Lin Sun

The Second Xiangya Hospital of Central South University, Ch’ang-sha-shih, Hunan, China

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Publications (96)260.42 Total impact

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    ABSTRACT: To evaluate the impact of RA on work capacity and identify factors related to work capacity impairment in patients with RA. A cross-sectional multicentre study was performed in 21 tertiary care hospitals across China. A consecutive sample of 846 patients with RA was recruited, of which 589 patients of working age at disease onset constituted the study population. Information on the socio-demographic, clinical, working and financial conditions of the patients was collected. Logistic regression analyses were used to identify factors associated with work capacity impairment. The rate of work capacity impairment was 48.0% in RA patients with a mean disease duration of 60 months (interquartile range 14-134 months), including 11.7% leaving the labour force early, 33.6% working reduced hours and 2.7% changing job. Multivariable logistic regression analysis showed that reduced working hours was significantly related to current smoking [odds ratio (OR) 2.07 (95% CI 1.08, 3.97)], no insurance [OR 1.94 (95% CI 1.20, 3.12)], in manual labour [OR 2.66 (95% CI 1.68, 4.20)] and higher HAQ score [OR 2.22 (95% CI 1.36, 3.60)]. There was an association of current smoking [OR 3.75 (95% CI 1.54, 9.15)], in manual labour [OR 2.33 (95% CI 1.17, 4.64)], longer disease duration [OR 1.01 (95% CI 1.00, 1.01)] and lower BMI [OR 0.90 (95% CI 0.82, 0.99)] with leaving the labour force early. There is a substantial impact of RA on the work capacity of patients in China. Social-demographic, disease- and work-related factors are all associated with work capacity impairment. © The Author 2015. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
    Rheumatology (Oxford, England) 03/2015; DOI:10.1093/rheumatology/kev014 · 4.44 Impact Factor
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    ABSTRACT: Abstract Ophiocordyceps sinensis (O. sinensis; syn. Cordyceps sinensis) has been used in clinical therapy for diabetic kidney disease (DKD) for more than 15 years. O. sinensis is a household name in china and it is available even in supermarket. However, the precise role of O. sinensis has not been fully elucidated with meta-analysis. The aim of this study was to review existing evidence on the effectiveness of O. sinensis for the treatment of DKD. We identified 60 trials involving 4288 participants. Overall, O. sinensis combined with ACEI/ARB had a better effect when compared to ACEI/ARB alone on 24 h UP (MD = -0.23 g/d, 95% CI: - 0.28 to -0.19, p < 0.00001), UAER (MD = -19.71 μg/min, 95% CI: -22.76 to -16.66, p < 0.00001), MAU (MD = -45.09 mg/d, 95% CI: -55.68 to -34.50, p < 0.00001), BUN (MD = -0.70 mmol/L, 95% CI: -1.02 to -0.39, p < 0.0001), SCr (MD = -8.37 μmol/L, 95% CI: -12.41 to -4.32, p < 0.0001), CRP (MD = -1.32 mg/L; 95% CI: -1.78 to -0.86; p < 0.00001), TG (MD = -0.51 mmol/L; 95% CI: -0.69 to -0.34, p < 0.00001), TC (MD = -0.64 mmol/L; 95% CI: -0.91 to -0.37, p < 0.00001), and SBP (MD = -2.01 mmHg; 95% CI: -3.45 to -0.58, p = 0.006). However, no effects were found for DBP, FBG, and HbA1C. This meta-analysis suggested that use of O. sinensis combined with ACEI/ARB may have a more beneficial effect on the proteinuria, inflammatory, dyslipidemia status as compared to ACEI/ARB alone in DKD III-IV stage patients, while there is no evidence that O. sinensis could improve the hyperglycemia status. However, with regard to low-quality and significant heterogeneity of included trials, to further verify the current results from this meta-analysis, long-term and well-designed RCTs with high-quality study are warranted to ascertain the long-term efficacy of O. sinensis.
    Renal Failure 02/2015; DOI:10.3109/0886022X.2015.1009820 · 0.78 Impact Factor
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    ABSTRACT: The diabetic milieu is believed to change the activity, or result in damage of podocytes - a key component of the glomerular filtration barrier and known to secrete matrix for glomerular basement membrane. This in turn contributes to diabetic nephropathy. However, how podocyte dysfunction is triggered in diabetic nephropathy remains ambiguous. Galectin-1 belongs to Galectin family that bind to β-galactoside residues of glycosylated proteins. We explored whether Galectin-1 is dysregulated in diabetic nephropathy using 3 different techniques, namely real-time polymerase chain reaction, western blotting and immunofluorescent staining, to follow the expression of Galectin-1 under high glucose levels in podocytes. High glucose consistently induced Galectin-1 expression. Immunohistochemistry using a Galectin-1-specific antibody also showed elevated Galectin-1 in renal tissues of diabetic patients with manifestation of nephropathy, indicating a correlation of Galectin-1 overexpression with diabetic nephropathy. Upregulation of Galectin-1 is associated with loss of podocin, which is important for the physiological function of podocytes and decreases in the renal tissues of diabetic nephropathy. Increased Galectin-1 is a causal event for the high glucose-induced loss of podocin, since silencing Galectin-1 in podocytes increased podocin expression in the presence of 25 mM glucose. Thus expression of Galectin-1 in diabetic nephropathy may serve as a marker and contribute to disease progression by interfering with podocin expression.
    Cell Biology International 02/2015; 39(2). DOI:10.1002/cbin.10363 · 1.64 Impact Factor
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    ABSTRACT: We report the outcome of a 52-year-old patient with diabetic nephropathy and receiving maintenance hemodialysis (HD) using low molecular weight heparin (LMWH) as an anticoagulant for 2 years. He presented right lower limb pain accompanied with difficulty in walking for 2 months, and had no history of bleeding tendency or trauma. Physical examination revealed marked swelling and tenderness on his right lower limb. By ultrasound and magnetic resonance imaging (MRI) diagnoses, the calf hematoma was diagnosed and identified with venous thrombosis. Following treatment with heparin-free HD, the swelling regressed and pain subsided, and a follow-up MRI showed complete dissolution of hematoma. However, similar symptoms recurred in the right upper limb after 2 months without any predisposition, he was just placed on HD with LMWH, and symptoms regressed following the aforementioned therapy. This suggests that HD patients, especially with diabetic nephropathy having extremity hematoma, should be watched for the development of spontaneous hemorrhage that can be differentially diagnosed by imaging tests, such as MRI, and can be effectively treated with heparin-free HD.
    Hemodialysis International 12/2014; DOI:10.1111/hdi.12246 · 1.36 Impact Factor
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    ABSTRACT: The aim of this study is to investigate the remission rate of rheumatoid arthritis (RA) in China and identify its potential determinants. A multi-center cross-sectional study was conducted from July 2009 to January 2012. Data were collected by face-to-face interviews of the rheumatology outpatients in 28 tertiary hospitals in China. The remission rates were calculated in 486 RA patients according to different definitions of remission: the Disease Activity Score in 28 joints (DAS28), the Simplified Disease Activity Index (SDAI), the Clinical Disease Activity Index (CDAI), and the American College of Rheumatology/European League Against Rheumatism (ACR/EULAR) Boolean definition. Potential determinants of RA remission were assessed by univariate and multivariate analyses. The remission rates of RA from this multi-center cohort were 8.6 % (DAS28), 8.4 % (SDAI), 8.2 % (CDAI), and 6.8 % (Boolean), respectively. Favorable factors associated with remission were: low Health Assessment Questionnaire (HAQ) score, absence of rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP), and treatment of methotrexate (MTX) and hydroxychloroquine (HCQ). Younger age was also predictive for the DAS28 and the Boolean remission. Multivariate analyses revealed a low HAQ score, the absence of anti-CCP, and the treatment with HCQ as independent determinants of remission. The clinical remission rate of RA patients was low in China. A low HAQ score, the absence of anti-CCP, and HCQ were significant independent determinants for RA remission.
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    ABSTRACT: Diabetic kidney disease (DKD) is associated with oxidative stress and mitochondrial injury. Myo-inositol oxygenase (MIOX), a tubular-specific enzyme, modulates redox imbalance and apoptosis in tubular cells in diabetes, but these mechanisms remain unclear. We investigated the role of MIOX in perturbation of mitochondrial quality control, including mitochondrial dynamics and autophagy/mitophagy, under high-glucose (HG) ambience or a diabetic state. HK-2 or LLC-PK1 cells subjected to HG exhibited an upregulation of MIOX accompanied by mitochondrial fragmentation and depolarization, inhibition of autophagy/mitophagy, and altered expression of mitochondrial dynamic and mitophagic proteins. Furthermore, dysfunctional mitochondria accumulated in the cytoplasm, which coincided with increased reactive oxygen species generation, Bax activation, cytochrome C release, and apoptosis. Overexpression of MIOX in LLC-PK1 cells enhanced the effects of HG, whereas MIOX siRNA or d-glucarate, an inhibitor of MIOX, partially reversed these perturbations. Moreover, decreasing the expression of MIOX under HG ambience increased PTEN-induced putative kinase 1 expression and the dependent mitofusin-2-Parkin interaction. In tubules of diabetic mice, increased MIOX expression and mitochondrial fragmentation and defective autophagy were observed. Dietary supplementation of d-glucarate in diabetic mice decreased MIOX expression, attenuated tubular damage, and improved renal functions. Notably, d-glucarate administration also partially attenuated mitochondrial fragmentation, oxidative stress, and apoptosis and restored autophagy/mitophagy in the tubular cells of these mice. These results suggest a novel mechanism linking MIOX to impaired mitochondrial quality control during tubular injury in the pathogenesis of DKD and suggest d-glucarate as a potential therapeutic agent for the amelioration of DKD.
    Journal of the American Society of Nephrology 09/2014; DOI:10.1681/ASN.2014050457 · 9.47 Impact Factor
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    ABSTRACT: BackgroundBacterial peritonitis is serious disease and remains a diagnostic challenge for clinicians. Many studies have highlighted the potential usefulness of procalcitonin (PCT) for identification of bacterial peritonitis, however, the overall diagnostic value of PCT remains unclear. Therefore, we performed a meta-analysis to assess the accuracy of PCT for detection of bacterial peritonitis.MethodsWe performed a systematic searched in MEDLINE, EMBASE, SCOPUS, China Biology Medicine Database (CBM), China National Knowledge Infrastructure Database (CNKI) and Cochrane databases for trials that evaluated the diagnostic role of PCT for bacterial peritonitis. Sensitivity, specificity and other measures of accuracy of PCT were pooled using bivariate random effects models.ResultsEighteen studies involving 1827 patients were included in the present meta-analysis. The pooled sensitivity and specificity of serum PCT for the diagnosis bacterial peritonitis were 0.83 (95% CI: 0.76–0.89) and 0.92 (95% CI: 0.87–0.96), respectively. The positive likelihood ratio was 11.06 (95% CI: 6.31–19.38), negative likelihood ratio was 0.18 (95% CI: 0.12–0.27) and diagnostic odds ratio (DOR) was 61.52 (95% CI: 27.58–137.21). The area under the receiver operating characteristic curve (AUROC) was 0.94. Use of a common PCT cut-off value could improve the DOR to 75.32 and the AUROC to 0.95. Analysis of the seven studies that measured serum C-reactive protein (CRP) indicated that PCT was more accurate than CRP for the diagnosis of bacterial peritonitis.ConclusionsOur results indicate that PCT determination is a relatively sensitive and specific test for the diagnosis of bacterial peritonitis. However, with regard to methodological limitations and significant heterogeneity, medical decisions should be based on both clinical findings and PCT test results.
    BMC Infectious Diseases 08/2014; 14(1):452. DOI:10.1186/1471-2334-14-452 · 2.56 Impact Factor
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    ABSTRACT: Matrix metalloproteinases (MMPs) are proteolytic enzymes belonging to the family of zinc-dependent endopeptidases that are capable of degrading almost all the proteinaceous components of the extracellular matrix (ECM). It is known that MMPs play a role in a number of renal diseases, such as, various forms of glomerulonephritis and tubular diseases, including some of the inherited kidney diseases. In this regard, ECM accumulation is considered to be a hallmark morphologic finding of diabetic nephropathy, which not only is related to the excessive synthesis of matrix proteins, but also to their decreased degradation by the MMPs. In recent years, increasing evidence suggest that there is a good correlation between the activity or expression of MMPs and progression of renal disease in patients with diabetic nephropathy in humans and in various experimental animal models. In such a diabetic milieu, the expression of MMPs is modulated by high glucose, advanced glycation end products (AGEs), TGF-β, reactive oxygen species (ROS), transcription factors and some of the microRNAs. In this review, we focused on the structure and functions of MMPs, and their role in the pathogenesis of diabetic nephropathy.
    Current Medicinal Chemistry 07/2014; DOI:10.2174/0929867321666140716092052 · 3.72 Impact Factor
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    ABSTRACT: A 28-year-old female suffered from nephrotic syndrome after a long-term use of mercury-containing, skin-lightening cream. The blood and urinary mercury content of this patient increased with use. Renal biopsy showed minimal change disease. Her symptoms were relieved 6 months after discontinuing use of the cream and receiving sodium dimercaptosulfonate and glucocorticosteroid treatments. Proteinuria disappeared, and blood and urinary mercury levels returned to normal. Previous reports of nephrotic syndrome caused by mercury-containing, skin-lightening creams have mostly been identified as be.ing due to membranous nephropathy. Minimal change disease has been reported in a few case reports published in the English language. Here we report a case of nephrotic syndrome with minimal change disease following exposure to a mercury-containing, skin-lightening cream. We also reviewed relevant published reports to summarize clinical features and treatments and to explore the possible mechanisms involved.
    Annals of Saudi medicine 05/2014; 34(3):257-61. DOI:10.5144/0256-4947.2014.257 · 0.71 Impact Factor
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    ABSTRACT: Emerging evidence has suggested that human peritoneal mesothelial cells (HPMCs) undergo epithelial‑mesenchymal transition (EMT) in peritoneal fibrosis. The molecular mechanisms underlying peritoneal fibrosis and the key molecules involved are not yet fully elucidated. In order to enhance the understanding of peritoneal fibrosis, the present study investigated the roles of integrin‑linked kinase (ILK) and glycogen synthase kinase 3β (GSK‑3β) in high glucose‑induced phenotypic alterations of HPMCs. It was observed that HPMCs exhibited a cobblestone morphology under normal glucose conditions, whereas under high glucose conditions they had a spindle morphology. Additionally, under high glucose conditions it was found that E‑cadherin expression was decreased and vimentin expression was increased in HPMCs, suggesting HPMCs underwent EMT. ILK expression in high glucose conditions was also increased in a dose‑ and time‑dependent manner. The role of ILK in the induction of EMT in HPMCs was further investigated using small interfering RNA (siRNA). Following knockdown of ILK gene expression by siRNA, low vimentin expression as well as high E‑cadherin expression were observed, suggesting that EMT was inhibited. ILK‑knockdown also inhibited phosphorylation of GSK‑3β. These results indicate that ILK‑knockdown inhibits EMT of HPMCs through inhibition of GSK‑3β phosphorylation. These findings suggest that ILK may be used as a novel diagnostic and therapeutic target for HPMC fibrosis in the future.
    Molecular Medicine Reports 04/2014; 10(1). DOI:10.3892/mmr.2014.2162 · 1.48 Impact Factor
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    ABSTRACT: Objective To estimate the annual direct and indirect costs of rheumatoid arthritis (RA) in China and identify the predictors for cost of illness. MethodsA cross-sectional study of cost of illness from the societal perspective was conducted on 829 patients with RA in 21 tertiary care hospitals in China between July 2009 and December 2010. Data on demographics, clinical variables, and components of costs were collected by physician interview. Costs were represented in 2009 US dollars using purchasing power parity estimates. Univariate and multivariate linear regression analyses were performed to identify the predictors for cost of illness. ResultsThe mean SD total cost of RA in China was $3,826 +/- $5,659 per patient-year, given a gross domestic product per capita of $6,798 in China in 2009. Direct costs and indirect costs comprised 90.0% and 10.0% of the total costs, respectively. Drug expense represented approximately half of the total costs, dominated by biologic agents (48.2%) and disease-modifying antirheumatic drugs (23.5%). Additionally, the cost of extracted herbal drugs and traditional Chinese medicine comprised approximate to 17.6% of the drug expense. Higher education level, noninsured status, longer disease duration, more extraarticular manifestations, and higher Health Assessment Questionnaire score independently predicted higher total costs. Conclusion Our results provide the first study of costs of RA in China. This study not only demonstrates the economic burden of RA, but also identifies the predictors that could be interventional factors to reduce the societal costs of RA in China.
    04/2014; 66(4). DOI:10.1002/acr.22160
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    ABSTRACT: Abstract Background: Vitamin E-coated dialyzer may have an effect on oxidative stress and inflammation status in hemodialysis (HD) patients. Therefore, we performed a systematic review to assess the anti-oxidation and anti-inflammatory effects of vitamin E-coated dialyzer in HD patients. Methods: The randomized controlled trials (RCTs) and quasi-RCTs of vitamin E-coated dialyzer versus conventional dialyzer for HD patients were searched from multiple databases. We screened relevant studies according to predefined inclusion criteria and performed meta-analyses using RevMan 5.1 software. Results: Meta-analysis showed vitamin E-coated dialyzer therapy could significantly decrease the serum thiobarbituric acid reacting substances (TBARS) (SMD, -0.95; 95% CI, -1.28 to -0.61; p < 0.00001), oxLDL (SMD, -0.61; 95% CI, -1.04 to -0.19; p = 0.005), interleukin-6 (IL-6) (SMD, -0.65; 95% CI, -0.97 to -0.32; p < 0.0001) and C-reactive protein (CRP) levels (SMD, -0.46; 95% CI, -0.87 to -0.05; p = 0.03) compared with that of the control group. However, vitamin E-coated dialyzer did not result in increasing the total antioxidant status (TAS) (SMD, 0.23; 95% CI, -0.16 to 0.61; p = 0.25) and the fractional clearance of urea index (Kt/v) levels (MD, -0.07; 95% CI, -0.14 to 0.00; p = 0.06), in addition, there was no significant difference in plasma superoxide dismutase (SOD) level compared with that of the conventional dialyzer & oral vitamin E group (SMD, 0.28; 95% CI, -0.20 to 0.75; p = 0.26). Conclusions: Vitamin E-coated dialyzer can reduce the oxidative stress and inflammation status reflected by the decreasing of serum TBARS, oxLDL, CRP, and IL-6 levels, and this new dialyzer does not affect the dialysis adequacy.
    Renal Failure 02/2014; 36(5). DOI:10.3109/0886022X.2014.890858 · 0.78 Impact Factor
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    ABSTRACT: Besides glomerulus tubulo-interstitium is often concomitantly affected in certain diseases, e.g., diabetic nephropathy, and activation of renin-angiotensin system, to a certain extent, worsens its outcome because of perturbations in hemodynamics and possibly tubulo-glomerular feedback. Certain studies suggest that pathobiology of tubulo-interstitial is influenced by small GTPases, e.g., Rap1. We investigated effect of Ang II on inflammatory cytokines, while at the same time focusing on upstream effector of Rap1, i.e., Epac1, and some of the downstream tubular transport molecules, i.e., NHE3. Ang II treatment of LLC-PK1 cells decreased Rap1a GTPase activity in a time- and dose-dependent manner. While Ang II treatment led to an increased membrane translocation of NHE3, which was reduced with Epac1 and PKA activators. Ang II-induced NHE3 translocation was notably reduced with transfection of Rap1a dominant positive mutants, i.e., Rap1a-G12V or Rap1a-T35A. While transfection of cells with dominant negative Rap1a mutants, i.e., Rap1a-S17A, or with Epac1 mutant, i.e., EPAC-ΔcAMP, normalized the Ang II-induced translocation of NHE3. In addition, Ang II treatment led to an increased expression of inflammatory cytokines, i.e., IL-1β, IL-6, IL-8 and TNF-α, which was reduced with Rap1a-G12V or Rap1a-T35A transfection; while it reverted to previous comparable levels following transfection of Rap1a-S17A or EPAC-ΔcAMP. Ang II-induced expression of cytokines was reduced with the treatment of NHE3 inhibitor, S3226, or with Epac1 and PKA activators. These data suggest that this novel Epac1-Rap1a-NHE3 pathway conceivably modulates the Ang II-induced expression of inflammatory cytokines, and this information may aid in developing strategies to reduce tubulo-intertstitial inflammation in renal diseases.
    AJP Renal Physiology 02/2014; 306(11). DOI:10.1152/ajprenal.00069.2014 · 4.42 Impact Factor
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    ABSTRACT: To explore tubulointerstitial nephritis antigen (TIN-ag) expression of chronic kidney disease (CKD) patients' renal tissue and the correlation to clinical phenotype. Through digital drawing lots, a total of 77 CKD patients from October 2012 to February 2013 at our department were randomly selected. All of them underwent biopsy. Based upon their pathological findings, they were divided into 2 groups of minimal change disease (MCD) and non-minimal change disease (NMCD). The stains of hematoxylin and eosin and Masson were used to observe renal pathological changes and immunofluorescence for detecting the TIN-ag expression of kidney tissue. The serum levels of creatinine, blood urea nitrogen, estimated glomerular filtration rate (eGFR), 24-hour urine output, 24-hour urine protein, α1-microglobulin, β2-microglobulin, pathological casts, N-acetyl-beta-glucosaminidase (NAG), specific gravity and other clinical parameters were monitored to examine their relationship between renal tissue TIN-ag expression. TIN-ag expression was distinct in renal tubular basement membrane of MCD patients while weak in primary focal segmental glomerulosclerosis (FSGS)(n = 16), IgA nephropathy (n = 23), MN (n = 14) and LN (n = 15) renal tissue. Immunofluorescence quantitative analysis showed that tubular TIN-ag fluorescence intensity of NMCD group was significantly lower than that of MCD group (4.84(3.02, 10.73) vs 20.79(8.19, 37.00), P < 0.01). In addition, TIN-ag expression in renal interstitial collagen area deposition of 0 grade group was higher than that of collagen area deposition 1-3 grades group (all P < 0.05). Serum α1-microglobulin and pathological urine cast, 24-hour urine protein of CKD patients were negatively correlated with kidney tubules TIN-ag expression (r = -0.312, -0.298, -0.214, all P < 0.05). Serum creatinine, blood urea nitrogen, serum β2-microglobulin and eGFR of CKD patients had no significant correlations with TIN-ag expression (P > 0.05). TIN-ag expression of CKD patients with lower expression levels of NAG was significantly higher than that of normal levels of NAG expression. TIN-ag expression of low urine specific gravity group was lower than that of normal urine specific gravity group (P < 0.05). TIN-ag expression of renal tissue tubule basement membrane in NMCD group is significantly lower than that in MCD group. TIN-ag expression is negatively correlated with renal tissue fibrosis. Expression of serum α1-microglobulin and concentrations of urinary pathology tube, 24-hour urine protein, NAG expression and urine specific gravity are negatively correlated with renal tissue TIN-ag expression in CKD patients.
    Zhonghua yi xue za zhi 01/2014; 94(4):246-50.
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    ABSTRACT: The heavy metal lead (Pb) is a major environmental and occupational hazard. Epidemiological studies have demonstrated a strong association between lead exposure and the presence of chronic kidney injury. Some studies have suggested that chelation therapy with calcium disodium ethylenediaminetetraacetic acid (calcium disodium EDTA) might help decrease the progression of chronic kidney disease among patients with measurable body lead burdens. However, calcium disodium EDTA chelation in lead exposure is controversial due to the potential for adverse effects such as acute tubular necrosis. Therefore, we investigated the available randomized controlled trials assessing the renoprotective effects of calcium disodium EDTA chelation therapy. Our meta-analysis shows that calcium disodium EDTA chelation therapy can effectively delay the progression of chronic kidney disease in patients with measurable body lead burdens reflected by increasing the levels of estimated glomerular filtration rate (eGFR) and creatinine clearance rate (Ccr). There appears to be no conclusive evidence that calcium disodium EDTA can decrease proteinuria.
    Nephrology 01/2014; 19(1):56-9. DOI:10.1111/nep.12162 · 1.86 Impact Factor
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    ABSTRACT: Diabetic kidney disease (DKD) is a leading cause of end-stage renal disease (ESRD). Renal tubular injury by overproduction of ROS in mitochondria plays a critical role in the pathogenesis of DKD. Evidences have shown that p66Shc was involved in renal tubular injury via mitochondrial-dependent ROS production pathway, but little is known about the upstream signaling of p66Shc that leads to tubular oxidative damage under high glucose conditions. In this study, an increased PKCδ and p66Shc activation and ROS production in renal tissues of patients with diabetic nephropathy were seen and further analysis revealed a positive correlation between the tubulointerstitial damage and p-PKCδ, p-p66Shc, and ROS production. In vitro, we investigated the phosphorylation and activation of p66Shc and PKCδ during treatment of HK-2 cells with high glucose (HG). Results showed that the activation of p66Shc and PKCδ was increased in a dose- and time-dependent manner, and this effect was suppressed by Rottlerin, a pharmacologic inhibitor of PKCδ. Moreover, PKCδ siRNA partially blocked HG-induced p66Shc phosphorylation, translocation, and ROS production in HK-2 cells. Taken together, these data suggest that activation of PKCδ promotes tubular cell injury through regulating p66Shc phosphorylation and mitochondrial translocation in HG ambient.
    Oxidative medicine and cellular longevity 01/2014; 2014:746531. DOI:10.1155/2014/746531 · 3.36 Impact Factor
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    ABSTRACT: A rapid protocol is necessary to determine the serum concentrations of prednisone. The HP1100 high-performance liquid chromatographic (HPLC) system was employed. The HP Lichrosphere C8 column (250 mm × 4 mm, i.d., 5 μm particle size) was used. The mobile phase was methanol, tetrahydrofuran and water in the ratio 25:25:50. The flow rate was 1.0 ml/min. The sample was monitored by UV absorbance at 240 nm. Acetanilide was used as the internal standard, and methanol was added into the serum for depositing the protein. The chromatography was effective and was not interfered with by the serum components. Good linearity was observed, within the range of 10-500 μg/L for prednisone, and the detection limit was 5 μg/L. The serum concentrations of prednisone between the nephrotic syndrome (NS) group and the control group were significantly different (P < 0.05), while there was no significant difference between the females and males of the NS group (P > 0.05). The serum ncentration of prednisone in the steroid-resistant group was lower than that in the steroid-sensitive group (P < 0.05). HPLC is a practical and reliable method to determine the serum concentration of prednisone with high accuracy, precision, linearity and repeatability.
    International Journal of Clinical and Experimental Medicine 01/2014; 7(12):5517-22. · 1.42 Impact Factor
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    ABSTRACT: The Wnt family of proteins belongs to a group of secreted lipid-modified glycoproteins with highly conserved cysteine residues. Prior results indicate that Wnt/ β -catenin signaling plays a prominent role in cell differentiation, adhesion, survival, and apoptosis and is involved in organ development, tumorigenesis, and tissue fibrosis, among other functions. Accumulating evidence has suggested that Wnt/ β -catenin exhibits a pivotal function in the progression of diabetic nephropathy (DN). In this review, we focused on discussing the dual role of Wnt/ β -catenin in apoptosis and epithelial mesenchymal transition (EMT) formation of mesangial cells. Moreover, we also elucidated the effect of Wnt/ β -catenin in podocyte dysfunction, tubular EMT formation, and renal fibrosis under DN conditions. In addition, the molecular mechanisms involved in this process are introduced. This information provides a novel molecular target of Wnt/ β -catenin for the protection of kidney damage and in delay of the progression of DN.
    12/2013; 2013:987064. DOI:10.1155/2013/987064
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    ABSTRACT: Rap1b ameliorates high glucose (HG)-induced mitochondrial dysfunction in tubular cells. However, its role and precise mechanism in diabetic nephropathy (DN) in vivo remains unclear. We hypothesize that Rap1 plays a protective role in tubular damage of DN by modulating primarily the mitochondria-derived oxidative stress.The role and precise mechanisms of Rap1b on mitochondrial dysfunction and of tubular cells in DN was examined in rats with Streptozotocin (STZ)-induced diabetes that have Rap1b gene transfer using an ultrasound microbubble-mediated technique as well as in renal proximal epithelial tubular cell line (HK-2) exposed to HG ambiance. The results showed that Rap1b expression decreased significantly in tubules of renal biopsies from patients with DN. Over-expression of a constitutively active Rap1b G12V notably ameliorated renal tubular mitochondrial dysfunction, oxidative stress, apoptosis in the kidneys of STZ-induced rats, which was accompanied with increased expression of transcription factor C/EBP-β and PGC-1α. Furthermore, Rap1b G12V also decreased phosphorylation of Drp1, a key mitochondrial fission protein, while boosting the expression of genes related to mitochondrial biogenesis and antioxidants in HK-2 cells induced treated with HG. These effects were imitated by transfection with C/EBP-β or PGC-1α siRNA. In addition, Rap1b could modulate C/EBP-β binding to the endogenous PGC-1α promoter and the interaction between PGC-1α and Catalase or mitochondrial superoxide dismutase. Indicating that Rap1b ameliorates tubular injury and slows the progression of DN by modulation of mitochondrial dysfunction via C/EBP-β:PGC-1α signaling.
    Diabetes 12/2013; 63(4). DOI:10.2337/db13-1412 · 8.47 Impact Factor
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    ABSTRACT: Objective: To evaluate the mortality and risk factors for acute kidney injury (AKI) in hospitalized patients by the risk, injury, failure, loss, end stage kidney disease (RIFLE) and acute kidney injury network (AKIN). Methods: We constructed a retrospective study of all AKI patients in the Second Xiangya Hospital of Central South University between February 2006 and January 2011. The diagnosis and classification of AKI were reconfirmed and categorized by RIFLE and AKIN criteria. To compare the clinical characteristics, mortality and associated risk factors in AKI patients by the RIFLE and AKIN stage, univariate analysis and multivariate logistic regression analysis were performed. Results: The patients were diagnosed as AKI by AKIN (n=1027) or by RIFLE criteria (n=1020). There was no significant difference in the hospital mortality, hospital length stay (days), or the proportion of complete recovery in each stage of AKI patients by RIFLE and AKIN (P>0.05). In the univariate analysis, age, pre-renal causes, proportion of hospital acquired AKI, mechanical ventilation, hypotension, the number of failed organs, acute tubular necrosis-index severity score (ATN-ISS), and the peak of serum potassium ion concentration were significantly higher in the non-survivors than in the survivors (P<0.05). Logistic regression analysis revealed that age older than 65, hospital acquired AKI, hypotension, number of failed organs, ATN-ISS scores, and the peak of serum potassium ion concentration were independent risk factors for hospital mortality. Conclusion: Both RIFLE and AKIN criteria have similar scientific value in assessing hospital mortality. AKI stage is associated with the recent prognosis of AKI patients.
    Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences 12/2013; 38(12):1243-1252. DOI:10.3969/j.issn.1672-7347.2013.12.007

Publication Stats

855 Citations
260.42 Total Impact Points

Institutions

  • 2010–2015
    • The Second Xiangya Hospital of Central South University
      Ch’ang-sha-shih, Hunan, China
  • 2014
    • Peking University
      Peping, Beijing, China
  • 2010–2014
    • Central South University
      • Department of Nephrology
      Ch’ang-sha-shih, Hunan, China
  • 2008–2014
    • Northwestern University
      • • Division of Hospital Medicine
      • • Department of Pathology
      Evanston, Illinois, United States
    • Society for Experimental Biology & Medicine
      Society Hill, New Jersey, United States
  • 2009–2013
    • Peking University Third Hospital
      Peping, Beijing, China
  • 2012
    • Peking University People's Hospital
      Peping, Beijing, China
  • 2011
    • Sun Yat-Sen University
      • Department of Rheumatology
      Guangzhou, Guangdong Sheng, China
  • 2006–2011
    • University of Illinois at Chicago
      Chicago, Illinois, United States
  • 2002
    • Okayama University
      • Medical School
      Okayama, Okayama, Japan