Objective To compare the diuretic efficacy of torasemide as a 2-hour continuous infusion and as a bolus injection of equal dose in patients with nephrotic syndrome,and to investigate a preferable administration mode of torasemide for these patients.Methods Twenty-three hospitalized patients were randomized to receive torasemide 20 mg or 40 mg per day by either 2-hour intravenous infusion or bolus injection,and interchanged after 48 hours of washout.Results Patients received torasemide by 2-hour intravenous infusion exhibited significantly higher daily urinary volume,chloride excretion,sodium excretion and fractional excretion of sodium (FENa) within 24 hours than those by bolus injection (P ＜ 0.05).Significantly lower bound-state torasemide excretion,higher ratio of urinary volume to torasemide excretion and a markedly larger area under the curve in the plasma concentrationtime profiles were also observed in the infusion group (P ＜ 0.05).Conclusion 2-hour continuous infusion delivers a better diuretic effect compared with a bolus injection of equal dose of torasemide in patients with nephrotic syndrome.

Objective: To explore the role of ROCK1 in oxidized low-density lipoprotein (ox-LDL) induced podocyte injury and its possible mechanism. Methods: The conditionally immortalized mouse podocyte cells were cultured in vitro and exposed to 20 μg/ml ox-LDL for 24 h. Western blotting was used to analyze the expression level of p-MYPT, nephrin, LC3-Ⅱ, p62, p-ULK1 in groups of control, ox-LDL, ROCK1 siRNA with ox-LDL, wtROCK1 with ox-LDL. Podocytes were incubated with DiI labeled ox-LDL for 4 h and fluorescence microscope was used to analyze lipid distribution. Results: Compared with control group, ox-LDL increased cell cholesterol accumulation, activated ROCK along with decreased nephrin, LC3-Ⅱ(P<0.05), and increased p62, and p-ULK1 expression (P<0.05). Over-expression of ROCK1 significantly decreased the expression of nephrin and LC3-Ⅱ, but up-regulated the levels of p62, p-ULK1 and cell cholesterol accumulation in ox-LDL stimulated podocytes (P<0.05). In contrast, Inhibition of ROCK1 protected podocyte by improved lipophagy. Conclusion ROCK1 mediated disfunction of lipophagy contributes to the ox-LDL induced podocyte injury.

Objective To find the differentially expressed long non-coding RNA (lncRNA) between db/db mice that with nephropathy (DN) or not (DM).Methods In this study,3 DM db/db mice and 2 DN db/db mice proven by renal biopsy were randomly selected,and 3 healthy db/m mice as normal control group.Then,differentially expressed lncRNAs,mRNAs and their fragments per kilobase million (FPKM) in kidney samples were detected by high-throughput next generation sequencing technology.Sequencing data were analyzed to filter out the differentially expressed lncRNA,and theirfunction was preliminarily investigated by bioinformatics analysis and functional enrichment analysis to predict their target genes.Total RNAs of kidneys from these 8 mice were extracted to run real time PCR (RT-qPCR) for verifying the outcomes of the high-throughput sequencing.Results The urinary microalbumin/creatinine ratio (UACR),serum creatinine,and glomerular basement membrane thickness of DN db/db mice were higher than those of DM db/db mice (all P ＜ 0.05),while there was not significant difference in glucose between DM and DN mice.Totally 160 lncRNAs were up-regulated and 99 lncRNAs were down-regulated in kidneys of DN mice compared with those of DM mice,in which the differentially expressed lncRNAs with FPKM value≥2 and differential expression≥ 1 fold between groups were screened and verified by RT-qPCR.Finally three lncRNAs whose variation trend were consistent with the outcomes of the high-throughput sequencing were obtained.Conclusion There was a significantly different expression pattern of lncRNA between the kidneys of DN and DM mice,which may be involved in the progress of DN.

Objective To evaluate the effect of over-expression of phosphatase and tensin homolog does on chromosome ten (PTEN) in podocytes on kidney under high fat diet (HFD) in vivo and clarify the mechanism how PTEN regulates scavenger receptor A (SR-A) expression exposed to oxidized low density lipoprotein (ox-LDL) in podocytes in vitro.Methods The podocyte-specific PTEN knockin (PPKI) mice were fed with HFD to establish mouse model of lipid-induced renal injury.Mice were divided into four groups:ND+Ctrl group,ND+PPKI group,HFD+Ctrl group and HFD+PPKI group.After 24 weeks of dietary intervention,all mice were tested for clinical and biochemical parameters,including serum creatinine (Scr) as well as urine albumin excretion rate (UAER);renal lipid content was measured by oil red O staining and cholesterol quantitative analysis;the pathological changes of glomeruli were observed by PAS staining and electron microscope.Podocyte injury was induced by ox-LDL in vitro.Western blotting was used to detect the changes of SR-A expression induced by ox-LDL after YAP-siRNA interfering (si-YAP),as well as YAP phosphorylation induced by ox-LDL after interfering by PTEN-siRNA (si-PTEN) and PTEN phosphatase inhibitor (Bpv-PTEN),and overexpressing by recombinant adenovirus (ad-PTEN).Results Compared with ND+Ctrl group,HFD+ Ctrl group significantly aggravated the levels of Scr and UAER,the expression of SR-A in podocytes,renal lipid content,mesangial matrix expansion,effacement of podocyte foot processes,and incrassation of glomerular basement membrane (all P ＜ 0.05).Conversely,compared with HFD+Ctrl group,HFD+ PPKI group obviously alleviated the above lipid-induced renal damage (all P ＜ 0.05).In vitro,the expression of SR-A in podocytes was up-regulated when stimulated with ox-LDL (P ＜ 0.05),and the knockout of YAP significantly down-regulated the expression of SR-A induced by ox-LDL (P ＜ 0.05).Exposed to ox-LDL,the expression of p-YAP increased in podocytes (P ＜ 0.05);over-expression of PTEN inhibited p-YAP up-regulation induced by ox-LDL (P ＜ 0.05),while either knockdown of PTEN or inhibition of PTEN phosphatase activity displayed opposite effect (all P ＜ 0.05).Conclusions Over-expression of PTEN in podocytes protected the kidney against damage from HFD in vivo and PTEN might suppress SR-A mediated lipid uptake via dephosphorylating p-YAP to prevent podocyte injury from ox-LDL.

Objective: To identify the anatomical positional relation of the internal jugular vein and the common carotid artery, and investigate the predictive factors associated with the stenosis rate of the internal jugular vein after catheterization in hemodialysis patients. Methods: A single-center cross-sectional survey study of 235 patients from the Department of Nephrology, Guangdong Provincial People's Hospital between August 2017 and June 2018 was performed. According to whether received hemodialysis treatment, The patients were divided into dialysis group (n=187) and control group (chronic kidney disease non-dialysis patients, n=48). Clinical data such as age, primary disease, history of deep vein catheterization, catheter indwelling time and dialysis age were collected. The positional relationship between the internal jugular vein and the common carotid artery was examined by Doppler ultrasound. Measure the cross-sectional area of the internal jugular vein in different neck anatomical planes and analyse of the incidence of internal jugular vein stenosis in the dialysis group. Chi-square test was used to compare the differences in the incidence of internal jugular vein stenosis between subgroups of different ages, with or without catheter retention, catheter indwelling time, dialysis age and presence or absence of diabetic nephropathy. Results: Doppler ultrasonography showed that in the 235 patients, there were four types of anatomical relationship between the internal jugular vein and the common carotid artery in the plane of the flat thyroid cartilage and the apex plane of the upper clavicle. The internal jugular vein was located on the lateral, anterolateral, anterior and medial sides of the common carotid artery, accounting for 16.23%, 36.52%, 41.11% and 3.14% respectively. There were significant differences in the anatomical relationship between the internal jugular vein and the common carotid artery between the left and right sides, different anatomical planes and patients of different ages (P<0.05). The rate of internal jugular vein stenosis in 187 hemodialysis patients was 47.1%. The right internal jugular vein stenosis rate was 66.4% and 44.1% in the age<65 years old group (n=128) and age≥65 years old group (n=59), respectively (P=0.004). The rate of internal jugular vein stenosis was 49.0% and 32.8% (P=0.018) in the catheter placement group (n=151) and the catheterless retention group (n=36), respectively. Two variables including age and history of catheterization were included in the logistic regression equation. The results showed that the history of catheterization was a risk factor for internal jugular vein stenosis (OR=1.668, 95% CI 1.083-2.568, P=0.020). Conclusions There is variability in the anatomical relationship between the internal jugular vein and the common carotid artery. Internal jugular vein stenosis is a common complication after indwelling catheters in hemodialysis patients. The history of internal jugular vein catheterization is a risk factor affecting internal jugular vein stenosis.