Objective To investigate the relationship between serum 25-hydroxycholecalciferol[25(OH)D3] deficiency and the risk of peritoneal dialysis associated peritonitis. Methods Baseline clinical data (before the peritoneal dialysis catheter insertion) of peritoneal dialysis patients treated with CAPD in the First Affiliated Hospital of Guangxi Medical University from May 1, 2013 to February 1, 2016 were retrospective analyzed. All the patients were followed-up until July 31, 2016. According to the baseline serum 25(OH)D3 levels, patients were divided into deficiency group (25(OH)D3＜15 ng/ml) and non deficiency group (25(OH)D3 ≥15 ng/ml), the baseline clinical data of the two groups were also analyzed. Kaplan-Meier method was used to compare the time-to-peritonitis of two groups. Cox proportional hazard model was used to analyze the relationship between the 25(OH)D3 deficiency and the risk of peritonitis. ROC curve was used to analyze the predictive value of the baseline serum 25(OH)D3 for the risk of PDAP in peritoneal dialysis patients. Results Compared with the 25(OH)D3 non deficiency group, 25(OH)D3 deficiency group had a significant increase incidence of peritonitis, high diastolic blood pressure and mean arterial pressure, but serum albumin, total serum protein decreased significantly (P＜0.05). Kaplan-Meier survival analysis showed that, compared with 25(OH)D3 non deficiency group, the time-to-peritonitis episode of patients with 25(OH)D3 deficiency were shorter (P＜0.05). Cox proportional hazard model showed that after adjusting for age, sex, hemoglobin, serum albumin, C-reactive protein, total Kt/V, eGFR, diabetes or not, 25(OH)D3 deficiency is the independent risk factor of peritoneal dialysis associated peritonitis (HR 5.247, 95%CI 1.180-23.340, P＜0.05). ROC curve showed the area under the curve that baseline serum 25(OH)D3 deficiency predict the occurrence of PDAP was 0.714, and the best cut-off point of baseline serum 25(OH)D3 was 11.35 ng/ml (sensitivity 75%, specificity 63%). Conclusions Peritoneal dialysis associated peritonitis occurred earlier in peritoneal dialysis patients whose baseline serum 25(OH)D3 deficiency. Baseline serum 25(OH)D3 deficiency is the independent risk factor of peritoneal dialysis associated peritonitis, which may predict the incidence of peritoneal dialysis associated peritonitis.

Objectives To investigate the effects of seasonal changes on peritoneal dialysis associated peritonitis (PDAP) in patients on peritoneal dialysis (PD), and to provide evidence for clinical prevention and treatment of PDAP. Methods All episodes of PD-related peritonitis during clinic follow-up in maintenance PD patients from Jan 1st, 2007 to Dec 31st, 2015 in Peking University People's Hospital were reviewed. The incidence of peritonitis, laboratory indexes, pathogens and clinical outcomes in different seasons were recorded and analyzed. One-way ANOVA and chi square test were employed to compare the incidence of PDAP and related data in different seasons, and Pearson correlation was used to analyze correlations between PDAP rate and monthly mean temperature and mean humidity. Results During nine years, a total of 119 PD patients occurred 190 times of peritonitis during home PD. The PDAP rate in summer was the highest, 0.21 episodes/year, followed by spring (0.16 episodes/year) and autumn (0.16 episodes/risk year), but there was no significant difference among peritonitis rates in four seasons. There were significant positive correlation between monthly mean temperature, monthly mean humidity and the peritonitis rate (mean temperature: r=0.828, P＜0.01; mean humidity r=0.657, P＜0.05). (2) As for bacteria, in Summer the PDAP rate caused by Staphylococcus aureus and Coagulase negative staphylococcus (CoNS), and Gram-negative bacteria was higher than that in other seasons, but there was no statistical difference. There were significant positive correlation between monthly mean temperature, mean humidity and the rate of CoNS peritonitis (mean temperature: r=0.704, P＜0.05; mean humidity: r=0.607, P＜0.05). (3) There were no statistical difference among results of PD related peritonitis in different seasons about general situation, clinical manifestation, causes of peritonitis and laboratory index before peritonitis episodes. PD procedure-related problems were the main cause of peritonitis in summer and autumn. (4) The cure rate of all peritonitis was 90%. The highest cure rate was in autumn and winter, while the lowest cure rate was in summer, but no statistical difference. Among the peritonitis episodes with treatment failure, 52.6% occurred in summer. Conclusions There is some correlation between the rate of PDAP and seasons. Higher temperature and higher humidity were significantly correlated with higher peritonitis rate, especially the rate of CoNS peritonitis. The prognosis of PDAP in summer was relatively poor, with higher proportion of hospitalization and lower cure rate.

Objective Intradialytic hypotension (IDH) is one of the common complications during hemodialysis, however its diagnostic criteria are highly controversial at present. In order to fully understand the prevalence of IDH in our center and figure out which diagnostic criteria is better for Chinese maintenance hemodialysis (MHD) patients, we choose several IDH definitions by reviewing published literatures and analyze their association with mortality. Methods The patients were recruited from Blood Purification Center of Ruijin Hospital undergoing hemodialysis during July 2012. Pre-, intra- and post-dialysis blood pressure were recorded. Patients' clinical characteristics, laboratory results and cardiac ultrasound results were collected. Based on several IDH definitions, we investigated the prevalence rate of IDH and its frequency among MHD patients. SPSS 23.0 was used to analyze data and conduct survival analysis. Results Totally 219 MHD patients underwent 16084 hemodialysis in 6 months. The prevalence rate, overall and individual frequency of IDH fluctuated between 45.21%-100.00%, 4.64%-37.60% and 0.00%-33.00% respectively. For every IDH criteria, the patients were recruited into the group IDH(+) if they ever met the corresponding definition, otherwise the group IDH(-). Survival analysis found that IDH (the criteria of an absolute systolic blood pressure (SBP)＜90 mmHg or with a decrease of SBP≥ 20 mmHg) could decrease the risk of patients' cardiovascular mortality but was not relevant to all-cause mortality. Further analysis showed these patients had better cardiac functions mainly reflecting in lower Pro-BNP (2880 ng/L vs 6909 ng/L), lower prevalence rate of left ventricular hypertrophy (52% vs 83%) and higher left ventricular ejection fraction (65.0% vs 62.5%) than IDH(-) patients. No correlation was found between other IDH criteria and mortality. Conclusions The prevalence rate, overall and individual IDH frequency of IDH are of high variability when diagnosed by different IDH criteria. All IDH episodes defined by our selected definitions are of no association with all-cause mortality. An absolute SBP＜90 mmHg or with a decrease of SBP≥20 mmHg can decrease the risk of cardiovascular mortality due to their better cardiac function. Large scale researches should be conducted to find optimal IDH definition and explore the association of IDH and mortality.

Objective To evaluate the diagnostic value of clinical laboratory indexes on judgment of hypovolemia in the patients with nephrotic syndrome (NS). Methods The blood volume of each 50 cases of healthy adult men and women was assessed with indocyanine green-pulse dye densitometry (ICG-PDD). The normal range of blood volume and the cut-off value of hypovolemia were determined. The blood volume of 81 patients with NS was also measured with ICG-PDD and then these patients were divided into the hypovolemic group (21 cases) and the non-hypovolemic group (60 cases) according to the cut-off value of hypovolemia. The test data of clinical laboratory indexes of the patients in the two groups were compared, and the indexes with statistic difference were screened out. Their diagnostic values on judgment of hypovolemia were evaluated by receiver operating characteristic (ROC) curve analysis, and finally the indexes with high judgment accuracy were selected. Results ①The cut-off values of hypovolemia are＜52.9 ml/kg for the male and＜52.5 ml/kg for the women, which were determined with ICG-PDD. ②The five clinical laboratory indexes, including orthostatic heart rate (OHR) increase＞10 bit per minute, fractional excretion of sodium (FENa)＜1, transtubular potassium gradient (TTKG)＞60%, blood urea nitrogen/serum creatinine ratio (BUN/Scr)＞20, and urine specific gravity (SG)＞1.020, were used to judge the hypovolemia in NS patients in this study. ROC curve analysis showed that the diagnostic accuracy in judgment of hypovolemia by one index or two indexes combination only belonged to medium level. However, the diagnostic accuracy in judgment of hypovolemia by the following three indexes combination, i.e. OHR increase+FeNa+BUN/Scr, FeNa+ BUN/Scr+SG, OHR increase+TTKG+BUN/Scr, or ORG increase+FeNa+TTKG, reached high level. Conclusion This study obtained the cutoff value of Chinese adults hypovolemia are＜52.9 ml/kg for the male and ＜52.5 ml/kg for the women, which are determined with ICG-PDD, through evaluation we recommend applying the above four specific combinations of three indexes for diagnosis of hypovolemia in NS patients.

Objective To investigate the prevalence and correlation factors of cardiovascular damage in patients with diabetic nephropathy (DN) and non-diabetic nephropathy (NDN). Methods A total of 278 chronic kidney disease (CKD) patients admitted to the First Affiliated Hospital of Jinan University from January 2014 to May 2016 were enrolled, including 78 case of DN and 200 case of NDN. Patients had cardiac and carotid ultrasonography test by colour doppler ultrasonography, and their clinical and biochemical data were collected. Multiple linear regression analysis and multivariable logistic regression analysis were applied to study the correlation factors of cardiovascular damage in CKD patients. Results Mean age was 48.22 years in the 278-patient cohort, which included 178(64.03%) men. Compared with NDN group, DN patients had higher left atrial dimension, interventricular septal thickness, left ventricular end-diastolic dimension, left ventricular posterior wall thickness, left ventricular mass index (LVMI), carotid intima-media thickness (cIMT) and carotid plaques ratio. Their estimated glomerular filtration rate (eGFR) and the ratio between the peak speed of the early filling wave and that of the atrial contraction wave (E/A ratio) were however lower (all P＜0.05). Prevalence of left ventricular hypertrophy (LVH), left ventricular relaxant function reduction and cIMT thickening in DN group were 67.95%, 70.27% and 57.14%, higher than those in NDN group (40.00%, 42.31% and 17.39%, respectively) (all P＜0.05). Along with the progress of CKD, LVMI and LVH proportion in patients with DN and NDN increased gradually. LVMI and LVH proportion in DN patients in CKD 1-2 phase and CKD 3-4 phase were higher than those in NDN patients (all P＜0.05). In all CKD phases, cIMT and cIMT thickening proportion in DN group were higher than those in NDN group (all P＜0.05). Just in CKD 1-2 phase, DN group had lower E/A ratio and higher proportion of left ventricular relaxant function reduction than NDN group (all P＜0.05). After multiple linear regression analysis, gender, BMI, hemoglobin, eGFR and DN were related with LVMI; age, serum calcium and DN were related with E/A ratio; age and DN were related with cIMT (all P＜0.05). In multivariate logistic regression, DN, hemoglobin and eGFR decrease were independently associated with LVH; age and BMI were independently associated with reduction of left ventricular relaxant function; age and DN were independently associated with cIMT thickening in all CKD patients (all P＜0.05). Conclusions DN patients have more severe cardiovascular damage than NDN patients, and DN may be associated with LVMI, E/A ratio, cIMT, LVH and cIMT thickening in all CKD patients.

Objective To investigate the relationship between dyslipidemia and nephrolithiasis in a population-based study. Methods All participants were investigated by questionnaires, physical examinations and laboratory tests including liver and renal function, lipid profile, serum fasting glucose, glycosylated hemoglobin. Nephrolithiasis was diagnosed by kidney B-ultrasonography. Subjects with estimated glomerular filtration rate (eGFR)＜60 ml?min-1?(1.73 m2)-1 were excluded. Results 10 316 individuals were enrolled with an average age of (54.88±10.27) years (range 17-88 years) and the ratio of male to female 1∶1.12. The prevalence of nephrolithiasis was 5.6%, 3.7% and 7.8% for whole population, women and men, respectively. In women, only eGFR in stone group was significantly lower than that in non-stone group (P＜0.05). However, participants in stone group were significantly older (P＜0.05), of higher blood pressure (P＜0.01), higher serum uric acid (P＜0.01), worse renal function (serum creatinine, P＜0.05; eGFR, P＜0.01), and higher low-density lipoprotein (LDL) (P＜0.05), compared with those in non-stone group in men. Logistic regression analysis showed that only eGFR (P＜0.05) was the independent influential factor for kidney stones in women; In men, LDL was an independent influential factor for nephrolithiasis with a hazard ratio of 1.149 (95%CI 1.003-1.317, P＜0.05), except for mean blood pressure and eGFR. After being divided into normal group, borderline high group and high LDL group according to the LDL level, with the increase of LDL, the prevalence of nephrolithiasis was significantly increased by 7.3%, 8.3% and 10.6% in men respectively. There was no significant relationship between total cholesterol, triglyceride, high-density lipoprotein and nephrolithiasis. Conclusions Dyslipidemia is associated with nephrolithiasis in men, and high LDL cholesterol is an independent risk factor for nephrolithiasis. Clinical lipid testing not only helps to reduce the risk of atherosclerotic disease, but also reduces the risk of kidney stones.

Objective To observe the role and related mechanism of chemerin and its receptor ChemR23 in glomerular endothelial cells (GEnCs) stimulated by high glucose. Methods Mouse GEnCs were cultured and divided into control group, 20.0 mmol/L high glucose group, 40.0 mmol/L high glucose group and mannitol control group. Then the expressions of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in cell culture supernatant as well as the expressions of intracellular protein and mRNA of chemerin, ChemR23, IL-6 and TNF-α were detected. Lentiviral transfection targeting ChemR23 was applied before high glucose- or Chemerin-stimulated, and expressions of supernatant and intracellular mRNA of IL-6 and TNF-α were measured. Meanwhile whether p38 mitogen-activated protein kinase (p38 MAPK) pathway was activated by high glucose was detected. The specific inhibitor of p38 MAPK was added prior to high glucose-stimulated, then supernatant and intracellular mRNA expressions of IL-6 and TNF-α was detected. The supernatant expressions of IL-6 and TNF-α were measured by ELISA. The intracellular protein expression and p38 MAPK phosphorylation activity were detected by Western blotting. The mRNA expression was detected by real time PCR. Results Compared with those in the control group, in high glucose groups the expressions of IL-6, TNF-α and chemerin were significantly increased (all P＜0.05), however, the expressions of ChemR23 did not change (all P＞0.05); the supernatant and mRNA expressions of IL-6 and TNF-α were also elevated in the chemerin group (all P＜0.05). Lentivirus baring shRNA could efficiently suppress ChemR23 expression, and the Chemerin- or high glucose-induced expressions of IL-6 and TNF-α were reduced (all P＜0.05). Also it could significantly reduce the expression of phosphorylated-p38 MAPK (p-p38 MAPK) induced by high glucose (P＜0.05), as high glucose group had higher p-p38 MAPK than control group (P＜0.05). While the high glucose-elevated expressions of IL-6 and TNF-α were significantly attenuated by p38 MAPK inhibitor (all P＜0.05). Conclusions High glucose stimulation can induce the expression of chemerin in GEnCs. By binding to ChemR23, chemerin activates p38 MAPK signaling pathway, and then promotes the expressions of IL-6 and TNF-α. These inflammatory cytokines aggravate inflammation of GEnCs.

Objective To investigate the effects of nephroblastoma over-expressed protein (CCN3) on the formation of extracellular matrix (ECM) induced by transforming growth factor -β1 (TGF-β1) in human mesangial cells (HMCs) and its underlying signal transduction mechanism related with microRNA-29(miRNA-29). Methods HMCs were pretreated with different doses of exogenous CCN3 (5 μg/L, 50 μg/L and 500 μg/L) or transfected with pcDNA3.1(+)-CCN3 before exposed to TGF-β1(2 μg/L), to observe the expression of fibronectin (FN), type Ⅰ collagen (COLⅠ) and miRNA-29a, b and c. The mimics or inhibitor of the miRNA-29a were transfected into HMCs to analyze whether miRNA-29a affect CCN3. The expressions of FN mRNA, COLⅠmRNA and miRNA-29 family were detected by real time PCR. The protein expressions of FN and COLⅠ were detected by Western blotting and cell immunofluorescence. Results (1) Compared with the normal control group, the expressions of FN and COLⅠ were up-regulated in TGF-β1 group, while the expressions of miRNA-29a, b, c were down-regulated in TGF-β1 group (all P＜0.05). (2) Compared with the TGF-β1 group, the expressions of FN and COLⅠ were decreased when pretreated with the different doses of exogenous of CCN3 or transfected with pcDNA3.1(+)-CCN3 (all P＜0.05). Meanwhile, the expression of miRNA-29a was significantly increased when pretreated with 50 μg/L and 500 μg/L CCN3 or transfected with pcDNA3.1(+)-CCN3 (all P＜0.05); whereas miRNA-29b and c had no statistical difference (all P＞0.05). (3) Compared with TGF-β1+CCN3 group, the expressions of FN and COLⅠ were decreased in CCN3+TGF-β1+miRNA-29a mimics group (all P＜0.05), whereas the expressions of FN and COLⅠ in CCN3+TGF-β1+miRNA-29a inhibitors group were increased (all P＜0.05). Conclusions CCN3 reduces the TGF-β1-induced production of ECM by the up-regulation of miRNA-29a.