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Guangzhou, China

Xia X.,Key Laboratory of Nephrology | Luo Q.,Key Laboratory of Nephrology | Li B.,Key Laboratory of Nephrology | Lin Z.,Key Laboratory of Nephrology | And 2 more authors.
Metabolism: Clinical and Experimental | Year: 2016

Background Studies have shown inconsistent results about the association between serum uric acid levels and mortality in patients with chronic kidney disease (CKD). Methods A systematic literature search in MEDLINE, Web of Science and bibliographies of retrieved articles was performed to identify studies investigating the association between serum uric acid and mortality in patients with CKD. Pooled hazard ratios (HR) and corresponding 95% confidence intervals (CIs) were calculated using random-effects models. Results A total of 24 studies with 25,453 patients with CKD were included. By meta-analysis, patients with the highest serum uric acid level were associated with a significantly higher risk for mortality (14 studies; HR, 1.52; 95% CI, 1.33-1.73) compared with patients with the lowest serum uric acid level. For dose-response analysis, a linear relationship (8 studies; Pfor non-linearity = 0.14) between serum uric acid levels and risk of mortality was found. Overall, an increase of 1 mg/dl in serum uric acid level was associated with an 8% increased risk of mortality (21 studies; HR, 1.08; 95% CI, 1.04-1.11). Conclusions Elevated serum uric acid levels are significantly associated with risk of mortality in patients with CKD. Further randomized controlled trials should attempt to determine whether it improves survival to target serum uric acid in patients with CKD. © 2016 Elsevier Inc.

Yu X.,Sun Yat Sen University | Yu X.,Key Laboratory of Nephrology | Yang X.,Sun Yat Sen University | Yang X.,Key Laboratory of Nephrology
American Journal of Kidney Diseases | Year: 2014

Due to limited medical and economic resources, particularly in the countryside and remote areas, the proportion of individuals with end-stage kidney disease who are treated with dialysis in China is only about 20%. For the rest, renal replacement therapy currently is not available. Peritoneal dialysis (PD) has been developed and used for more than 30 years in China to treat patients with end-stage kidney disease. Several national PD centers of first-rate scale and quality have sprung up, but the development of PD varies widely among geographic regions across China. The Chinese government has dedicated itself to continually increasing the coverage and level of medical service for patients with end-stage kidney disease. Under the guidance of the government and because of promotion by kidney care professionals, presently there are more than 40,000 prevalent PD patients in China, representing approximately 20% of the total dialysis population. Recently, a National Dialysis Unit Training Program for countywide hospitals has been initiated. Through the efforts of programs like this, we believe that awareness of PD and advances in the underlying technology will benefit more patients with end-stage kidney disease in China. © 2014 by the National Kidney Foundation, Inc.

Yu X.,Sun Yat Sen University | Yu X.,Key Laboratory of Nephrology | Yang X.,Sun Yat Sen University | Yang X.,Key Laboratory of Nephrology | And 2 more authors.
Peritoneal Dialysis International | Year: 2014

Managing a rapidly growing peritoneal dialysis program with more than 1000 patients involves multiple challenges, labor constraints, logistics, and excessive geographic distance. This paper describes how Sun Yat-sen University, Guangzhou, China, manages those issues, while simultaneously improving quality of the care and, subsequently, clinical outcomes. © 2014 International Society for Peritoneal Dialysis.

Yu X.-Q.,Sun Yat Sen University | Yu X.-Q.,Key Laboratory of Nephrology | Li M.,Sun Yat Sen University | Li M.,Key Laboratory of Nephrology | And 32 more authors.
Nature Genetics | Year: 2012

We performed a two-stage genome-wide association study of IgA nephropathy (IgAN) in Han Chinese, with 1,434 affected individuals (cases) and 4,270 controls in the discovery phase and follow-up of the top 61 SNPs in an additional 2,703 cases and 3,464 controls. We identified associations at 17p13 (rs3803800, P = 9.40 × 10 -11, OR = 1.21; rs4227, P = 4.31 × 10 -10, OR = 1.23) and 8p23 (rs2738048, P = 3.18 × 10 -14, OR = 0.79) that implicated the genes encoding tumor necrosis factor (TNFSF13) and α-defensin (DEFA) as susceptibility genes. In addition, we found multiple associations in the major histocompatibility complex (MHC) region (rs660895, P = 4.13 × 10-20, OR = 1.34; rs1794275, P = 3.43 × 10 -13, OR = 1.30; rs2523946, P = 1.74 × 10 -11, OR = 1.21) and confirmed a previously reported association at 22q12 (rs12537, P = 1.17 × 10 -11, OR = 0.78). We also found that rs660895 was associated with clinical subtypes of IgAN (P = 0.003), proteinuria (P = 0.025) and IgA levels (P = 0.047). Our findings show that IgAN is associated with variants near genes involved in innate immunity and inflammation. © 2012 Nature America, Inc. All rights reserved.

Zhou Q.,Sun Yat Sen University | Zhou Q.,Key Laboratory of Nephrology | Yang M.,Sun Yat Sen University | Lan H.,Chinese University of Hong Kong | And 2 more authors.
American Journal of Pathology | Year: 2013

Although epithelial-mesenchymal transition (EMT) and the subsequent development of peritoneal fibrosis are key processes leading to the peritoneal failure related to peritoneal dialysis (PD), mechanisms underlying these processes remain largely unclear. In the present study, we found that miR-30a was significantly down-regulated in peritoneal tissues, with progressive fibrosis in patients with continuous ambulatory peritoneal dialysis and in a rat model of PD. In vitro, transforming growth factor (TGF)-β1-induced EMT, identified by de novo expression of α-smooth muscle actin and a loss of E-cadherin in both human and rat peritoneal mesothelial cells, was associated with down-regulation of miR-30a but up-regulation of Snai1, suggesting a close link between miR-30a and Snai1 in TGF-β1-induced peritoneal fibrosis. It was further demonstrated in vitro that miR-30a was able to bind the 3′ untranslated region of Snai1 and overexpression of miR-30a blocked TGF-β1-induced up-regulation of Snai1 and, therefore, inhibited EMT and collagen expression. To determine the functional role of miR-30a, we overexpressed miR-30a in the peritoneal tissue in a rat model of PD and found that overexpression of miR-30a blocked both Snai1 and EMT and inhibited peritoneal fibrosis, with improvement of peritoneal dysfunction. In conclusion, miR-30a negatively regulates Snai1-mediated EMT during peritoneal fibrosis in vitro and in vivo. Blockade of peritoneal fibrosis by overexpressing miR-30a in a rat model of PD reveals a therapeutic potential of miR-30a for peritoneal fibrosis associated with PD. © 2013 American Society for Investigative Pathology.

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