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  • 2015 Volue 31 Issue 7      Published: 15 July 2015
      

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    Objective    To investigate the value of clinical parameters in predicting the initiation of renal replacement therapy(RRT) in acute kidney injury (AKI) patients with cardiorenal syndrome (CRS).    Methods    A total of 75 AKI patients hospitalized with CRS were enrolled. All patients received pharmacologic therapy on the beginning 3 days. The patients whose heart function improved were divided into control group (n=39), and the patients whose heart function worsened were divided into RRT group (n=36). Clinical and laboratory data on the first day and the fourth day were collected and analyzed. The factors on the first day were labeled as “Ⅰ”, and those on the fourth day were labeled as “Ⅱ.” The ratio of some parameters calculated were labeled as “Ⅱ/Ⅰ”. Area under curve (AUC) of receiver operating characteristic curve (ROC) of these factors was used to evaluate the sensitivity and specificity in predicting the initiation of RRT.    Results   The patients in RRT group had significantly higher levels of BNP-Ⅱ, BNPⅡ/Ⅰand creatinineⅡ/Ⅰ(P<0.01), and lower levels of 24 hours urine volume-Ⅰ and 24 hours urine volume-Ⅱ(P<0.01). From ROC curve analysis, the AUC of 24 hours urine volume-Ⅰ, 24 hours urine volume-Ⅱ, creatinineⅡ/Ⅰ, BNP-Ⅱlevels and BNPⅡ/Ⅰ to predict RRT were 0.736, 0.875, 0.747, 0.779 and 0.894 respectively. When the cutoff values of 24 hours urine volume-Ⅰ, 24 hours urine volume-Ⅱ, BNP-Ⅱlevels, BNPⅡ/Ⅰ and creatinineⅡ/Ⅰ were 905 ml (sensitivity 75%, specificity 94.9%), 1450 ml (sensitivity 75%, specificity 100%), 3360 ng/L (sensitivity 72.2%, specificity 100%), 1.37 (sensitivity 75%, specificity 100%) and 1.25 (sensitivity 72.2%, specificity 94.4%) respectively, the value of the parameters to predict RRT was high.   Conclusions    The 24 hours urine volume, BNP levels after treatment and the dynamic changes of BNP levels and creatinine levels can be used as predictors of the initiation of RRT in the AKI patients with CRS.

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    Objective    To analyze the early renal function of donors after nephrectomy. Methods    Clinical data of 467 cases of living kidney donors during the period from April, 2010 and November, 2014 in our center were retrospectively analyzed. Data on serum creatinine (Scr), glomerular filtration rate (GFR), serum uric acid (UA), and urine microproteins before operation and three days, seven days, one month and three months after operation were collected to evaluate the impact of nephrectomy on early renal function after operation for donators.    Results    Before operation and three days, seven days, one month, three months after operation, the average serum creatinine (Scr) level was (59.9±12.8), (85.8±21.0), (91.2±21.3), (92.8±21.6), (91.0±21.3) μmol/L, respectively; The GFR were (113.5±25.3), (75.1±17.9), (70.3±15.2), (68.5±16.0), (69.5±15.1) ml/min, respectively; The levels of uric acid were (292.60±79.58), (142.18±55.28), (228.41±66.39), (321.31±83.72), (346.61±87.21) μmol/L, respectively; All these data above-mentioned after operation reached statistical significance compared with that before operation (P<0.05). Parameters including urine IgG, urine albumin, urine retinol-binding protein and urine β2-microglobulin post-operation time point were significantly different when compared with relative parameters pre-operation (P<0.05).    Conclusions    Nephrectomy has significant influence on GFR, uric acid, and urine microprotein for donors in the early stage after operation. It's worth to evaluate nephrectomy's long-term effect on the renal function of donors in clinical practice.

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    Objective    To investigate the serum level of placental growth factor (PLGF) and explore its relationship with left ventricular structure and function in chronic kidney disease (CKD) patients.    Methods    Seventy-two non-dialysis CKD patients and sixteen age- and sex- matched healthy controls were included in this study. Serum PLGF level was measured by ELISA. Cardiac structure and function were assessed by two dimensional echocardiography.    Results    (1)The serum level of PLGF in CKD patients[3.32(2.97, 19.77) ng/L] was significantly higher compared to the healthy controls [2.33(2.27, 2.49) ng/L] (P<0.01). It progressively increased  with the decline of renal function (P<0.05/6). (2)The interventricular septum (IVS), left ventricular posterior wall (LVPW) was significantly higher while the ejection  fraction was significantly lower in CKD patients. (3)The serum PLGF level was higher in patients with left ventricular hypertrophy (LVH) than those without LVH [19.05(3.31, 21.05) ng/L vs 2.99(2.60, 3.32) ng/L, P<0.05]. The prevalence of LVH in the group above median PLGF level was significantly higher than that in the group below the median PLGF level (70% vs 18%, P<0.01). (4)PLGF level was positively correlated with left ventricular mass index (LVMI), systolic pressure, diastolic pressure, 24 h urine protein, Scr, UA, BUN, iPTH, the history of high blood pressure and was negatively correlated with LVEF, hemoglobin, albumin, eGFR (P<0.05). Multiple regression results showed that UA, Scr, LVEF, Hb were associated with PLGF level independently (P<0.01).    Conclusions    CKD patients have elevated level of PLGF. It has a relationship with cardiac structure and function. It may participate in the occurrence of cardiovascular events.

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    Objective    To investigate the long-term outcome of Chinese lupus nephritis (LN) patients undergoing peritoneal dialysis (PD).    Methods    All LN patients with end-stage renal disease (ESRD) initiating PD between May 1, 1995 and Apr 30, 2013 at Renji Hospital, Shanghai Jiao Tong University School of Medicine, China, with complete data (n=33) were enrolled. Another 33 age-, gender- and comorbidity-matched non-LN patients receiving PD were selected as the control group for the study. All patients were followed up from the date of PD initiation until death, cessation of PD, transfer to other centers or the end of this study (Dec 31, 2013). Kaplan-Meier analysis and Log-Rank test were applied to compare patient survival, technique survival and peritonitis-free survival between two groups.    Results    Compared to the control group, LN patients had higher eGFR, anti-dsDNA and hs-CRP level at the starting of PD. By the end of the study, in the LN group 13 (39.4%) patients died, 8(24.2%) patients switched to hemodialysis (HD), 5(15.2%) patients transplanted and 2(6.1%) patients transferred to other centers. Infection was the most common cause of death in the LN group (9 patients, 69.2%), and majority of death was caused by PD-related peritonitis (6 patients, 46.2%), while cardiovascular disease (CVD) was the leading cause of death in the control group (5 patients, 83.3%). Kaplan-Meier analysis showed that LN patients had significantly lower patient survival (χ2=8.455, P=0.004). For both LN group (6 patients, 75.0%) and control group (4 patients, 66.7%), peritonitis was the leading cause of transfer to HD. Compared to the control group, LN patients had significantly lower technique survival (χ2=6.753, P=0.009). Peritonitis rates were 1 episode/20.5 patient-months in the LN group and 1 episode/67.6 patient-months in the control group respectively. LN patients had significantly shorter peritonitis-free survival (χ2=8.256, P=0.004) when compared to their counterparts in the control group.    Conclusion      LN patients with ESRD receiving PD have inferior clinical outcome. Peritonitis is the most common cause of death and technique failure in LN patients.

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    Objective    To investigate the expression and clinical significance of serum microRNA (miRNA) expression profiling in the occurrence and progression of diabetic nephropathy.    Methods     The miRNA expression profiling was detected by miRNA TaqMan Low Density Array chip from 10 patient with diabetic nephropathy, 10 diabetes patients with normoalbuminuria and 10 health control. Real-time quantitative PCR was applied to verify the result of miRNA array in serum samples of 66 patients with diabetic nephropathy (36 patients with microalbuminuria, 30 patients with macroalbuminuria), 40 diabetes patients with normoalbuminuria and 40 health control. And the relationship of differetial expression with clinical features was analyzed.    Results    miR-150-5p, miR-155-5p, miR-30e-5p and miR-3196 being validated by real-time quantitative PCR differentially expressed in 3 groups of serum samples from the diabetes patients with microalbuminuria (n=36), with normoalbuminuria (n=40) and health control (n=40) (P<0.05). Serum miR-150-5p (P=0.005) and miR-155-5p (P=0.006) changed significantly between diabetes patients with microalbuminuria (n=36) and with macroalbuminuria (n=30). Compared with the diabetes patients with microalbuminuria, serum miR-150-5p and miR-155-5p increased by 2.3 and 1.5 times in macroalbuminuria group, respectively. Estimated glomerular filtration rate and urinary albumin excretion rate significantly correlated with serum miR-150-5p and miR-155-5p level.    Conclusions    miR-150-5p and miR-155-5p may be involved in the process of pathological mechanisms of diabetic nephropathy. Serum miR-150-5p and miR-155-5p may be regarded as potential biomarkers to diagnosis the occurrence and development of diabetic nephropathy.

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    Objective    To investigate the effects of β-adrenoceptor (β-AR) activation on the apoptosis in human mesangial cells and it’s mechanism.    Methods    Cultured HMC were used in experiments and were divied into four groups: the control group; β-AR activation (β-AR agonist NE/Pra) group; β-AR inhibitor (Prop) group;antioxidants group. The experiments technology including PCR, confocal scanning microscope, immunofluorescence and Tunel.    Results    The results of RT-PCR and confocal scanning microscope showed that β1-AR and β2-AR were expressed in human HMC. β-AR activation induced reactive oxygen species (ROS) increase in human MCs, the relative levels of ROS were elevated as early as 0.5 h after β-AR activation, and gradually increased and peaked at 4 h on a concentration and time dependent manner. Tunel results demonstrated that β-AR activation induced apoptosis with ROS on a concentration and time dependent manner, β-AR blocking agent-propranolol significantly inhibited β-AR activation induced apoptosis. Antioxidants including vitamin C and NAC could inhibited β-AR activation induced apoptosis (all P<0.01).    Conclusions    β-AR is functionally expressed in human mesangial cell, furthermore β-AR activation-induced ROS increase mediate apoptosis. Antioxidants can inhibit β-AR activation induced apoptosis.

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    Objective    To investigate the effect of high mobility group box chromosomal protein 1 (HMGB1) knockdown on improving renal function and decreasing cell proliferation of glomeruli in lupus nephritis (LN) MRL/Faslpr mice.    Methods    Twenty-four MRL/Faslpr mice were randomly divided into 3 groups: LN model group, shHMGB1 group and  empty plasmid group. Besides, eight MRL/MpJ mice, age and mass matched to the MRL/Faslpr mice, were chosen as normal control group (shNC group). Electroporation technology was used for in vivo transfection in treatment group.shHMGB1 group and empty plasmid group were transfected by electroporation technology for shHMGB1 plasmids and empty plasmid, LN model group and normal control group were transfected only with saline. Automatic biochemical analyzer was used to detect serum urea nitrogen (BUN) and creatinine (Scr) levels and  24 h urinary protein (UP) was tested. HE staining was used to detect the pathological change of renal tissues; real-time PCR, immunofluorence staining and Western blotting were used to detect the mRNA and protein expression of HMGB1 and PCNA.    Results    (1) The HMGB1 mRNA and protein expression in LN group increased compared with those in control group, HMGB1 mRNA and protein expression in shHMGB1 group reduced compared with those in LN model group (all P﹤0.05). (2) 24 h UP of MRL/Faslpr mice in shHMGB1 group significantly reduced compared with those in LN group (P﹤0.05). (3) Immunofluorence and Western blotting showed that positive signal of proliferating cell nuclear antigen (PCNA) was mainly located in nuclei, PCNA mRNA and protein in glomeruli of LN model group increased compared with those of control mice (P﹤0.05). Interestingly, PCNA expression in glomeruli of shHMGB1 group remarkably reduced (P﹤0.05).    Conclusions    shHMGB1 significantly improves renal function and decreases cell proliferation of glomeruli in LN MRL/Faslpr mice.

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    Objective    To investigate the effects of the fibrin-derived peptide Bβ15-42 (FgBβ15-42) on renal inflammation in acute kidney injury (AKI) induced by renal ischemia reperfusion (IR).    Methods    SD rats were randomly divided into sham group (the abdominal cavity were closed after separating the renal artery), IRI group (renal arteries of rats were occluded with microvascular clamps for 60 min), negative treated group (rats were injected with 3.6 mg/kg random peptide by tail vein) and FgBβ15-42 treated group (rats were injected with 3.6 mg/kg FgBβ15-42 by tail vein). Rats were sacrificed at 24 h or 48 h after reperfusion. Blood and kidney samples were collected and histological changes and renal function were examed. The mRNA and protein expressions of  intercellular cell adhesion molecule-1 (ICAM-1) and interleukin-1β (IL-1β ) were examined by immunohistochemistry, real-time PCR and Western blotting.    Results    Compared with sham group,Scr and BUN were obviously increased in IRI group (all P<0.05),  pathologic changes of kidney were more serious (P<0.05). Compared with IRI group, in FgBβ15-42 treated group Scr and BUN were obviously decreased (all P<0.05), the injury of kidney tubulointerstitial was less serious (P<0.05). Compared with sham group, there was increased ICAM-1 and IL-1β in IRI group (all P<0.05), and they all peaked at 24 h. After treated with FgBβ15-42, the expression of ICAM-1, IL-1β were significantly decreased in kidneys compared to IRI group (all P<0.05).    The above indexes had no significant differences between negative treated group and IRI group (all P>0.05).    Conclusions    FgBβ15-42 can protect kidneys against ischemia reperfusion injury in rats. The mechanism may be associated with down-regulated expressions of ICAM-1 and IL-1β in the kidney.