Objective To explore the clinicopathological features and renal outcomes of primary IgA nephropathy (IgAN) patients with chronic tonsillitis. Methods Patients with biopsy-proven primary IgAN admitted to The First Affiliated Hospital, Sun Yat-sen University from January 2006 to December 2011 were enrolled. The clinicopathological features and renal outcomes of patients with and without chronic tonsillitis were retrospectively compared. The primary outcome was progression to end stage renal diseases and/or doubling of serum creatinine. Results A total of 981 primary IgAN patients were enrolled and 98 patients (9.99%) had a history of chronic tonsillitis. Compared with patients without chronic tonsillitis, IgAN patients with chronic tonsillitis exhibited significantly higher prevalence of acute episodes of tonsillitis as a predisposition (P＜0.001), higher serum IgA levels (P=0.012), and higher prevalence of macrohematuria (P=0.006). No significant difference in renal pathological features was observed in patients with and without chronic tonsillitis. Moreover, the renal outcomes were similar as regards IgAN patients with and without chronic tonsillitis. Conclusion IgAN patients with chronic tonsillitis had higher prevalence of acute episodes of tonsillitis and macrohematuria as well as higher serum IgA levels. However, IgAN patients with and without chronic tonsillitis showed no significant difference in renal pathological features and renal outcomes.

Objective To investigate the risk factors and prognosis of peritoneal dialysis (PD) related bacterial peritonitis. Methods The clinical data of patients with PD related bacterial peritonitis from January 2006 to September 2016 in our hospital were retrospectively analyzed and followed up until December 2016. Patients were divided into two groups according to the frequency of peritonitis, single episode group and multiple episodes group (no less than two episodes of peritonitis). According to efficacy of therapy, the episodes of peritonitis were divided into two groups, cured group (no relapse, recurrence or repeat episodes) and failure group (relapse, recurrent or repeat infection after the therapy of initial episode). Logistic regression and Cox regression were used to analyze the risk factors for outcomes. Results Five hundred and fifty-nine patients had PD related bacterial peritonitis, including 339 patients in the single episode group and 220 patients in the multiple episodes group. Logistic analysis showed low serum albumin level (OR=787, P＜0.001) and malnutrition (OR=0.422, P＜0.001) at baseline were independent risk factors for multiple episodes (P＜0.001). The technical survival was better in the single episode group than that in the multiple episodes group (75.2% vs 36.2%, P=0.001) while the difference of survival rate was not significant between the two groups (48.2% vs 24.1%, P=0.592). Five hundred and thirteen episodes of peritonitis were analyzed, including 147 episodes in failure group (88 relapse episodes, 16 recurrent episodes and 43 repeat episodes) and 366 episodes in cured group. There were 78 patients in failure group and 253 patients in cured group. Logistic analysis showed prolonged response time (OR=1.200, P＜0.001), Gram-positive bacteria infection (OR=1.736, P=0.022), higher hs-CRP level (OR=1.004, P=0.013), lower serum albumin level (OR=0.936, P=0.008) were independent risk factors for failure of therapy. Multivariate Cox regression showed prolonged response time (HR=1.120, P=0.032), Gram-positive bacteria infection (HR=2.462, P=0.002), higher hs-CRP level (HR=1.007, P=0.009) were independent risk factors for failure of therapy and higher serum albumin level (HR=0.942, P=0.048) was an independent protection factor. Conclusions Low serum albumin level and malnutrition at baseline are independent risk factors for patients with multiple peritonitis episodes. Prolonged response time, Gram-positive bacteria infection, the high hs-CRP level are independent risk factors for relapse or recurrent or repeat episodes while high serum albumin level was an independent protection factor.

Objective To observe the changes of irisin in patients before and after hemodialysis (HD), as well as the differentiation of irisin change in patients with diabetes mellitus and protein energy waste. Methods Clinical parameters of patients on maintenance hemodialysis (MHD) in Shanxi People's Hospital from September 2016 to November 2016 were collected. A total of 33 cases were enrolled——14 cases of diabetic MHD group and 19 cases of non-diabetic MHD group as divided according to etiology. Based on the presence of protein energy waste, patients were also grouped into 17 cases with and 16 cases without protein waste. Before and after HD, the non parametric test was used to compare the changes of irisin in each group. Results After HD, the irisin value of 33 patients with ERSD decreased, with the difference being statistically significant [0.666(0.218, 1.365) ng/L vs 0.977(0.202, 1.820) ng/L, P=0.01]. The difference was not statistically significant in the diabetes MHD group; statistically significant in the non diabetes group [0.666(0.178, 1.351) ng/L vs 0.913(0.100, 1.497) ng/L, P﹤0.05]; and not statistically significant in the protein energy group. The irisin of diabetic MHD group and non-diabetic MHD group were compared after HD: the difference was not statistically significant. Conclusions After HD, plasma irisin levels were reduced in patients with end-stage renal disease. Diabetes and protein wasting effects are not important for irisin at HD.

Objective To evaluate the relationship between coronary artery calcification (CAC) and outcomes in maintenance hemodialysis (MHD) patients. Methods Eighty-six patients who were on MHD between October 2014 and May 2015 in the blood purification center of our hospital were enrolled prospectively. CAC was measured and scored by multiple slice computed tomography (MSCT). According to the CAC score (CACs), the patients were divided into mild CAC (CACs＜100) group and severe CAC (CACs≥100) group. Kaplan-Meier analysis was performed to analyze the survival rates of the two groups, and a COX proportional hazards regression model was used to estimate the risk factors of all-cause mortality and cardiovascular disease mortality in MHD patients. Results Severe CAC (CACs≥100) was present in 62.8% (54/86) patients. The median of follow-up duration was 28.9(23.8, 29.4) months. During the follow up, 2(6.3%) patients in CACs＜100 group and 18 (33.3%) patients in CACs≥100 group died. Kaplan-Meier survival analysis demonstrated that patients in CACs≥100 group had higher all-cause mortality and cardiovascular mortality as compared with patients in CACs＜100 group (P=0.007, P=0.030). Multivariate COX regression analysis demonstrated that CACs≥100 (HR=7.687, 95%CI 1.697-34.819, P=0.008) and low single-pool Kt/V (HR=0.092, 95%CI 0.020-0.421, P=0.002) were independent risk factors for all-cause mortality. Old age (HR=1.192, 95%CI 1.100-1.291, P＜0.001), short duration of dialysis (HR=0.598, 95%CI 0.445-0.804, P=0.001), low 25-hydroxy vitamin D3 (HR=0.461, 95%CI 0.326-0.630, P＜0.001), and low total cholesterol (HR=0.405, 95%CI 0.213-0.772, P=0.006) were independent risk factors for cardiovascular disease mortality. Conclusions The CACs is significantly related with overall survival in MHD patients. Large multicenter prospective studies are to be evaluated the association between CACs and long-term survival in MHD patients.

Objective To elucidate the efficiency lncRNA GAS5 and miR-21 as biomarkers in diabetes mellitus and diabetic nephropathy. Methods The patients were divided into three groups, diabetic nephropathy group (DN group proven by renal biopsy, n=25, 14 males and 11 females), diabetes group (DM group, with normal urine albumin creatinine ratio, n=10, 4 males and 6 females), and normal control group (NC group, n=9, 4 males and 5 females). The expressions of lncRNA GAS5 and miR-21 in serum samples were detected by real-time quantitative PCR. The correlation between serum lncRNA GAS5 and miR-21 expressions and the clinical parameters was analyzed by T-test, Pearson, Spearman test and multivariate linear regression analysis. Differences of lncRNA GAS5 and miR-21 in different groups were analyzed by one-way analysis of variance. The ROC curve was used to analyze the diagnostic efficacy of lncRNA GAS5 and miR-21 in diabetes and diabetic nephropathy. All data were analyzed by SPSS 20.0 and GraphPad software, with P＜0.05 as considered statistically significant. Results (1) The expression of serum lncRNA GAS5 was significantly down-regulated and serum miR-21 was significantly up-regulated in both diabetes mellitus and diabetic nephropathy patients compared to the NC group all (P＜0.05). (2) In DN patients, the expression of serum lncRNA GAS5 was gradually up-regulated along with the increment of 24 h urinary protein. The expression of serum miR-21 was gradually up-regulated along with renal biopsy stage IIb-Ⅲ of DN (P＜0.05). (3) FBG and HbA1c were all negatively correlated with serum lncRNA GAS5 (P＜0.05), and FBG was independently correlated with serum lncRNA GAS5 (P＜0.05). Urine microalbumin, Total cholesterol(TC), Scr, Urea and SBP were all positively correlated with serum miR-21(P＜0.05). Albumin (ALB) and estimated GFR (eGFR) were negatively correlated with serum miR-21(P＜0.05), and ALB was independently correlated with serum miR-21 (P＜0.05). (4) The diagnostic efficiency of serum lncRNA GAS5, miR-21 and lncRNA GAS5/miR-21 as "diagnostic signature" for DM were was good (P＜0.05). (5) The diagnostic efficiency of serum miR-21 and lncRNA GAS5/miR-21 as "diagnostic signature" for DN were was good (P＜0.05). Conclusions (1) Serum lncRNA GAS5 had good diagnostic efficiency in diabetes mellitus. The sensitivity of lncRNA GAS5/miR-21 for diagnosis of diabetes was 85.71%, and specificity was 88.89%. (2) The level of serum miR-21 can be used as a noninvasive diagnostic marker for diabetic nephropathy.

Objective To investigate the association between cumulative exposure blood to pressure (cum BP) and new-onset chronic kidney disease (CKD). Methods In this prospective cohort study, 101 510 employees of Kailuan Group receiving annual health examination during 2006 to 2007 were observed. The participants received the second, third, and fourth annual health examinations during 2008 to 2009, 2010 to 2011, and 2012 to 2013 year respectively. Their urinary and serum creatinine were tested, and participants with incomplete SBP, DBP data and CKD were excluded. Further excluding those who somehow failed to take annual health examination, with incomplete data, or new-onset CKD 27 809 participants were selected in the analysis. According to cum BP exposure quintile grouping: Q1＜3.70 scores; Q2: 3.70-6.16 scores; Q3: 6.17-8.45 scores; Q4: 8.46-10.95 scores; Q5≥10.96 scores. Multivariate Logistic regression was used to analyze the association between cum BP level and new-onset CKD by cum BP exposure quintile grouping. Results The rise of cum BP exposure level caused the increased incidence of CKD. The incidences of CKD in the five quintile groups were 2.59%, 3.11%, 4.19%, 5.81%, and 7.73% respectively (P＜0.01). Compared with Q1 group, multivariate logistic regression analysis showed that after the adjustment of age, gender, education, income, smoking, drinking, BMI, FBG, TC, TG, LDL, HDL, UA and CRP, the incidences of CKD gradually increased in the Q2, Q3, Q4, and Q5 cum BP quintile groups, and OR(95%CI) values were 1.08(0.86-1.35), 1.26(1.01-1.58), 1.57(1.27-1.95), 1.78(1.43-2.21) respectively (P for trend＜0.01). Similar results were obtained in different genders. For each single point increase of cum BP exposure level, the incidence of CKD increased 6% in the general population (P for trend＜0.01), increased 8% in male (P for trend＜0.01), and 3% in female (P for trend=0.12). Conclusion As the cumulative exposure to blood pressure increases, the risk of CKD incidence rises, especially in men.

Objective To investigate the role and mechanism of sulforaphane (SFN) in vascular calcification induced by oxidative stress. Methods The uremic vascular calcification model was established by treating rat vascular smooth muscle cells (RASMCs) with β-glycerophosphate. RASMCs were divided into 6 groups: normal control (NC) group, 1 μmol/L SFN group, 5 μmol/L SFN group, calcification group, 1 μmol/L SFN+calcification group, 5 μmol/L SFN+calcification group, and were all cultured for 72 h. Cell viability was measured by MTT. RASMCs calcification was visualized by Von Kossa staining. Calcium content was quantified by the microplate test, and mRNA level of FGF-23 was tested by real-time PCR. The expressions of OPN, Runx-2, Nrf-2 and Sirt-1 were evaluated by Western blotting. Confocal microscope was employed to observe mitochondria damage in RASMCs and the production of ROS in RASMCs was measured by reactive oxygen species assay. Results (1) SFN did not affect cell viability of the NC group, but both low dosage and high dosage increased the cell viability of calcification group (all P＜0.05). (2) Compared with calcification group, SNF treatment decreased the calcium concentration, intracellular calcium deposition and the mRNA level of FGF-23 (all P＜0.05). (3) Compared with calcification group, SNF treatment decreased the fluorensence intensity, mitochondria injury and the protein expressions of OPN and Runx-2, but increased the protein expressions of Nrf-2, Sirt-1 and cleaved caspase-3 (all P＜0.05). Conclusion SNF can effectively protect RASMCs against vascular calcification induced by oxidative stress, since it prevents the ROS production and mitochondria dysfunction through Nrf-2 and Sirt-1.

Objective To explore the effects and possible mechanism of histone deacetylase inhibitor SAHA on the interstitial fibrosis induced by diabetes. Methods The SD rats were divided into three groups: control group (Con, n=9), diabetes mellitus (DM) group (n=9) and SAHA treatment group (n=9). The diabetic rat model was established by injecting streptozotocin (STZ) through tail vein. After 8 weeks, the SAHA treatment group rats were fed with a SAHA solution (25 mg?kg-1?d-1) by gastric gavage. After 16 weeks, all rats were sacrificed to detect relevant biochemical parameters, and observe the changes of pathomorphology in kidney. In addition, immunohistochemistry staining and Western blotting were employed to detect the protein expressions of transforming growth factor-β1 (TGF-β1), Smad2, Smad3, p-Smad2, p-Smad3, Smad7, collagen-Ⅰ and collagen-Ⅲ, respectively. Results Compared with Con group, the levels of blood glucose (BG), urinary trace albumin/urinary creatinine (ACR), triglyceride (TG) and total cholesterol (TC) in the diabetic group were all increased significantly (all P＜0.05), the protein expressions of TGF-β1, p-Smad2, p-Smad3, collagen-Ⅰ and collagen-Ⅲ in kidney were all increased in diabetic group (all P＜0.05), and the expression of Smad7 was significantly reduced (P＜0.05). Compared with DM group, the levels of ACR was reduced, the renal fibrosis was alleviated, the protein expressions of TGF-β1, p-Smad2, p-Smad3, collagen-Ⅰ and collagen-Ⅲ in SAHA group were all decreased (all P＜0.05), and the expression of Smad7 was increased significantly (P＜0.05). Conclusion SAHA may restore the protein level of Smad7 by enhancing protein stability, then promote the moderate transduction of TGF-β1/Smads signaling pathway, which reduce the fibrosis of renal tubules in diabetic rats.

Objective To explore the expression of miroRNA-21 (miRNA-21) in myocardial fibroblasts stimulated by indoxyl sulfate (IS) and its role on paracrine factors of myocardial fibroblasts. Methods Myocardial fibroblasts which derived from C57BL/6J mice were divided into control group and IS group, and their expressions of miRNA-21 were detected by real time PCR after 48 h. MiRNA-21 inhibitor transfection was applied to silence miRNA-21 expression. Myocardial fibroblasts were divided into creatinine (Scr) group (Scr treated for 48 h), Scr+IS group (Scr and 50 μmol/L IS treated for 48 h), Scr+miRNA-21 inhibitor group (miRNA-21 inhibitor treated for 24 h and then Scr treated for 48 h) and Scr+miRNA-21 inhibitor+IS group (miRNA-21 inhibitor pretreated for 24 h and then Scr and IS treated for 48 h). Enzyme-linked immunosorbent assay was performed to evaluate the expressions of interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Western blotting was applied to detect the expressions of transforming growth factor-β (TGF-β), matrix metalloproteinases 2 (MMP2), matrix metalloproteinases 9 (MMP9) and tissue inhibitor of metalloproteinases 1 (TIMP1). Results The expression of miRNA-21 was obviously increased in IS group than that in control group (P＜0.01). Compared with those in Scr group, the expressions of IL-1, IL-6, TNF-α, TGF-β, MMP2 and MMP9 significantly increased (all P＜0.05), while the expression of TIMP1 decreased (P＜0.05). When the expression of miRNA-21 was inhibited, the expressions of IL-1, IL-6, TNF-α, TGF-β and MMP2 in Scr+miRNA-21 inhibitor+IS group significantly decreased than those in Scr+IS group (all P＜0.05), and the expression of TIMP1 decreased further (P＜0.05). Conclusions IS can promote the expression of miRNA-21 in myocardial fibroblasts. MiRNA-21 plays an important role in regulating inflammatory factors and pro-fibrogenic cytokines in myocardial fibroblasts.

Objective To explore the reversibility of early stage tubular interstitial injury as well as the timing of reparation through the pig relief of unilateral ureteral obstruction (R-UUO) model. Methods Eight three-month-old female Guangxi BA-MA mini pigs were selected for the construction of R-UUO models. Five time points were set which were UUO 0 day, UUO 3 days, R-UUO 7 days, R-UUO 14 days, and R-UUO 21 days. Renal function, histological structure, and protein expressions of α-smooth muscle actin (α-SMA), vimentin and E-cadherin were evaluated at different time points. Results After 3 days of UUO, compared with UUO 0 day, serum creatinine levels were increased obviously and the kidney tissues presented varying degrees of damage. The expressions of α-SMA and vimentin were increased and E-cadherin expression was decreased (P＜0.05). Following R-UUO after 3 days of UUO, compared to UUO, serum creatinine levels were significantly decreased. Renal pathological tissue damage was repaired. The expressions of α-SMA and vimentin were decreased and E-cadherin expression was increased (P＜0.05). Conclusions The pig R-UUO animal model may provide a good platform to study the kidney injury and repair. The tubular injury may be fully reversed and repaired when removing the pathogenic factors if the renal tubular injury was at an earlier stage.