Objective To investigate the prevalence of chronic kidney disease (CKD) and risk factors in the adult population of Tianshan district in Urumqi, Xinjiang. Methods A total of 2131 residents from 4 communities in Tianshan district of Urumqi city were randomly selected using a stratified, multistage sampling. All the residents were interviewed and tested for morning spot urine of albumin to creatinine ratio (ACR) (abnormal≥30 mg/g), morning spot urine dipstick of hematuria ( abnormal >3 red blood cells/HP or greater) and pyuria ( abnormal> 5 white blood cells/HP) confirmed by microscopy. Renal function was determined with abbreviated MDRD equation [reduced estimated glomerular filtration rate (eGFR)<60 ml&#8226;min-1&#8226;(1.73 m2)-1]. The associations of kidney damage indicators with age, gender, hypertension, diabetes mellitus, income, education, cholesterol, triglyceride and smoking were examined. Results Eligible data of 2131 subjects were collected in the study．After the adjustment of age and gender component, the prevalence of albuminuria was found in 2.63% (95%CI：1.78%-3.48%) of subjects, hematuria in 7.43%(95%CI：6.11%-8.75%) and reduced renal function in 1.72%(95%CI：1.08%-2.35%). Approximately 9.99%(95%CI：8.47%-11.55%) of subjects had at least one indicator of kidney damage. Multivariate logistic regression revealed that albuminuria, hematuria, age and hyperuricemia were independently associated with reduced renal function. Hematuria and reduced renal function were independently associated with albuminuria. Albuminuria, reduced renal function and female were independently associated with hematuria. Conclusion In urban adult population over 35 years old of Urumqi, a big city in western China, the prevalence of CKD is 9.99%, the recognition is 2.44% and the risk factors of CKD are similar to those of other domestic big cities and western developed countries.

Objective To investigate the clinicopathological characteristics and prognosis of Henoch-Schonlein purpura nephritis with diffused endothelial cell proliferation (DEP-HSPN) in children. Methods Data of 8 DEP-HSPN cases in Nanjing Children’s Hospital within recent ten years were retrospectively reviewed. The clinicopathological features, efficacy and prognosis were compared between DEP-HSPN cases and 48 cases of non-DEP-HSPN. Non- DEP-HSPN cases were divided into two groups according to the clinical classification or the pathological classification. Results (1) In DEP-HSPN, HSP developed nephritis within 4 to 15 days after the initial onset of purpuric rashes. Hematuria was present in all the 8 patients. The main clinical manifestation of DEP-HSPN was nephritic-nephrotic syndrome (4 cases), nephrotic level proteinuria (3 cases) and acute nephritic syndrome (1 case). Four cases had macrohematuria. Six cases had abdominal symptoms and two cases had arthritis. Pathology of all the cases showed grade Ⅲ-b lesion with diffused endocapillary proliferation and segmental necrotizing lesion of the capillary wall, always accompanied with intraglomerular inflammatory cell infiltration. Crescent was found in 4 cases. (2) Compared to non-DEP-HSPN grades Ⅲ, DEP-HSPN showed a shorter course of disease. Macrohematuria, heavy proteinuria, nephritic-nephrotic syndrome, and segmental necrotizing lesion of capillary wall were more common in DEP-HSPN. Compared to non-DEP-HSPN with nephrotic level proteinuria, DEP-HSPN had a lower rate of crescent. (3) Methylprednisolone pulse therapy in early stage, then prednisone combined with cyclophosphamide were used in the treatment of DEP-HSPN. After an average follow-up period of seven months, one patient showed complete remission, five showed persistent microhematuria, and two showed persistent microhematuria accompanied with minor proteinuria. No significant difference of prognosis was found between DEP-HSPN and non-DEP-HSPN. Conclusions DEP-HSPN has an acute onset. The main clinical manifestation of DEP-HSPN is nephritic-nephrotic syndrome and nephrotic level proteinuria, always accompanied with macrohematuria. Immunosuppressant treatment in the early stage of disease is effective for a short-term outcome.

Objective To investigate the prevalence and risk factors of chronic kidney disease (CKD) in the general adult population in the Hulunbeir Prefecture, Inner Mongolia Autonomous Region where many minorities of north China live. Methods Sampling survey was performed in the residents aged 20 years and older in the Hulunbeir Prefecture. All the investigated subjects were tested for urinary albumin to creatinine ratio (ACR); hematuria by microscopy of urinary sediment; and GFR estimated by modified MDRD equation for Chinese adults (eGFR). The related risk factors of CKD were also investigated. Results A total of 4522 subjects were enrolled in the study. The prevalence of albuminuria was 7.11%, hematuria was 2.64% and reduced eGFR [60 ml&#8226;min-1&#8226;(1.73 m2)-1] was 2.75%. The prevalence of hypertension was 38.90%; hyperglycemia 6.61% ; hyperlipidemia 2.72%; increased waist 24.79% and metabolic syndrome 15.02%. After the subjects with combined microalbuminuria, hematuria and reduced eGFR were excluded, the prevalence of CKD was 12.95%. Logistic regression analysis and stratified analysis showed increased age, increased waist, elevated systolic pressure, hyperglycemia, hypertriglyceridemia and metabolic syndrome were independently associated with albuminuria; increased age, elevated systolic pressure and hyperglycemia were independently associated with reduced eGFR; increased age was independently associated with hematuria. Conclusions The prevalence of adult CKD is 12.95% in the Hulunbeir Prefecture, Inner Mongolia Autonomous Region. Independent risk factors of CKD include increased age, increased waist, hypertension, abnormal blood glucose or lipid, and metabolic syndrome.

Objective To investigate the characteristics of BK virus (BKV) infection in renal transplant recipients. Methods A total of 243 renal recipients from our clinic within 48 months after transplantation were enrolled as the trial group and 82 healthy people as the control group. Urine and peripheral blood samples of these two groups were harvested for urinary sediment BKV cytology by Decoy cell counting and BKV DNA by real-time PCR. Results The positive rates of urinary Decoy cell, BKV viruria and viremia were 35.4%, 36.6% and 16.9% in trial group, and 4.9 %, 20.7% and 2.9% in control group, respectively. In trial group, the medians of urinary Decoy cell, urinary BKV and peripheral blood BKV were 6/10 HPF, 1.50×104 copy/ml and 6.87×103 copy/ml respectively, while in control group, they were 2/10 HPF, 1.10×104 copy/ml and 2.24×103 copy/ml. Compared with the healthy people, the positive rates and the levels of BKV DNA in urine and peripheral blood of recipients were significantly higher. The amount of urinary Decoy cells was positively correlated to urinary BKV load(r=0.636, P<0.01). Conclusions BKV replication is easier to happen in renal recipients as compared to healthy people. Counting of urinary Decoy cells is convenient, useful and sensitive to evaluate BK viruria and viremia in renal transplant recipients. BKV DNA detection in urine and peripheral blood can be used to screen the evidence of BK reaction in order to prevent irreversible graft damage by BKV.

Objective To establish a citrate pharmacokinetics model which is applied to evaluate the risk of citrate accumulation in patients with liver dysfunction in the continuous renal replacement treatment (CRRT) with regional citrate anticoagulation (RCA). Methods The source of citrate for extracorporeal anticoagulation, the body clearance and filter elimination of citrate, which were the three major citrate fluxes of systemic citrate level, were combined into a single-pool, first order kinetic equation. The data from a published clinical study of systemic citrate kinetics in the intensive care unit patients with or without liver cirrhosis were adapted and the citrate kinetic equation was applied to predict the risk of systemic citrate accumulation in patients with normal, impaired and absent liver clearance while different RCA-CRRT protocols were carried out. Results The single pool, first order citrate kinetic modeling equation was as follows:
. There was excellent agreement between published citrate measurements and our predictions. Kinetic modeling showed that the plasma citrate concentration of patients with normal citrate body clearance was no more than 1 mmol/L during common RCA-CRRT. The model predicted that when the single pass fractional extraction of citrate on the artificial kidney was above 66%, systemic steady citrate concentration would be among the safe range even in patients of impaired body metabolism of citrate. Conclusions The citrate kinetic model of RCA-CRRT can predict the risk of systemic citrate accumulation and provide the basis for designing the safe RCA-protocols for the patients with impaired body clearance of citrate.

Objective To assess the efficacy of fish oil in the treatment of IgA nephropathy using the method of Meta-analysis. Methods Randomized controlled trials of fish oil in the treatment of IgA nephropathy were searched in the database of Cochrane library, PubMed, EMBASE and CNKI. Data extracted from the literatures were analyzed with Revman software (version 5.0). Results In comparison with the controlled group, proteinuria in the fish oil group was significantly decreased [SMD=-0.27, 95%CI(-0.52 to -0.03), P=0.03], while the renal function deteriorated [SMD=0.30，95%CI(0.05 to 0.55), P=0.02]. Conclusion Fish oil can decrease the proteinuria of IgA nephropathy, but can not prevent renal function from deterioration.

Objective To investigate the antiproliferative effect of rosiglitazone, a thiazolidinedione(TZD) on autosomal dominant polycystic kidney disease (ADPKD) cystic lining epithelial cells and to explore the underlying molecular mechanism. Methods ADPKD cystic lining immortalized epithelial (WT9-12) cells were stimulated by rosiglitazone with different concentrations. After treatment, MTT method was performed to detect the level of proliferation; flow cytometry was used to determine the cell cycle distribution and the apoptosis rate. Western blotting was used to detect the protein expressions of mTOR, p70S6K, 4E-Bp1, PPARγ. PPARγ siRNA was transfected into WT9-12 cells to knock down the expression of PPARγ. Results Treatment of WT9-12 cells with rosiglitazone resulted in a dose-dependent and time-dependent strong inhibition of cell proliferation, an accumulation of cells in the G0/G1 phase (rosiglitazone 50 &#61549;mol/L 65.43%, rosiglitazone 100 &#61549;mol/L 64.02%, control 49.65%) and 6% apoptosis at high concentration(rosiglitazone 200 &#61549;mol/L). Rosiglitazone reduced the phosphorylation of p70S6K in a dose-dependent and time-dependent manner. The levels of phosphorylated mTOR and 4E-Bp1, the latter being a downstream substrate of mTOR related mRNA translation initiation, were not changed by rosiglitazone. Cells were pre-incubated with GW9662, a PPARγ antagonist, before the treatment with rosiglitazone, the inhibition of p70S6 kinase phosphorylation by rosiglitazone was partially prevented by GW9662 (P<0.01). Then PPARγ siRNA was transfected into WT9-12 cells, in contrast to untransfected control or cells transfected with an irrelevant siRNA, rosiglitazone did not cause an obvious inhibition of p70S6 kinase phosphorylation in PPARγ knock-down. Conclusion Rosiglitazone inhibits the proliferation of ADPKD cystic lining epithelial cells, and down-regulates p70S6 kinase phosphorylation through mTOR-independent and PPARγ-dependent signal pathway.

Objective To investigate the effects of parathyroid hormone (PTH) on the synthesis and secretion of collagen Ⅲ and fibronectin (FN), and the expressions of plasminogen activator inhibitor-1 (PAI-1), matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA in cultured human renal tubular epithelial cells (HK-2). Methods HK-2 cells were cultured in DMEM-F12 medium supplemented with 5% FBS. Cells were exposed to different concentrations of PTH (0, 10-12, 10-11, 10-10, 10-9, 10-8 mol/L) for 48 h, or 10-8 mol/L PTH at different time (0, 12, 24, 48, 72 h). The gene expressions of collagen Ⅲ, FN, PAI-1, MMP-1, and TIMP-1 were detected by semi-quantitative RT-PCR. The protein expression of collagen Ⅲ was detected by Western blotting. The level of FN in the supernatant was assayed by enzyme linked immunosorbent assay (ELISA). Results PTH increased gene expressions of collagen Ⅲ, FN, PAI-1 and TIMP-1 in a dose- and time-dependent manner, but decreased MMP-1 gene expression. Then the ratio of MMP-1/TIMP-1 was decreased. PTH increased the collagen Ⅲ protein expression in cultured HK-2 cells and the level of FN in the supernatant of cultured HK-2 cells in a dose- and time-dependent manner. Conclusion PTH can up-regulate PAI-1, TIMP-1 gene expressions, and down-regulate MMP-1 gene expression, resulting in elevation of extracellular matrix (ECM) synthesis and reductim of degradation.

Objective To observe the expression and localization of CIP4 (Cdc42 interacting protein-4) in the renal fibrosis and the effect of CIP4 on the expression of E-cadherin, vimentin and β-catenin tyrosine phosphorylation. Methods In vitro, the human tubular epithelial cells (HK-2 cell line) were cultured with 10 μg / L TGF-β1 for 72 h. The protein expressions of CIP4, E-cadherin, vimentin and β-catenin tyrosine phosphorylation were measured by Western blotting; the expression of CIP4 mRNA was detected by RT-PCR. The intracellular distribution of CIP4 was observe by confocal microscope. In vivo, Masson staining was used to evaluate the level of renal fibrosis; the expression and distribution of CIP4 in renal tissue were detected by immunohistochemistry. HK-2 cells were transfected with pcDNA3.1-CIP via lipofectamine 2000. The expressions of E-cadherin, vimentin and β-catenin tyrosine phosphorylation level in the transfected cells were detected by Western blotting. Results The expressions of CIP4 mRNA and protein were up-regulated in renal tubular EMT cells. Most of CIP4 protein localized in cell membrane, and some was in cytoplasm. After stimulation by TGF-β1, the expression of CIP4 protein both in cytoplasm and nucleus was greatly increased (P＜0.05), especially in cytoplasm. In vivo, CIP4 was expressed in renal tubular epithelia, but little expressed in glomeruli. In renal from 5/6 nephrectomized rats, CIP4 expression was significantly increased. In the CIP4 transfectants, the expression of CIP4, vimentin and β-catenin tyrosine phosphorylation level were up-regulated (P＜0.05), but E-cadherin expression was suppressed(P＜0.05). Conclusion The overexpression of CIP4 is likely to take part in the epithelial-to-mesenchymal transition process, thereby promoting the renal fibrosis.

Objective To investigate the association of the expressions of glomerular nephrin, vascular endothelial growth factor (VEGF) and its receptor(VEGFR) with proteinuria in preeclampsia rats. Methods A rat model of preeclampsia was developed by inhibitor of nitric oxide synthase (L-NAME). The systolic blood pressure (SBP) and 24 h urine protein were compared among the normal female group(n=6), the normal pregnant group(n=8), nonpregnant control group(n=6) and preeclampsia group(n=8). The kidney biopsies of each group were observed by light and electron microscopy. The glomerular nephrin was detected by Western blotting and real-time PCR. Immunofluorescence was used to detect the expression of WT1. The level of glomerular VEGF and VEGFR (Flt-1 and Flk-1) were evaluated by Western blotting. Results The level of glomerular nephrin protein in the rats with preeclampsia (0.0726±0.0074) was significantly lower compared with normal female group (0.3795±0.0509), normal pregnant group (0.2361±0.0437) and nonpregnant control group (0.7265±0.0503) (P<0.01, respectively), while the levels of nephrin mRNA were not significantly different among 4 groups. The expression of WT1 was not significantly different among 4 groups as well. The level of glomerular VEGF in preeclampsia group (1.5429±0.0898) was significantly higher compared with normal female group(1.1870±0.1160), normal pregnant group (1.3741±0.1165) and nonpregnant control group (1.0155±0.0742)(P<0.01, respectively). VEGFR(Flt-1 and Flk-1) was also significantly higher in preeclampsia rats compared with other control groups (P<0.05, respectively). Conclusions In preeclampsia rats, nephrin is decreased significantly and the glomerular VEGF-VEGFR is increased significantly compared with the other control groups. The abnormal expression of nephrin and VEGF-VEGFR may be involved in the preeclampsia proteinuria. The underlying mechanism of this phenomenon needs further research.