Background: The prevalence of chronic kidney disease (CKD) has increased and will continue to rise worldwide. However, data regarding the prevalence of CKD in a rural area of China are limited. We therefore investigated the prevalence and associated risk factors of impaired renal function and urinary abnormalities in an adult rural population in southern China.Methods: Between December 2006 and January 2007, residents older than 20 years from four villages in Zhuhai city were randomly selected using a stratified, multistage sampling technique. All participants were interviewed and tested for hematuria, albuminuria and estimated glomerular filtration rate (eGFR). The associations between age, gender, diabetes mellitus, hypertension, hyperuricemia, education level and indicators of renal damage were examined.Results: Overall, 1,214 subjects were enrolled in this study. After adjustment for age and gender, the prevalence of albuminuria was 7.1% (95% CI: 4.5, 8.1), reduced eGFR was 2.6% (95% CI: 1.7%, 3.3%), and hematuria was 4.6% (95% CI: 3.3%, 6.0%). Approximately 13.6% (95% CI: 12.0%, 15.1%) of the patients had at least one indicator of renal damage, but only 8.3% were previously aware. Age, diabetes, hyperlipidemia, hypertension, hyperuricemia, use of nephrotoxic medications, coronary heart disease and history of CKD were independently associated with impaired renal function and urinary abnormalities. Additionally, age, diabetes, and hypertension were independently associated with albuminuria. Age, hypertension, hyperuricemia, central obesity, and coronary heart disease were independently associated with reduced renal function.Conclusions: The high prevalence and low awareness of impaired renal function and urinary abnormalities in this population illustrates the urgent need to implement a CKD prevention program in the rural areas of southern China.

Background: The effect of hyperuricemia on chronic kidney disease (CKD) is controversial, and little is known about gender as it relates to hyperuricemia and CKD. Methods: This was a cross-sectional study of 7,053 adults in the general Chinese population in Southern China using a multi-stage stratified sampling method. In which associations between hyperuricemia and indicators of CKD (defined by albuminuria (urinary albumin-to-creatinine ratio >= 30mg/g) or decreased modified MDRD equation estimated GFR (<60ml/min per 1.73m(2)) were tested using multivariate logistic regression. Results: After adjustment for potential confounders, hyperuricemia was associated with increased risk of reduced renal function and CKD but not albuminuria, with odds ratios (ORs) (95% CI) of 4.39 (3.38-5.70, P < 0.001), 1.54 (1.31-1.82, P < 0.001) and 0.96 (0.78-1.17, P = 0.671), respectively. The interaction between gender and hyperuricemia with CKD was significant (P = 0.010); and stratified analysis showed a stronger association of hyperuricemia with CKD in males (OR (95% CI): 2.04 (1.56-2.67), P < 0.001) than in females (1.45 (1.17-1.80), P = 0.001). Conclusions: We observed an independent association of hyperuricemia with CKD that was stronger in males, and this independent association in male might imply some gender specific mechanisms. These results should be confirmed in future prospective studies. Copyright (C) 2012 S. Karger AG, Basel

The optimal therapy for adult steroid-resistant nephrotic syndrome (SRNS) remains a therapeutic challenge. We investigated the efficacy and safety of tacrolimus as a promising regimen in Chinese adult patients.A prospective, multicenter trial was conducted in 9 nephrology centers from 2006 to 2008, in patients with SRNS (defined as failure to respond to 1 mg/kg/day of prednisone for 8, and 16 weeks, in focal segmental glomerulosclerosis). Patients were treated with tacrolimus (TAC) plus prednisone for 12 months. TAC dose was titrated to achieve a target trough blood concentration of 5-10 ng/ml for the first 6 months and 4-6 ng/ml for the subsequent 6 months. The primary outcomes included complete or partial remission [complete remission (CR): proteinuria < 0.3 g/24 h, with serum albumin a parts per thousand yen3.5 g/dl and stable renal function; partial remission (PR): proteinuria between 0.3 and 3.5 g/24 h and a decrease of at least 50 % from the baseline level, with serum albumin a parts per thousand yen3.0 g/dl and stable renal function]. Secondary end-points included relapse rate, changes of clinical parameters (proteinuria, serum albumin, and lipid profile) and adverse events.Twenty-four patients with SRNS were enrolled. After 6 months of therapy, CR was achieved in 58.3 % of patients and PR in 16.7 %, yielding a final response rate of 75.0 %. The decrease in proteinuria was 43.1 +/- A 17.5 % after the first month of treatment (P < 0.001). Complete or PR was achieved in 6 of 8 patients with minimal change disease, 4 of 6 patients with mesangioproliferative glomerulonephritis (MsPGN), 6 of 7 patients with focal segmental glomerulosclerosis (FSGS), and all 2 patients with IgA nephropathy. Two patients (1 with MsPGN and 1 with FSGS) experienced relapses during the subsequent 6 months of follow-up. Adverse events included infection, hand tremor, diarrhea, acute reversible or persistent nephrotoxicity.In conjunction with prednisone, TAC may be an alternative therapeutic regimen for adult SRNS patients. However, adverse events in these patients should be carefully monitored, especially at the beginning of treatment. Randomized controlled trials with longer follow-up are warranted.

Background: Familial juvenile hyperuricemic nephropathy (FJHN) is an autosomal dominant disorder characterized by early onset of hyperuricennia, decreased fractional renal urate excretion and progressive interstitial nephropathy. Mutations in the uromodulin (UMOD) gene encoding uromodulin/Tamm-Horsfall, a glycosylphosphatidylinositol (GPI)-anchored protein, cause this disease. Methods: One Chinese family with 13 FJHN-affected individuals is described. Clinical data, blood and urine samples of 7 affected members (all alive patients in this family) and 15 unaffected members were collected. Mutation analysis of the UMOD gene was performed by polymerase chain reaction and direct sequencing. Urinary uromodulin from affected or unaffected members of this family and healthy controls was examined by enzyme-linked immunosorbent assay kit. Expression of uromodulin in renal tissue was shown with immunofluorescence. Results: A novel mutation (p.T605G) within the uromodulin GPI anchor signal segment was identified in the affected individuals of this FJHN family. There was a markedly increased expression of uromodulin in renal tissue and significantly decreased urinary excretion of uromodulin in affected patients with an estimated glomerular filtration rate < 60 ml/mm/1.73 m(2). Conclusions: The present study reported a novel mutation in exon 9 of UMOD in the Chinese Han population, within the GPI anchor signal segment of uromodulin. Since the GPI anchor is linked with the release or secretion of proteins, our finding may provide further evidence for the underlying mechanism of decreased urinary excretion of uromodulin in FJHN. Copyright (c) 2012 S. Karger AG, Basel

本研究我们主要围绕着“分析IgA肾病(IgAN)患者外周血和肾脏组织中调节性T细胞(Treg)/Th17/Th1/Th2细胞的数量和其对B细胞分泌IgA的影响，结合临床表现、病理类型、治疗反应、临床结局进行分层分析”进行研究。其中在“IgA肾病遗传易感基因及其相关致病机理”研究方面，我中心在该研究领域有突破性的重大进展。通过全基因组关联分析研究，首次发现了中国人群中IgA肾病独有的两个新的易感基因位点，证明了遗传因素在IgA肾病的发病机制中起重要作用，并能够影响IgA肾病的发病过程及临床表现。研究结果对科学家们更深入地了解IgA肾病发生的分子机制，探索IgA肾病风险预测标记，并为未来IgA肾病的早期诊断、个体化治疗和新的干预靶点及新药研发提供了坚实的基础。 通过本研究，我们对Treg/Th17细胞及其它非T细胞依赖途径对B细胞分泌IgA1的影响在IgAN发病中的作用及MMF治疗IgAN的疗效及耐受性方面有了初步的认识。本研究旨在应用最新免疫学基础研究理论，利用我国丰富的临床病例资源与合作方先进的基础研究成果和技术方法，分析T细胞不同亚群在IgA肾病发病机制中的作用及可能机制，并且开展前瞻随机对照临床研究探讨MMF治疗IgA肾病疗效和耐受性。为临床防治IgA肾病提供目标和依据。 In this project,we focus on‘Analyzing the quantity of regulatory T cells(Treg)/Th17/Th1/Th2 in Peripheral blood and kidney tissue of patients with IgA nephropathy(IgAN),and its effect on B cells secreting IgA,integrating clinical manifestation,pathological type,response to treatment,clinical outcomes for stratified analysis’.Among studies of‘IgAN susceptibility genes and related pathogenesis’,we had a major breakthrough in this field.Using genome wide association study(GWAS),for the first time we found two new susceptibility loci in Chinese IgAN,demonstrating genetic factor plays an important role in the pathogenesis of IgAN,and affecting disease process and clinical manifestation.The paper was published in the international journal of Nature Genetics.The study results offer solid foundation for helping scientists better understand the molecular pathogenesis of IgAN,exploring disease risk predicted markers,also achieving early diagnosis,individual treatment,finding new targeting points and drugs for the disease in the future. The effects of Treg/Th17 cells and other T cell independent way in B cells secreting IgA1 were indicated in our study.We also comprehended the efficacy and tolerance of MMF in the treatment of IgAN.The aim of study is to exploring the role of T cell subsets in the pathogenesis of IgAN,using updated immune theory,our abundant clinical resources and advanced technologies,outstanding achievements of our partner.On this beneficial platform,we also carried out a prospective randomized control study“The efficacy and tolerance of low dose of prednisone combined with MMF in the treatment of IgAN”to probe new evidence of IgAN treatments.