Objectives To investigate whether the presence of metabolic syndrome (MS) modifies overall survival and cardiovascular (CV) outcomes among patients undergoing long-term peritoneal dialysis (PD) and to explore suitable diagnostic criterion for PD patients. Methods A total of 258 patients on PD in Peking University Third Hospital between October 2008 and March 2009 were enrolled and followed until June 2017. According to the diagnostic criteria of WHO, IDF and ATP Ⅲ, the patients were divided into MS group and non-MS group. The median following time was 51.9 (26.8, 97.9) months. Overall survival and cardiovascular death were analyzed by the Kaplan-Meier method. The analyses were also done among non-diabetic PD patients. The influence of MS and its components on outcomes was analyzed by Cox regression models. Results Among 258 PD patients, 106(41.1%) fulfilled the WHO criteria, 121(46.9%) the IDF criteria, and 167(64.7%) the ATP criteria. 139 cases were dead, among which 50(36.0%) cases were caused by CV diseases. The patients with MS had worse outcomes than those without MS by WHO and IDF criteria (cumulative survival rates of WHO criteria: 21.3% vs 44.8%, P﹤0.01; cumulative surviva rats of IDF criteria: 23.3% vs 45.7%, P﹤0.01). It was the same even in non-diabetic PD patients. The patients with MS had more CV death than those without MS by WHO and IDF criteria (both P﹤0.05). Among non-diabetic PD patients, the results remained the same only by IDF criteria (P﹤0.05). By ATP criteria, above analyses showed no difference. By multivariate Cox regression analysis, MS and serum albumin (all P﹤0.01) were independently associated with increased risk for overall and cardiovascular survival. Among MS components, waist girth, low-density lipoprotein cholesterol (LDL-C) levels and blood sugar (all P﹤0.01) were significant risk factors for adverse survival outcomes. Conclusions In patients undergoing PD, both overall survival and cardiovascular survival were worse in patients with MS than those without MS. Waist girth, blood sugar and serum LDL-C were the main risk factors. For PD patients the IDF criterion for MS was recommended.

Objective To evaluate the relationship between low vitamin D level and metabolic syndrome (MS) in maintenance hemodialysis (MHD) patients. Methods A total of 143 patients who had received MHD from Jan 2016 to Jan 2017 in the dialysis center of our hospital were enrolled. Their clinical and laboratory data were collected. The serum 25(OH)D3 levels were measured by chemiluminescence instrument. According to the levels of 25(OH)D3, patients were divided into three groups: sufficient group (＞30 μg/L), insufficient group (15-30 μg/L) and deficient group (＜15 μg/L) to explore how the 25(OH)D3 were associated with MS and abnormal metabolic parameters, including central obesity, raised triglycerides (TG), reduced high-density lipoprotein cholesterol (HDL-C), raised systolic blood pressure (SBP), raised diastolic blood pressure (DBP) and increased fasting blood glucose (FBG). The risk factors of MS and abnormal metabolic factors were analyzed by multivariate logistic regression model. Results Among the 143 MHD patients, the median of serum 25(OH)D3 was 24.30(12.90, 29.50) μg/L and the prevalence of MS was 45.45%(65 cases). Among 3 groups the prevalence of MS, the abdominal circumference and the serum TG showed statistical differences, and they increased with the severity of 25(OH)D3 deficiency (all P＜0.05). The body mass indexes of patients in the insufficient and deficient groups were elevated compared with that in the sufficient group (all P＜0.05). SBP, TG and FBG in deficient group were significantly higher but HDL-C was lower than those in the other two groups (all P＜0.05). The more abnormal metabolism existed, the lower 25(OH)D3 levels patients had (H=61.316, P＜0.001). Multivariate logistic regression analysis showed that in MHD patients low 25(OH)D3 negatively correlated with MS (OR=0.889, 95%CI 0.846-0.934, P＜0.001) and abnormal metabolic factors central obesity (OR=0.913, 95%CI 0.874-0.953, P＜0.001), raised TG (OR=0.932, 95%CI 0.894-0.971, P=0.001), reduced HDL-C (OR=0.901, 95%CI 0.845-0.959, P=0.001), raised SBP (OR=0.898, 95%CI 0.847-0.953, P＜0.001) and raised FBG (OR=0.956, 95%CI 0.920-0.994, P=0.024). Conclusions The prevalence of MS is high in MHD patients and low levels of 25(OH)D3 may be an independent risk factor for MS and abnormal metabolic factors.

Objective To understand the prevalence, treatment and influence factors of hypertension in maintenance hemodialysis (MHD) patients in Anhui Province. Methods A total of 2724 adult patients on MHD from January 1st 2014 to March 31st 2014 in 26 hospitals of southern, northern and central Anhui Province were investigated. Their demographic characteristics, primary disease, complications, medications, dialysis and laboratory examination were explored. The prevalence treatment rate and control rate of hypertension were analyzed. Associated factors for controlling hypertension [systolic blood pressure (SBP)＜140 mmHg and diastolic blood pressure (DBP)＜90 mmHg] were assessed by logistic regression analysis. Results (1) The prevalence of hypertension in the hemodialysis patients was 87.0%. Their treatment rate and control rate were 93.2% and 23.9% respectively. The average of SBP was (145.90±21.18) mmHg, and the DBP on average was (83.60±12.21) mmHg. The most commonly used anti-hypertensive drug is calcium channel blocker (88.2%). Over one third (45.7%) of patients were treated with two kinds of anti-hypertensive drug, 26.2% with 1 kind, 21.7% with 3 kinds, and 6.4% with 4 kinds or more. (2) Compared with non-hypertension patients, patients with hypertension have older age, higher body mass index (BMI), phosphorus, SBP and DBP, as well as lower hemoglobin and Kt/V (all P＜0.05). (3) The multivariate logistic regression analysis showed that Ca＞2.50 mmol/L (OR=2.084, 95%CI 1.008-4.307, P=0.047) positively correlated with controlling hypertension, while smoke (OR=0.594, 95%CI 0.356-0.911, P=0.046) and BMI 18.5～23.9 kg/m2 (OR=0.516, 95%CI 0.293-0.907, P=0.022) negatively correlated with it. Conclusions High prevalence yet low control rate of hypertension in MHD patients in Anhui Province were observed. Hypocalcemia may be a protective factor for hypertension control, while smoke and BMI may be risk factors for it.

Objective To improve clinicians' understanding of post-transplant lymphoproliferative disorder (PTLD) after renal transplantation, a rare case of this disease was reported and literature was reviewed. Method The clinical data and pathological changes of the allograft, immunohistochenmistry (IHC) and in situ hybridization (ISH) were analyzed. In addition, the relevant literature was reviewed. The clinicopathological features and differential diagnoses of PTLD were discussed. Result A renal mass (5.6 cm×5.4 cm), which was suggestive of primary renal malignancy, had been detected on the patient after received renal transplantation for a year and a half. Grossly, the mass was 7cm in diameter, with fleshy texture. Microscopically, the renal parenchyma was destructed and infiltrated with massive inflammatory cells, mostly lymphoid cells and occasionally Reed-Sternberg-like cells. IHC showed CD20 and CD79a were predominantly expressed in lymphoid cells. ISH showed diffused Epstein-Barr virus encoded RNAs (EBERs) positivity. The above findings were consistent with PTLD, polymorphic B cell hyperplasia (polymorphic PTLD), with concurrent Epstein-Barr virus infection. Conclusion Lymphoid infiltration in a renal allograft needs to be differentiated from T-cell rejection, viral infection, nephropyelitis, as well as PTLD. Early detection and proper management of PTLD may help improve the graft survival rate.

Objective To explore the effect of acteoside (one of the ingredients of Total Glycosides Extracted from Rehmannia capsules) on treatment of proteinuria and protection of podocytes. Methods In this study, puromycin nephropathy rat model was successfully established. After detecting the degree of proteinuria, the expression of podocyte injury markers and the degree of podocyte foot process fusion were investigated by electron microscope. In addition, puromycin treated podocyte injury model was also successfully established in vitro. Podocyte viability, migration, cytoskeleton and injury marker were detected. Results In vivo study showed that acteoside could effectively reduce proteinuria (P＜0.05), restore the expression of podocyte injury markers such as nephrin and synaptopodin (all P＜0.05), and alleviate the degree of podocyte foot process fusion. In vitro study showed that acteoside could effectively restored podocyte viability (P＜0.05), reduce abnormal migration ability (P＜0.05), protecte cytoskeleton and restore the expression of podocyte injury marker nephrin (P＜0.05). Conclusions This study confirms that acteoside can reduce the degree of proteinuria in puromycin nephropathy rat model in vivo and alleviate the degree of podocyte injury in vitro as well as enrich the molecular mechanism of Total Glycosides Extracted from Rehmannia capsules in treatment of proteinuria.

Objective To investigate the effect of pyrin domain 3 (NLRP3) inflammasome in the process of contrast induced human kidney cell apoptosis. Methods Human kidney 2 (HK-2) cells were cultured in DMEM-F12 medium with 5% FBS. Cells were divided into control group, Contrast group (O group), NLRP3-siRNA+Iohexol group (si-NLRP3+O group), ASC-siRNA+Iohexol group (si-ASC+O group), and mannitol group (M group). Different concentrations of hypotonic contrast agent were added to HK-2 cell culture plates for 24, 48 and 72 h. Flow cytometry was used to detect apoptosis. NLRP3 and ASC mRNA expressions were detected by RT-PCR. The expressions of NLRP3, ASC, caspase-8/cleaved caspase-8, Bcl-2/Bax, caspase-1/cleaved caspase-1, and caspase-3/cleaved caspase-3 protein were detected by Western blot. The levels of interleukin (IL) 1β and IL-18 in supernatant were detected by ELISA. Results Compared with the control group, the rate of apoptotic cells, as well as the expressions of NLRP3, ASC and cleaved caspase-1 proteins were increased in HK-2 cells of contrast group. The expressions of NLRP3 and ASC mRNA in the contrast group also increased, so did IL-1β and IL-18 levels (all P＜0.05), suggesting that NLRP3 inflammasome in HK-2 cells was activated by contrast. Compared with the control group, the expressions of cleaved caspase-8, Bax and cleaved caspase-3 protein were increased, and the expression of anti-apoptotic protein Bcl-2 was decreased (all P＜0.05). Compared with the contrast group, the rate of apoptotic cells in the si-NLRP3+contrast group and si-ASC+contrast group was significantly decreased; the expression of cleaved caspase-1 was decreased; the expressions of Bax and cleaved caspase-3 were decreased, and Bcl-2 level was increased. The expressions of IL-1β and IL-18 in the supernatant of cells were decreased (all P＜0.05). Conclusion Contrast agent can activate the NLRP3 pathway in HK-2 cells and induce apoptosis, which could be reduced by blocking the NLRP3 pathway.

Objective To investigate the mechanism of cellular senescence in ischemia reperfusion injury (IRI)-induced acute kidney injury (AKI) that leads to chronic kidney disease (CKD) in elderly mice. Methods An acute kidney injury model was established in C57Bl/6 male mice at ages 8-10 weeks (young group) or 20-24 months (old group) by bilateral IRI. The animals were randomly divided into 4 groups as follows: Young-Sham (n=8), Old-Sham (n=8), Young-IRI (n=8), and Old-IRI groups (n=8). All mice were weighted, and their blood was collected from the tail vein at days 1, 3, and 7 after surgery. The mice were killed on day 14 after surgery, and their kidneys were harvested for further analysis. Serum was used for the creatinine test. The changes of the renal tissue morphology and pathology were assessed using hematoxylin-eosin staining and sirius red staining. Immunofluorescence staining of collagenⅠ, F4/80, phosphor-histone H3 (p-HH3), and Ki67 were performed to determine the stage of the collagen deposit, macrophage filtration, and cell cycle G2/M arrest. The collagenⅠ expression was analyzed using western blot. The expression levels of TNF-α, IL-6, TGF-β, and collagenⅠ were determined using real-time PCR. Results Compared with that in the sham group, the serum creatinine levels in both Young-IRI and Old-IRI groups were obviously increased. The Young-IRI group recovered completely on day 7. The Old-IRI group had higher creatinine levels than the Young-IRI group at each time point. Morphology and pathology analyses revealed that acute injury was repaired in the Young-IRI group, but slight inflammatory cell filtration and collagen deposition were observed in the Old-Sham and Old-IRI groups, respectively. Immunofluorescence staining revealed some F4/80-positive macrophage filtration, collagenⅠdeposition, and p-HH3 and Ki67 double-positive nuclear tubular epithelial cells in the Old-Sham group, but considerably more positive results were found in the Old-IRI group. Western blot analysis revealed that collagenⅠ expression level was higher in the Old-IRI group than in the Young-IRI group (P＜0.01) and in the Old-Sham group than in the Young-Sham group (P＜0.05). Real-time PCR demonstrated that the mRNA expression levels of cytokines and fibrosis markers, including of TNF-α, IL-6, TGF-β, and collagenⅠ, in the Old-Sham and Old-IRI groups were increased as compared with those in the Young-Sham and Young-IRI groups (P＜0.05). Conclusions The levels of kidney inflammation, fibrosis, and cell-cycle arrest are lower in the old mice. After IRI injury, a sustained and ongoing inflammatory reaction is involved and more cells are arrested in the cell cycle G2/M, which inhibit renal repair and promote fibrosis progression.

Objective To observe the expression of Notch1 signaling pathway in the aorta of chronic kidney disease (CKD) rats with vascular calcification and to explore the role of this signaling pathway activation in aortic calcification of CKD. Methods A total of 40 male SD rats were randomly divided into normal group (Nor group) and CKD with vascular calcification group (CKD+VC group). Rats in each group were sacrificed at 4 weeks, 6 weeks and 8 weeks respectively after the success of modeling. Their 24-hour urine was reserved to test 24 hour urine protein (24 h Upro); blood sample was collected from abdominal aorta to test blood urea nitrogen (BUN), serum creatinine (Scr), Ca and P. The histopathology of renal was detected by HE staining. The aortic calcification was detected by alizarin red S staining. Immunohistochemistry (IHC) was used to test the protein expressions of alpha -smooth muscle actin (α-SMA), Runt-related transcription factor 2 (Runx2), Notch1, recombination signal-binding protein for immunoglobulin kappa J region (RBP-Jκ), Msh homeobox 2 (Msx2), Jagged1 and Notch1 intracellular domain (N1-ICD) in the aorta. Real time PCR was applied to detect the mRNA expressions of α-SMA, smooth muscle 22 alpha (SM22α), Runx2, alkaline phosphatase (ALP), Notch1, RBP-Jκ, Msx2 and Jagged1. Results Compared with those in Nor group, 24 h Upro, BUN and Scr increased in the CKD+VC group at 4th, 6th and 8th weeks (all P＜0.05). Numerous continuous calcified nodules were detected in the vascular wall of the CKD+VC group, but none in Nor group. As compared with Nor group, the expression of α-SMA was low, while the expression of Runx2 was relatively high in the CKD+VC rats at each time point (all P＜0.05). The expressions of Notch1, RBP-Jκ, Msx2, Jagged1 and N1-ICD in the Nor group were slightly appeared in the aortic wall, while in CKD+VC group these signal protein expressions increased relatively during the experimental period (all P＜0.05). As compared with Nor group, the expressions of α-SMA and SM22α mRNA were low, yet the expressions of Runx2 and ALP mRNA were high in the CKD+VC rats at each time point (all P＜0.05). The mRNA levels of Notch1, RBP-Jκ, Msx2 and Jagged1 in the CKD+VC group at each time point were significantly up-regulated as compared with the Nor group (all P＜0.05). Conclusions There exist phenotypic changes in smooth muscle cells and activations of Notch1/RBP-Jκ/Msx2 signaling pathway in CKD rats with vascular calcification. It may be one of the important signal transduction pathways.