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Objective To examine the correlation of serum neutrophil gelatinase-associated lipocalin (NGAL) with dialysis adequacy,microinflammatory state and iron metabolism,and to assess the value of NGAL in identifying the dialysis adequacy in maintenance hemodialysis (MHD) patients.Methods A total of 150 MHD patients and 50 healthy control people were enrolled in the study.Clinical data were collected and serum NGAL,CRP,transferrin saturation,serum ferritin were measured.MHD patients were divided into adequacy group and non-adequacy group according to spKt/V value.Serum NGAL between two groups was compared and correlation of NGAL with spKt/V,inflammatory factors,and other clinical indexes was examined by Pearson,multivariate regression Logistic model and area under curve (AUC) of ROC.MHD patients were followed up for 3 months.Similar correlation analysis was carried out before and after follow up between two groups.Results Serum NGAL of MHD patients was higher compared to healthy people [(445.45±50.34) μg/L vs (50.02 ±6.45) μg/L].Among 150 MHD patients,95 were classified into adequacy group,while 55 into non-adequacy group according to spKt/V value.Serum NGAL was significantly higher in adequacy group as compared to non-adequacy group [(589.14±56.34) μg/L vs (360.13±46.23) μg/L,P＜0.05].Serum NGAL was positively correlated to spKt/V,CRP,TSAT [r=0.652,0.825,0.785,all P＜0.05],but not to serum ferritin.Serum NGAL was also correlated to spKt/V,CRP,TSAT by multivariate regression Logistic model.AUC showed that NGAL level could reflex the condition of dialysis adequacy.During the follow up,all adequacy patients remained the same adequacy status.Thirty-eight out of 55 non-adequacy patients were qualified for complete adequacy after intervention.The serum NGAL before and after intervention was (368.14±56.21) μg/L and (360.56±46.23) μg/L respectively without significant difference.Conclusions Serum NGAL is obviously higher in MHD patients with dialysis adequacy compared to those without dialysis adequacy.Serum NGAL is positively correlated to spKt/V,CRP,TSAT.NGAL can reflex the condition of dialysis adequate in MHD patients.
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Objective To investigate the effect of parathyroid hormone (PTH) on the transition and connective tissue growth factor (CTGF) expression of human renal proximal tubular epithelial cell line HK-2 . Methods The expression of CTGF mRNA and protein of HK-2 cells were measured by real time RT-PCR and Western blot respectively . The effect of PTH on the phenotypic transformation of HK-2 cells was examined by light microscopy . The expression of α-smooth muscle actin (α-SMA) in HK-2 cells was detected by immunofluorescence . Results Basal level of CTGF mRNA and the protein expression were detected in HK-2 ceils . PTH upregulated the expression of CTGF mRNA and protein with the maximal response at the concentration of 10-10 mol/L and the best stimulating time was at 72 h . After exposure to PTH (10-10tool/L) for 12 hours, the highest level of luciferase activity was 1 .96 fold as compared to control (1 .888±0 .078 vs 0 .989±0 .030, P＜0 .01 ) . Untreated cells showed negligible expression of ±-SMA,whereas ±-SMA expression was significantly increased in cells treated with PTH . Conclusion PTH up-regulates CTGF expression and induces transition of HK-2 cells .
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Objective To evaluate the effect of parathyroid hormone (PTH) on the expression of connective tissue growth factor (CTGF) in human renal tubular epithelial cells, and to explore the role of MAPK signaling pathway. Methods Real time RT-PCR, Western blot, and reporter gene assay were employed to detect PTH-induced CTGF expression in HK-2 cells. Inhibitors (PD98059 and U0126) of MAPK signaling pathway were used to confirm involved signal pathway. Results HK-2 cells had basic expression level of CTGF mRNA and protein, which were increased significantly after treatment with PTH. The luciferase activity was up-regulated to a higher level as compared with control group after treatment with 10-10 mol/L PTH for 12 h [(1.8884±0.0780) vs (0.9891±0.0300) A, P<0.01]. Moreover, a small amount of p-ERK1/2 was detected in normal HK-2 cells, but it was increased significantly in response to PTH activation, most remarkably when treated with 10-10 mol/L PTH for 30 min. Inhibitors of MAPK signaling pathway, PD98059 and U0126, noticeably inhibited the expression of CTGF mRNA and protein as well as gene promoters in HK-2 cells. Conclusion PTH can induce higher expression of CTGF in HK-2 cells probably via MAPK signaling pathway.
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25 is also an important impact factor among various components.