA).TGF-β1 and TGF-β2 mRNA levels were measured by real-time PCR.Vascular endothelial marker VE-cadherin and mesenchymal marker α-SMA were detected by immunofluorescent stain and observed by confocal microscopy.Results Compared with NG,the expression of claudin5 protein in HG (15 or 30 mmol/L) was up-regulated while expression of α-SMA protein was down-regulated (P ＜0.05).Both TGF-β1 and TGF-β2 mRNA levels increased as well (P ＜ 0.05).However,when compared with HG,the claudin 5 levels increased while α-SMA decreased in TGF-β inhibition group.No significant changes were observed in hyperosmotic or solvent control group.Confocal microscopy showed the transformation of cells from a cobblestone-liked shape to a spindle one,and a decreasing expression of VE-cadherin while an increasing α-SMA in HG group (P ＜ 0.05),whereas TGF-β inhibition partly attenuated those changes in both morphological and protein levels.Conclusions High glucose treatment of glomerular endothelial cells results in an increase in the level of TGF-β1 and TGF-β2 mRNA and leads to endothelial-mesenchymal transiton.Inhibition of TGF-β partly prevents this process,indicating that TGF-β plays a crucial role in high-glucose-induced glomerular endothelial-mesenchymal transiton.
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Objective To explore the effect of high glucose on the renin-angiotensin system (RAS) in rat glomerular endothelial cells and its probable mechanism.Methods Rat glomerular endothelial cells were stimulated by culture medium containing 5 mmol/L or 30 mmol/L glucose (with or without pre-treatment of captopril and chymostatin) for 12 h,24 h,48 h,72 h.ELISA,real-time PCR,Western blotting and confocal immunofluorescence microscopy were employed to examine the follows:the angiotensin Ⅱ (Ang Ⅱ ) concentration in cell lysate and the culture medium; the mRNA levels of angiotensinogen and renin; the protein levels of angiotensin Ⅱtype 1 receptor (AT1R),angiotensin Ⅱ type 2 receptor (AT2R),renin and angiotensinogen in cell lysate; localization of intracellular AT1R,AT2R and renin.Results Exposure to high glucose for only 12 h or 72 h resulted in a significant increase of Ang Ⅱ levels in the culture medium compared with control cells (P＜0.05),but only exposure to high glucose for 72 h resulted in a significant increase of Ang Ⅱ levels in the cell lysate compared with control cells (P＜0.05).However,exposure to high glucose for 24 h or 48 h had no effects on Ang Ⅱ levels in the cell lysate or culture medium.The captopril and chymostatin were able to antagonize high glucose induced Ang Ⅱ generation when exposure time was 72 h but not 12 h.Exposure to high glucoseincreased the mRNA level of angiotensinogen,but reduced the level of renin mRNA,meanwhile angiotensinogen protein increased,and AT1 protein reduced,but protein levels of AT2R and renin were unchanged.However,the transformation of AT2R from the cell nucleus to cytoplasm was observed.Conclusions High glucose can activate the local renin-angiotensin system in rat glomerular endothelial cells,and the probable mechanism may contribute to ACE and non-ACE pathways.The effects of high glucose on glomerular endothelial cells may also involve in the substrate and receptors of Ang Ⅱ.
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Objective To investigate the effect of advanced glycation end products (AGEs) on the disruption of tight junctions in rat glomerular endothelial cells (rGEnCs) and the role of renin-angiotensin system (RAS) in this pathological procedure.Methods Primary cultured rGEnCs were incubated with AGEs at concentrations of 20 mg/L,40 mg/L and 80 mg/L,for 6 h,12 h and 24 h respectively.The cells were treated with captopril (1 mmol/L) or valsartan (10 μ mol/L)to block RAS.The endothelial permeability was investigated by transendothelial electrical resistance and the flux of fluorescein isothiocyanate-conjugated bovine serum albumin.The expression of AGEs receptor (RAGE),tight junction proteins [occludin,claudin-5,junctional adhesion molecules A (JAM-A) and zona occludens-1 (ZO-1)]and RAS components [angiotensinogen,renin and angiotensin Ⅱ type 1 receptor (AT1)]were detected by Western blotting.Immunofluorescence was used to demonstrate the disruptions of the tight junction proteins.The activity of angiotensin converting enzyme (ACE) was evaluated by UV spectrophotometry.Angiotensin Ⅱ (Ang Ⅱ ) was measured by enzyme immunoassay.Results The monolayer permeability,the expression of RAGE,the activity of ACE,the concentration of Ang Ⅱ and the expression of AT1 of rGEnCs were increased after induced by AGEs.Meanwhile,AGEs decreased the expression of occludin,claudin5 and JAM-A and induced disruption of tight junction proteins.Pretreatment with anti-RAGE antibody (100 mg/L),captopril or valsartan could attenuate the detrimental effect of AGEs.Conclusion The changes of permeability induced by AGEs in glomerular endothelial cells are partly mediated by RAS through RAGE.