Background Diabetic nephropathy (DN) is a main cause of chronic renal failure. Despite decades of extensive study, the molecular mechanisms underlying diabetic tubulointerstitial injury remain unclear. We aim to identify key transcription factor genes involved in diabetic tubulointerstitial injury. Methods A microarray dataset (GSE30122) from Gene Expression Omnibus (GEO) was downloaded. A total of 38 transcription factor genes based on 166 differentially expressed genes (DEGs) were identified by UCSC_TFBS. Results The regulatory network showed connections between the top 10 transcription factors and their target DEGs. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of targeted DEGs indicated that extracellular space, extracellular exosome, cell surface and complement and coagulation cascades were most significantly enriched. Utilizing Nephroseq v5 online platform, the mRNA expression pattern analysis of transcription factor genes demonstrated that mRNA expression of CDC5 , CEBPA , FAC1 , HFH1 , IRF1 , NFE2 and TGIF1 increased in renal tubulointerstitium of DN patients compared with normal controls while that of CEBPB and FOXO4 decreased in renal tubulointerstitium of DN patients compared with normal controls. Correlation analysis between mRNA expression of transcription factor genes in renal tubulointerstitium and clinical features showed that AP1 , BACH1 , CDC5 , FAC1 , FOXD1 , FOXJ2 , FOXO1 , FOXO4 , HFH1 , IRF1 , POU3F2 , SOX5 , SOX9 , RSRFC4 , S8 and TGIF1 may be related to diabetic tubulointerstitial injury. Conclusions (1) CDC5 , FAC1 , FOXO4, HFH1 , IRF1 and TGIF1 may be key transcription factor genes. (2)Transcription factors involved in diabetic tubulointerstitial injury may become prospective targets for diagnosis and treatment of DN.

While β-hemolytic streptococcus (β-HS) infections are known to predispose patients to acute poststreptococcal glomerulonephritis, there is evidence that implicates α-hemolytic streptococcus (α-HS) in IgA nephropathy (IgAN). The alternative pathway of the complement system has also been implicated in IgAN. We aimed to explore the association between α-HS and complement activation in human tonsillar mononuclear cells (TMCs) in IgAN. In our study, α-HS induced higher IgA levels than IgG levels, while β-HS increased higher IgG levels than IgA levels with more activation-induced cytidine deaminase, in TMCs in the IgAN group. Aberrant IgA1 O-glycosylation levels were higher in IgAN patients with α-HS. C3 and C3b expression was decreased in IgAN patients, but in chronic tonsillitis control patients, the expression decreased only after stimulation with β-HS. Complement factor B and H (CFH) mRNA increased, but the CFH concentration in culture supernatants decreased with α-HS. The percentage of CD19 + CD35 + cells/complement receptor 1 (CR1) decreased with α-HS more than with β-HS, while CD19 + CD21 + cells/complement receptor 2 (CR2) increased more with β-HS than with α-HS. The component nephritis-associated plasmin receptor (NAPlr) of α-HS was not detected on tonsillar or kidney tissues in IgAN patients and was positive on cultured TMCs and mesangial cells. We concluded that α-HS induced the secretion of aberrantly O-glycosylated IgA while decreasing the levels of the inhibitory factor CFH in culture supernatants and CR1 + B cells. These findings provide testable mechanisms that relate α-HS infection to abnormal mucosal responses involving the alternative complement pathway in IgAN.

IgA nephropathy (IgAN) is the most common primary glomerular disease. The characteristic pathology involves immune complexes formed by the deposition of IgA1 and underglycosylated IgA1 aggregates in the mesangial area, which may be accompanied by the deposition of IgG and/or IgM and complement components. However, the molecular mechanisms of IgAN remain unclear. In the present study, microarray analysis showed that the expression of microRNA-630 (miR-630) was significantly reduced in palatal tonsils from IgAN patients compared with chronic tonsillitis. Additionally, bioinformatic analysis showed that Toll-like receptor 4 (TLR4) was the predicted target gene of miR-630 and was regulated by miR-630. When miR-630 was overexpressed in palatal tonsil mononuclear cells from IgAN patients, the expression of TLR4 was reduced and the content of IgA1 in the cell culture supernatant was decreased, and the level of galactosylation in the IgA1 hinge region was increased. Moreover, immunohistochemical analysis showed that the expression of TLR4 in IgAN patients was significantly increased. After knocking down the expression of TLR4, both the concentration of IgA1 and the binding force of IgA1 with broad bean lectin were significantly reduced in IgAN. Furthermore, the mechanism study demonstrated that TLR4 might regulate the expression of IL-1β and IL-8 through NF-κB signaling pathway to modulate the concentration of IgA1 and the glycosylation level of IgA1. This interesting finding may offer new insight into the molecular mechanism of IgAN.

Many studies have focused on finding predictors for mild IgAN progression. However, the cases of severe IgAN with a high proportion of global glomerulosclerosis have received inadequate attention. A group of 172 primary IgAN patients with 50–75% global glomerulosclerosis was studied retrospectively between April 2007 and October 2017. Patients were divided into three groups according to the serum triglyceride tertiles: < 1.42 µmol/L (Group 1), 1.42–2.29 µmol/L (Group 2), and > 2.29 µmol/L (Group 3). Groups 1 and 2 comprised non-hypertriglyceridemia subjects, while Group 3 was defined as the hypertriglyceridemia (HTG) group. The patients were followed for 4–96 months (median 39.43 months). The study end point was defined as a 50% decline in estimated glomerular filtration rate (eGFR) or ESRD. A high proportion of global glomerulosclerosis is not absolutely correlated with severe clinical features and poor renal outcome. In our retrospective observation, eGFR decreased by less than 10% of the baseline during follow-up in 43.6% of the patients. However, in our patients with HTG, the cumulative renal survival rate was significantly lower compared to those without HTG. Multivariate Cox regression analysis also showed that triglyceride is an independent predictor of poor renal outcomes. Furthermore, in the HTG group, the cumulative renal survival rates were higher in patients treated with Tripterygium wilfordii Hook F (TwHF) compared to those without TwHF. A high proportion of global glomerulosclerosis combined with HTG at biopsy have better predictive validity for the disease progression of IgAN than global glomerulosclerosis alone. TwHF may partially affect the renal outcome of severe IgAN with HTG, and this may relate to its regulation of lipid metabolism and immunoinflammatory response.

Renal ischemia-reperfusion injury (IRI), a major cause of acute kidney injury as well as a contributor to a rapid kidney dysfunction and high mortality rates, is a complex yet not fully understood process. Investigation on the underlying molecular mechanism including the inflammation initiation and progression can help to have a better understanding of the disease, and thereby lead to a potential therapeutic approach. We established renal IRI mouse model groups differing in their ages. These renal IRI mice were treated either only with si-nuclear receptor subfamily 4, group A, member 1 (NR4A1) or together with si-β-catenin by tail vein injection to analyze the role of NR4A1 and β-catenin in the development of renal IRI. Serum creatinine (SCr) and blood urea nitrogen (BUN) levels were examined for renal function analysis. Levels of the apoptosis markers B-cell lymphoma-2 (Bcl-2), Bcl-2 associated protein X (Bax), and cleaved caspase-3 were determined. NR4A1 gene was up-regulated in the renal tissues of all mice with IRI, which showed a much higher level in the old mice with IRI. si-NR4A1 treatment resulted in reduced SCr and BUN levels and a decrease of cell apoptosis, indicated by lower expression of Bax and cleaved Caspase-3, while in contrast increased levels of Bcl-2 were detected. Interestingly, also the β-catenin level was increased by knockdown of NR4A1. Furthermore, si-β-catenin reversed the effect of knockdown of NR4A1, leading to aggravated renal function damage, severe pathological injury and increased apoptosis. Thus, silencing NR4A1 ameliorates renal IRI via β-catenin signaling pathway activation. Down-regulated NR4A1 confirms renoprotective properties against renal IRI via the activation of β-catenin signaling pathway in old mice.

Background: Despite the progression of dialysis techniques, the mortality of hemodialysis (HD) patients is still high in China. Here, a retrospective study was performed to investigate the neglected risk factors of all-cause mortality during maintenance HD (MHD). Methods: We investigated 117 MHD patients who died between 2011 and 2016 in the Second Xiangya Hospital of Central South University HD center. In order to analyze the risk factors of 48 months all-cause death, the methods of Kaplan-Meier and Cox regression were used. Results: Multivariate analyses of adjusted age and gender showed that MHD patients with estimated glomerular filtration rate <7 or >10 mL/min/1.73 m2 and anemia (hemoglobin <100 g/L) at the initiation of dialysis are independently associated with the higher death risk. Using central venous catheter vascular access, cerebrovascular comorbidities, diabetes, low-flux dialyzer, and dialysis frequency ≤2 times weekly were also the independent risk factors of death within 48 months. Conclusions: This study indicated that the status of HD initiation is a risk factor of long-term survival in MHD patients, which were usually ignored for lacking of nephrology care prior and could potentially be identified and modified to improve the survival prognosis. Video Journal Club “Cappuccino with Claudio Ronco” at https://www.karger.com/Journal/ArticleNews/223997?sponsor=52

Diabetic nephropathy (DN) is a primary cause of renal failure. However, studies providing renal gene expression profiles of diabetic tubulointerstitial injury are scarce and its molecular mechanisms still await clarification. To identify vital genes involved in the diabetic tubulointerstitial injury, three microarray data sets from gene expression omnibus (GEO) were downloaded. A total of 127 differentially expressed genes (DEGs) were identified by limma package. Gene set enrichment analysis (GSEA) plots showed that sister chromatid cohesion was the most significant enriched gene set positively correlated with the DN group while retinoid X receptor binding was the most significant enriched gene set positively correlated with the control group. Enriched Gene Ontology (GO) annotations and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of DEGs mostly included extracellular matrix organization, extracellular space, extracellular matrix structural constituent, and Staphylococcus aureus infection. Twenty hub genes from three significant modules were ascertained by Cytoscape. Correlation analysis and subgroup analysis between hub genes and clinical features of DN showed that ALB, ANXA1, APOH, C3, CCL19, COL1A2, COL3A1, COL4A1, COL6A3, CXCL6, DCN, EGF, HRG, KNG1, LUM, SERPINA3, SPARC, SRGN, and TIMP1 may involve in diabetic tubulointerstitial injury. ConnectivityMap analysis indicated the most significant three compounds are 5182598, thapsigargin and 5224221. In conclusion, this study may provide new insights into the molecular mechanisms underlying diabetic tubulointerstitial injury as well as potential targets for diagnosis and therapeutics of DN.

Background: Aberrant O-glycosylation IgA1 production is a major factor in the pathogenesis of IgA nephropathy, but the underlying mechanism is still unclear. IgA1 glycosylation modification is in Golgi, and downregulation of the Golgi peripheral membrane protein Golgi matrix protein 130 (GM130) could lead to glycosylation deficiency. In this study, we aimed to explore the role of GM130 in glycosylate deficiency IgA1 (Gd-IgA1) production. Methods: We enrolled 27 IgA nephropathy patients, 12 patients with chronic tonsillitis, 15 non-IgAN chronic kidney disease patients, and 15 healthy volunteers as healthy control. We explored GM130 expression in Tonsillar tissue by immunofluorescence staining and Western blotting and expression in peripheral blood mononuclear cells (PBMCs) by flow cytometry. The concentration of IgA1 and level of O-glycosylation were determined by ELISA and Vicia Villosa lectin-binding assay. Real-time PCR and Western blot were used to analyze the levels of β1,3-Gal transferase (C1GALT1) and ST6GalNAC2, respectively. To explore the contribution of GM130 in IgA1 O-glycosylation modification, cells were subjected to experiments for evaluation of GM130 silencing by GM130-siRNA transfection. Results: GM130 expression was significantly decreased in tonsil tissues and PBMC of IgAN patients; the expression of C1GALT1 decreased and Gd-IgA1 level increased significantly in patients with IgAN patients. The expression of GM130 was negatively related to Gd-IgA1 production. By siRNA transfection, our results clearly indicated that the downregulation of GM130 can increase IgA1 O-glycosylation deficiency, which is thought to reduce C1GALT1 expression but not affect the expression of ST6GalNAC2. Conclusion: We identified and demonstrated that GM130 plays an important role in IgA1 O-glycans deficiency in IgAN patients, by negatively regulating C1GALT1 expression. We believe that this finding will provide theoretical foundations for a new mechanism of Gd-IgA1 production in IgAN patients.

OBJECTIVE:To investigate the correlation of different types of urinary abnormalities or different proteinuria and hematuria with the pathological injury of kidney in IgA nephropathy with isolated hematuria and/or mild proteinuria.
 Methods: Patients with primary IgA nephropathy, isolated hematuria and/or mild proteinuria were enrolled in the Department of Nephrology, the Second Xiangya Hospital, Central South University from January 2013 to January 2018. According to the difference of red blood cell count in urinary sediment and quantitative of 24-hour urinary protein (24 h-UP) during renal biopsy, the patients were grouped in 3 ways: a simple hematuria group, a hematuria and proteinuria group, and a simple proteinuria group; a proteinuria I group, a proteinuria II group, and a proteinuria III group; a hematuria I group, a hematuria II group, and a hematuria III group. The clinical parameters such as age, mean arterial pressure, blood urea nitrogen, serum creatinine, blood uric acid, 24 h-UP, and renal pathological damage were compared.
 Results: A total of 157 patients met the inclusion criteria, including 71 males and 86 females. The most common pathological type was focal and/or segmental glomerulosclerosis. The Lee's classification were dominated by grade III and IV, and the renal pathological injury was heavy. Immunoglobulin deposition was dominated by simple IgA deposition. The most common fluorescence intensity of IgA deposition was +++. 97 (61.78%) patients were accompanied by complement deposition and were mainly composed of simple complement C3 deposition. There were 18 patients (11.47%) in the simple hematuria group, 111 patients (70.70%) in the hematuria and proteinuria group, and 28 patients (17.83%) in the simple proteinuria group. Compared with the simple hematuria group, the proportion of patients with mild injury was lower in the simple proteinuria group, and the proportion of patients with moderate-to-severe injuries was increased (χ2=7.053, P=0.008). Compared with the hematuria and proteinuria group, the proportion of patients with mild injury was lower in the simple proteinuria group, and the proportion of patients with moderate-to-severe injury was increased (χ2=4.294, P=0.038). Compared with the proteinuria I group, the proportion of patients with mild injury was lower in the proteinuria III group, and the proportion of patients with moderate-to-severe injury was increased (χ2=5.433, P=0.020). There was no significant difference in the proportion of patients with renal pathological injury among different hematuria groups (P>0.05).
 Conclusion: The clinical manifestations of patients with IgA nephropathy with hematuria and/or mild proteinuria are inconsistent with renal pathological damage. Some patients with mild clinical manifestations have severe renal pathological damage and the renal pathological damage is more serious in simple proteinuria. The more proteinuria, the heavier the renal pathological damage.

Damaged or dysfunctional mitochondria are toxic to the cell by producing reactive oxygen species and releasing cell death factors. Therefore, timely removal of these organelles is critical to cellular homeostasis and viability. Mitophagy is the mechanism of selective degradation of mitochondria via autophagy. The significance of mitophagy in kidney diseases, including ischemic acute kidney injury (AKI), has yet to be established, and the involved pathway of mitophagy remains poorly understood. Here, we show that mitophagy is induced in renal proximal tubular cells in both in vitro and in vivo models of ischemic AKI. Mitophagy under these conditions is abrogated by Pink1 and Park2 deficiency, supporting a critical role of the PINK1-PARK2 pathway in tubular cell mitophagy. Moreover, ischemic AKI is aggravated in pink1 andpark2 single- as well as double-knockout mice. Mechanistically, Pink1 and Park2 deficiency enhances mitochondrial damage, reactive oxygen species production, and inflammatory response. Taken together, these results indicate that PINK1-PARK2-mediated mitophagy plays an important role in mitochondrial quality control, tubular cell survival, and renal function during AKI.

Diabetic nephropathy (DN) is a major cause of end-stage renal disease. Although intense efforts have been made to elucidate the pathogenesis, the molecular mechanisms of DN remain to be clarified. To identify the candidate genes in the progression of DN, microarray datasets GSE30122, GSE30528, and GSE47183 were downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) were identified, and function enrichment analyses were performed. The protein-protein interaction network was constructed and the module analysis was performed using the Search Tool for the Retrieval of Interacting Genes and Cytoscape. A total of 61 DEGs were identified. The enriched functions and pathways of the DEGs included glomerulus development, extracellular exosome, collagen binding, and the PI3K-Akt signaling pathway. Fifteen hub genes were identified and biological process analysis revealed that these genes were mainly enriched in acute inflammatory response, inflammatory response, and blood vessel development. Correlation analysis between unexplored hub genes and clinical features of DN suggested that COL6A3, MS4A6A,PLCE1, TNNC1, TNNI1, TNN2, and VSIG4 may involve in the progression of DN. In conclusion, DEGs and hub genes identified in this study may deepen our understanding of molecular mechanisms underlying the progression of DN, and provide candidate targets for diagnosis and treatment of DN.

Background/Aims: Tonsillectomy may be an important method to achieve a long-term remission of IgAN, but patients’ physical status may limit their access to this surgery. We proposed an encouraging solution through inhibiting GADD34 expression in order to promote tonsillar mononuclear cells (TMCs) apoptosis and reduce nephropathic IgA secretion. Methods: A total of 12 IgAN and 9 non-IgAN patients were involved from March 2015 to May 2016. After TMCs were extracted by density gradient centrifugation and stimulated by inactivated hemolytic streptococcus, the mRNA and protein expression of GADD34, GRP78, CHOP, Bcl-2, Bcl-XL, AID, Iα-Cα, and cleaved caspase-3 were examined by fluorescent RT-PCR and Western blotting. Guanabenz treatment and siRNA interference were applied to downregulate GADD34 in tonsillar mononuclear cells from IgAN patients, and P-eIF2α expression was examined by Western Blotting. Cell apoptosis was evaluated by Annexin V FITC/PI flowcytometry, and IgA secretion in cultural supernatant was inspected by enzyme linked immunosorbent assay. Results: After stimulation, the expression of GADD34 was significantly increased in IgAN patients (P< 0.05). Cell apoptosis was mitigated and IgA secretion level was elevated (P< 0.05). To be noticed, CHOP expression had no significant difference between two groups. After guanabenz treatment and siRNA interference, a prolonged elevation of P-eIF2α expression was observed. Cell apoptosis was reinforced and IgA secretion level was decreased (P< 0.05). Conclusion: GADD34 may be a potential therapeutic target for IgAN treatment due to its effect on cell apoptosis.

The classical theory of heat conduction (Fourier theory) predicts an infinite speed for thermal disturbance propagation, which is physically unrealistic. By extending the classical Fourier heat conduction and Fick's diffusion, this paper presents a hyperbolic diffusion law with different phase lags of thermal and moisture fluxes to simulate coupled heat-moisture diffusion-propagation behavior. Transient hygrothermal and elastic response of an infinitely long cylinder subjected to sudden hygrothermal loadings at the surface is studied. By using Laplace transform and decoupling technique, a closed form solution of temperature, moisture, displacements and stresses is determined. The analytical results show that the thermal and moisture relaxation times or phase lags of heat and moisture fluxes play a significant role in the early stage of transient response after heat/moisture shock. The classical results corresponding to vanishing phase lags can be recovered from the present ones. For non-vanishing phase lags, hygrothermal waves have finite propagation speeds. Numerical results are calculated and displayed graphically to show the influence of the phase lags of heat and moisture fluxes on transient hygrothermoelastic fields. A comparison between classic model and hyperbolic hygrothermal coupling model is given. Based on the non Fourier heat conduction and non-Fick diffusion, some shortcomings induced by the classical Fourier's and Fick's laws can be effectively avoided. (C) 2018 Elsevier Ltd. All rights reserved.

Objective To detect the expression of molecular marker protein and miR-200c in the mesothelial cells of the peritoneal dialysate effluent fluid of peritoneal dialysis( PD) patients,and to investigate the association between miR-200c and human peritoneal mesothelial cell( HPMC)epithelial-mesenchymal transition( EMT). Methods Twelve patients recently given continuous ambulatory peritoneal dialysis( initial PD group) and 16 patients undergoing peritoneal dialysis for more than 6 months( PD over 6 months group) were randomly chosen for the isolation,culture and identification of effluent cells. Real-time PCR and Western blotting were used to detect the expression levels of miR-200c,and the levels of four cellular marker proteins: E-cadherin,vimentin,fibronectin( FN) and COL-1,in effluent cells. Results Cells isolated from effluents of dialysis fluid were identified as HPMCs. The morphology of effluent cells varied according to how long patients undergoing PD. The relative expression of miR-200c in the effluents HPMCs of the initial PD group was( 7. 546 ± 0. 341),and the relative expression of miRNA-200c in the effluent HPMCs of the PD over 6 months group was( 1. 701 ± 1. 070)( P < 0. 01). The level of E-cadherin mRNA and protein expression was significantly lower in the PD over 6 months group than in the initial PD group,while vimentin,FN and COL-1 mRNA and protein expression levels were significantly increased in the PD over 6 months group as compared with those in the PD initial group. Conclusions Cells isolated from effluents of dialysis fluid were identified as HPMCs,and the expression of miRNA-200c in HPMCs were confirmed. With the prolongation of PD time,miR-200c expression was significantly reduced and associated with EMT,suggesting that miR-200c may be associated with peritoneal fibrosis.

SUV39H1, the histone methyltransferase (HMTase) of histone H3 lysine 9 trimethylation (H3K9me3), is a known transcriptional repressor of inflammatory genes. The effect of SUV39H1 on inflammatory gene promoters under high-glucose stimulation in vascular smooth muscle cells (VSMCs), macrophages, and cardiomyocytes has been studied, but how SUV39H1 functions in renal tubules under diabetic conditions is unclear. Renal biopsy specimens of ten diabetic nephropathy (DN) subjects and seven non-DN minimal change diseases (MCD) subjects were collected. SUV39H1, IL-6, and MCP-1 expression in renal tissues were measured using immunohistochemical, while SUV39H1, H3K9me3, IL-6, and MCP-1 in human proximal tubular epithelial cells (HK-2) under varying glucose conditions were assayed by Western blot and ELISA. SUV39H1 was overexpressed in HK-2 cells; the regulation of SUV39H1 and H3K9me3 on NF-κB, IL-6, MCP-1, caspase 3, and apoptosis was measured. SUV39H1 was expressed more in diabetic human renal tubules. HK-2 cells with high glucose up-regulated IL-6 and MCP-1 in a dose- and time-dependent manner, and SUV39H1 expression was reduced with greater glucose and prolonged stimulation. Expression of H3K9me3 was synchronized with SUV39H1. Moreover, overexpression of SUV39H1 in high glucose environment was accompanied with increased H3K9me3 and decreased inflammation and apoptosis. SUV39H1 dysregulation may be involved in DN progression. Overexpression of SUV39H1 may reduce renal inflammation and apoptosis via epigenetic modulation, thus plays a protective role in DN.

Acute kidney injury (AKI) and chronic kidney disease (CKD) are interconnected. Although AKI-to-CKD transition has been intensively studied, the information of AKI on CKD is very limited. Nonetheless, AKI, when occurring in patients with CKD, is known to be more severe and difficult to recover. CKD is associated with significant changes in cell signaling in kidney tissues, including the activation of transforming growth factor-beta, p53, hypoxia-inducible factor, and major developmental pathways. At the cellular level, CKD is characterized by mitochondrial dysfunction, oxidative stress, and aberrant autophagy. At the tissue level, CKD is characterized by chronic inflammation and vascular dysfunction. These pathologic changes may contribute to the heightened sensitivity of, and nonrecovery from, AKI in patients with CKD.

Proteinuria and decline of renal function are associated with progression of kidney disease. The Renin Angiotensin Aldosterone System (RAAS) plays an important role in blood pressure regulation, fluid volume, and sodium balance. Overactivity of RAAS contributes to the pathogenesis of a variety of clinical conditions including progress of chronic kidney disease (CKD). This review summarizes the use of RAAS inhibitors as dual therapy or monotherapy in different stages of kidney disease. Experimental and clinical studies have demonstrated RAAS inhibitors prevent proteinuria, kidney fibrosis and slow decline of renal function and thus play a protective role in both early and end stages of kidney disease. While combination use of RAAS inhibitors showed higher efficiency compared with monotherapy, it is also associated with higher incidence of adverse events. Besides ACEI/ARBs, more mechanism research of mineralocorticoid receptor antagonists in kidney disease should be performed.

Objective To investigat the symptom burden of patients with maintenance hemodialysis (MHD) and explore the influencing factors of them,in order to provide the basis for improving the quality of life of these patients.Methods A total of 230 patients with MHD were enrolled in Xiangtan Central Hospital from January 2016 to December 2016,the general condition and disease-related data of them were collected,and the symptom burden of them over the past week was assessed by improved symptom burden scale.Results ① The average age of these patients were (56.8 ± 14.1)years,the sex ratio for men and women was 1.37∶ 1,the median time of dialysis was 24 months,and the frequency of dialysis was (9.16 ± 2.36)times;② The symptom score in MHD patients was (65.72 ± 28.46)points,the top 5 symptoms which had higher incidence were fatigue (72.2％),dry mouth (63.5％),itching (61.3％),falling asleep difficultly (54.3％),drying (49.2％),the top 5 symptoms which were more troubling were restless legs syndrome (2.54 ± 0.73),falling asleep difficultly (2.48 ± 0.83),bone/joint pain (2.45 ± 0.69),fatigue (2.31 ±0.77),easy to wake up (2.16 ±0.78);③ Age,sex,occupation,dialysis age,inorganicphosphorus and serum calcium had an effect on the symptom burden of MHD patients (P ＜ 0.05).Condusions We should focus on patients who are older,female,retired or no occupation,longer dialysis age,calcium or phosphorus metabolism disorders,provide targeted care and treatment,in order to reduce the symptom burden and improve the life quality of them.

Objectives To explore control rates of CKD-MBD markers in hemodialysis patients in the first hospital of changsha,and evaluate the association between CKD-MBD markers and mortality.Methods A retrospective general data and laboratory test results of 177 HD patients who received regular outpatient HD in the hospital from January 2014 until December 2016 were performed.The control rate of CKD-MBD markers were evaluated based on the KDIGO clinical guidelines.According to the clinical outcome,the patients were divided into the death group (n =35) and the survival group (n =142).iPTH,P and Ca were compared between the two groups by generalized estimating equation.A logistic regression model was used to evaluate the relationship between serum Ca,P and iPHT levels and the risk for all-cause mortality.Results In the 177 cases,normal serum Ca was found in 102 (57.6％)cases,normal phosphate in 51 (28.8％) cases and normal iPTH in 81 (45.8％) cases.There were differences in our study between surviving and non-surviving patients' Ca and iPTH,and no difference in P.In our study,all-cause mortality was associated with increased levels of Ca and P in hemodialysis patients,and iPTH levels were not significantly associated with all-cause mortality.Conclusions The results of the study are different from the results of previous observational studies in Europe and the United States.Whether the suggestions of KDIGO Guidelines are suitable for Chinese hemodialysis patients still needs further evidences.