The interaction between injured proximal tubular epithelial cells (PTECs) and the microenvironment has been widely associated with post-AKI fibrosis; however, the underlying mechanisms remain largely unclear. In this study, we identified three distinct injury patterns of the tubular basement membrane (TBM) in kidney tissues from patients with acute kidney injury. Phosphorylated H3Ser10 and transforming growth factor-β1 (TGFB1) were co-localized in PTECs exhibiting TBM injury. To mimic this condition, we employed a low-attachment culture system (LACS). LACS induced in PTECs a morphology resembling that of maladaptive repaired PTECs, accompanied by G2/M cell-cycle arrest, as well as upregulation and secretion of TGFB1. The expression of TGFB1 was markedly suppressed when PTECs were re-attached to normal culture dishes or to medium supplemented with Matrigel. Furthermore, TGFB1 expression was not directly linked to G2/M arrest in PTECs. Mechanistically, knockdown of TGFB1 or SMAD3 attenuated the LACS-induced upregulation of SOX9, whereas SOX9 knockdown did not downregulate TGFB1 expression. We further demonstrated that TBM injury-induced upregulation of TGFB1 is mediated by ETV5. Collectively, these findings indicate that TBM damage triggered by AKI promotes renal fibrosis via activation of the ETV5/TGFB1/SMAD3/SOX9 pathway in proximal tubular epithelial cells following AKI.

Uremic cardiomyopathy (UCM) remains the leading cause of cardiovascular mortality in patients with end-stage renal disease (ESRD). Experimental animal models serve as essential tools for elucidating the potential mechanism underlying UCM. However, experimental UCM models are often challenged by inter-individual variability and inconsistent success rates. Reliable phenotypes are not guaranteed by current animal models of UCM. In this study, Tei index from echocardiography was investigated for its potential value in construction of murine UCM model based on 5/6 nephrectomy (Nx). Comprehensive echocardiographic assessment, measurement of blood pressure and serum creatinine, histological analysis, and quantitative polymerase chain reaction (qPCR) were performed to reveal the relationship between Tei index and construction of UCM model. The Tei index was significantly elevated in Nx mice despite preserved cardiac function and structural integrity at 8 weeks post-nephrectomy. A longitudinal follow-up to the 12th week revealed that the Nx mice with higher Tei index (Nx HT) presented distinct features of hemodynamic remodeling, left ventricular hypertrophy and diastolic dysfunction. Furthermore, pronounced myocardial hypertrophy and extensive myocardial interstitial fibrosis were confirmed in the Nx HT group. This study validates the Tei index as a sensitive and non-invasive parameter for the early evaluation and prediction of UCM murine model induced by 5/6 nephrectomy.

X-linked agammaglobulinaemia (XLA) is a rare congenital immunodeficiency caused by pathogenic mutations in the Bruton's tyrosine kinase (BTK) gene, characterised by a reduction in mature B cells and low levels of immunoglobulins, which predispose patients to recurrent infections. However, renal involvement in adult XLA patients is extremely rare. Here, we report a man in his early 20s with XLA who experienced recurrent severe infections, resulting in elevated serum creatinine, nephrotic-range proteinuria and haematuria. Laboratory analysis revealed the absence of mature B cells and significantly reduced immunoglobulin levels. A kidney biopsy confirmed a diagnosis of membranoproliferative glomerulonephritis (MPGN), and genetic testing identified a BTK gene mutation. This is a rare case of XLA complicated by MPGN prior to intravenous immunoglobulin therapy, which expands the pathological spectrum of renal involvement.

Background Sepsis-induced acute kidney injury (S-AKI) is a common complication in critically ill patients. Therefore, reliable biomarkers for predicting S-AKI outcomes are necessary. Serum cell-free DNA (cfDNA) is a circulating extracellular DNA fragment used as a noninvasive screening tool for many diseases, including sepsis. This study aimed to investigate the prognostic value of cfDNA in S-AKI patients and its relationship with some other parameters.Methods A total of 89 S-AKI patients admitted to the intensive care unit (ICU) from June 2021 to December 2021 were enrolled in this study. The patients were categorized into the low cfDNA group (< 855 ng/ml) and high cfDNA group (≥ 855 ng/ml) and were followed up for three months. CfDNA was extracted from serum and quantified using Quant-iT PicoGreen dsDNA Reagent.Results Overall survival was significantly lower in the high cfDNA group than in the low cfDNA group (Log-Rank p = 0.012). Univariate Cox proportional hazard model showed that cfDNA was significantly associated with all-cause mortality (HR [hazard ratio] 2.505, 95% CI [95% confidence interval] 1.184-5.298, p = 0.016). Also, serum cfDNA was a significant risk factor for all-cause mortality after adjusting for covariates (HR 2.191, 95% CI 1.017-4.721, p = 0.045). Moreover, cfDNA was positively correlated with several baseline parameters, including serum creatine, aspartate aminotransferase, alanine aminotransferase, prothrombin time, and International Normalized Ratio.Conclusion High serum cfDNA level is associated with higher mortality among the S-AKI population, indicating that cfDNA is a valuable biomarker for S-AKI prognosis.

BACKGROUND:The application value of myocardial work (MW) in evaluating myocardial function and predicting major adverse cardiovascular events (MACE) in maintenance hemodialysis (MHD) patients has not been fully explored. PURPOSE:Comparing noninvasive MW parameters between MHD patients and healthy controls, and further determining its value in predicting MACE in MHD patients. METHODS:A prospective single-institution study included 92 MHD patients without prior cardiovascular disease and 40 age- and sex-matched healthy controls. Conventional echocardiographic data, global longitudinal strain (GLS), and MW parameters (global work index [GWI], global constructive work [GCW], global work efficiency [GWE], global wasted work [GWW]) were derived and compared between MHD and the control. Logistic regression was used to determine the predictive value of these parameters for MACE. The receiver operating characteristic curve was utilized to compare the predictive differences of MACE between GWE and GLS. RESULTS:Compared with healthy individuals, MHD patients had significantly reduced GWE, GLS and elevated LVMI, GWW (all p < 0.001), while there was no significant difference in left ventricular ejection fraction. Twenty eight (30%) MHD patients experienced MACE. Two nested models adding GWE and GLS, respectively, showed that age (p < 0.005), GWE (p = 0.034), and GLS (p = 0.014) were independent predictors of MACE. The AUC derived from GWE for predicting MACE was significantly higher than that derived from GLS (0.836 vs. 0.743, p = 0.039). CONCLUSIONS:Myocardial work is a novel tool for assessing left ventricular myocardial performance in MHD patients. GWE is an independent predictor of MACE.

BACKGROUND:The gut microbiota plays a crucial role in regulating host metabolism and producing uremic toxins in patients with end-stage renal disease (ESRD). Our objective is to advance toward a holistic understanding of the gut ecosystem and its functional capacity in such patients, which is still lacking.RESULTS:Herein, we explore the gut microbiome of 378 hemodialytic ESRD patients and 290 healthy volunteers from two independent cohorts via deep metagenomic sequencing and metagenome-assembled-genome-based characterization of their feces. Our findings reveal fundamental alterations in the ESRD microbiome, characterized by a panel of 348 differentially abundant species, including ESRD-elevated representatives of Blautia spp., Dorea spp., and Eggerthellaceae, and ESRD-depleted Prevotella and Roseburia species. Through functional annotation of the ESRD-associated species, we uncover various taxon-specific functions linked to the disease, such as antimicrobial resistance, aromatic compound degradation, and biosynthesis of small bioactive molecules. Additionally, we show that the gut microbial composition can be utilized to predict serum uremic toxin concentrations, and based on this, we identify the key toxin-contributing species. Furthermore, our investigation extended to 47 additional non-dialyzed chronic kidney disease (CKD) patients, revealing a significant correlation between the abundance of ESRD-associated microbial signatures and CKD progression.CONCLUSION:This study delineates the taxonomic and functional landscapes and biomarkers of the ESRD microbiome. Understanding the role of gut microbiota in ESRD could open new avenues for therapeutic interventions and personalized treatment approaches in patients with this condition.

Tubulointerstitial lesions play a pivotal role in the progression of IgA nephropathy (IgAN). Elevated N-acetyl-beta-D-glucosaminidase (NAG) in urine is released from damaged proximal tubular epithelial cells (PTEC) and may serve as a biomarker of renal progression in diseases with tubulointerstitial involvement. We evaluated the predictive value of urinary NAG (uNAG) for disease progression in 213 biopsy-proven primary IgAN patients from January 2018 to December 2019 at Zhongshan Hospital, Fudan University. We compared the results with those of serum cystatin C (sCysC). Increased uNAG and sCysC levels were associated with worse clinical and histological manifestations. Only uNAG level was independently associated with remission status after adjustment. Patients with high uNAG levels (> 22.32 U/g Cr) had a 4.32-fold greater risk of disease progression. The combination of baseline uNAG and clinical data may achieve satisfactory risk prediction in IgAN patients with relatively preserved renal function (eGFR ≥ 60 ml/min/1.73 m2, area under the curve [AUC] 0.760). Our results suggest that uNAG is a promising biomarker for predicting IgAN remission status.

Background and Purpose. Hemodialysis patients face a higher risk of ischemic stroke. p-Cresyl sulfate is a typical protein-bound uremic toxin that contributes to chronic kidney disease and cardiovascular disease progression, as well as mortality in hemodialysis patients. The present study was aimed at elucidating the association between p-cresyl sulfate and the risk of ischemic stroke in hemodialysis patients. Method. Patients on hemodialysis over 6 months were enrolled in this prospective cohort study and were divided into 2 groups based on plasma p-cresyl sulfate level. The primary end point was the first episode of ischemic stroke during follow-up. The association between p-cresyl sulfate and ischemic stroke incidence was analyzed by Kaplan-Meier method and Cox proportional hazard model. Results. 220 patients were enrolled in this study. 44 patients experienced episodes of first ischemic stroke during follow-up for 87.8 (47.6-119.5) months. Kaplan-Meier analysis demonstrated that the incidence of ischemic stroke in the high p-cresyl sulfate group was significantly higher than that in the low p-cresyl sulfate group (Log-Rank P=0.007). Cox regression analysis as well proved that p-cresyl sulfate level was significantly associated with the first incidence of ischemic stroke (HR (hazard ratio) 2.332, 95% CI (95% confidence interval) 1.236-4.399, P=0.009). After being adjusted for other confounding risk factors, the results persisted significant (model 11: HR 2.061, 95% CI 1.030-4.125, P=0.041). Conclusion. Plasma p-cresyl sulfate predicts the first incidence of ischemic stroke in hemodialysis patients.

Background Trimethylamine-N-Oxide (TMAO) is a proatherogenic and prothrombotic metabolite. Our study examined the association of plasma TMAO level with cardiovascular and all-cause mortality in hemodialysis (HD) patients. Methods Patients who were at least 18 years-old and received HD for at least 6 months were enrolled within 6 months. Patients with coronary heart disease, congestive heart failure, arrhythmia, or stroke within 3 months before study onset were excluded. The primary endpoints were cardiovascular and all-cause death, and the secondary endpoint was cerebrovascular death. Results We recruited 252 patients and divided them into a high-TMAO group (>4.73 μg/mL) and a low-TMAO group (≤4.73 μg/mL). The median follow-up time was 73.4 months (interquartile range: 42.9, 108). A total of 123 patients died, 39 from cardiovascular disease, 19 from cerebrovascular disease, and 65 from other causes. Kaplan-Meier analysis indicated that the high-TMAO group had a greater incidence of cardiovascular death (Log-Rank: p = 0.006) and all-cause death (Log-Rank: p < 0.001). Cox regression analysis showed that high TMAO level was significantly associated with cardiovascular and all-cause mortality. After adjustment for confounding, this association remained significant for cardiovascular mortality (TMAO as a continuous variable: HR: 1.18, 95%CI: 1.07, 1.294, p < 0.001; TMAO as a dichotomous variable: HR: 3.44, 95%CI: 1.68, 7.08, p < 0.001) and all-cause mortality (TMAO as a continuous variable: HR: 1.14, 95%CI: 1.08, 1.21, p < 0.001; TMAO as a dichotomous variable: HR: 2.54, 95%CI: 1.71, 3.76, p < 0.001). Conclusions High plasma TMAO level is significantly and independently associated with cardiovascular and all-cause mortality in HD patients.

目的 采用二维斑点追踪显像(speckle tracking imaging,STI)技术评价硫酸吲哚酚(indoxyl sulfate,IS)在肾功能不全(chronic renal failure,CRF)大鼠模型中的心脏毒性.方法 方法30只6周龄SD大鼠,随机入组肾功能不全CRF手术对照组、CRF+ IS处理(IS)组和假手术(sham operation,SOR)组,每组10只.对CRF组和IS组实施5/6肾切除术建立肾功能不全模型,建模成功后,IS组给予隔天腹腔注射IS(100mg/kg)约24周.每组大鼠在基线和注射结束1周时采集左室短轴二维超声图像,分析获得应变及应变率参数并进行组间及组内比较.实验完成后取心脏标本行病理学检查.结果 IS组中3只大鼠在IS注射12～20周中发生猝死,实验结束时SOR组10例,CRF组10例,IS组7例纳入统计分析.3组的左室内径均较基线明显增大,IS组和CRF组的室壁厚度均较基线明显增厚,IS组肥厚程度更为显著(P均＜0.01).实验前后,径向应变(radial strain,RS)在CRF组显著增加(P=0.017),但在IS组及SOR组差异无统计学意义.舒张功能参数环向应变率(circumferential peak E'/peak/A',E'/A'-SRc)和径向应变率(radial peak E'/peak/A',E'/A'-SRr)在IS组和CRF组均较基线显著降低,且实验后IS组显著低于CRF组(P均＜0.01).CRF组及IS组的心脏重量均显著大于SOR组(P均＜0.05).心肌细胞面积在SOR组、CRF组及IS组依次增大,且心肌纤维化程度在SOR组、CRF组和IS组依次增加(P均＜0.05).结论 IS可以加重肾功能不全大鼠的心肌损害,表现为心肌细胞的肥厚,坏死和纤维化,且左室舒张功能的下降早于收缩功能受损,应变率显像的舒张功能指标可敏感检测IS导致的左室舒张功能改变.

BackgroundRight ventricular (RV) dysfunction is a major cause of death in patients undergoing maintenance hemodialysis (MHD). We used 3‐dimensional speckle‐tracking echocardiography (3DSTE) to evaluate long‐term impacts of MHD on RV function.HypothesisIn this study, RV dysfunction in MHD patients will be revealed and studied in depth by 3DSTE.MethodsEchocardiography was performed on 110 consecutively enrolled individuals: 30 controls and 80 patients with MHD. Conventional echocardiographic parameters and 3DSTE parameters were obtained and compared between groups. Univariate and multivariate logistic regression analysis identified independent predictors of intradialytic hypotension (IDH).ResultsCompared with the control group, RV end‐diastolic volume (RVEDV) was markedly enlarged (46.1 ± 11.8 mL/m2 vs 42.3 ± 8.6 mL/m2; P = 0.047), whereas RV ejection fraction (RVEF) was significantly lower in the MHD group (50.6% ± 5.8% vs 55.2% ± 3.7%; P < 0.001). RV global, septal, and lateral wall longitudinal strains were also decreased in the MHD group (−18.2 ± 3.6 vs −22.6 ± 4.3%; −13.1 ± 3.8 vs −17.5 ± 5.5%; and −23.4 ± 4.7 vs −27.7 ± 4.0%, respectively; all P < 0.001). RVEF (odds ratio [OR]: 0.72, 95% confidence interval [CI]: 0.51 to 1.01, P = 0.038) and history of diabetes (OR: 11.14, 95% CI: 1.16 to 106.71, P = 0.036) were 2 independent predictors of IDH. Ultrafiltration rate was an independent factor associated with RVEF (β = −0.01, 95% CI: −0.019 to 0.001, P = 0.039).ConclusionsRVEF by 3DSTE could be an important predictor of IDH in MHD patients, and lower ultrafiltration rate was protective for RVEF. 3DSTE may have potential in RV evaluation and risk stratification in MHD patients.

Introduction: Patients with chronic kidney disease, especially those with end-stage renal disease, have an increased risk of death. Previous studies have suggested neutrophil/lymphocyte ratio (NLR) was related to worse outcome in patients undergoing hemodialysis (HD). However, monocyte/lymphocyte ratio (MLR) has not been evaluated in HD patients. In this study, we prospectively studied the predictive value of MLR for all-cause and cardiovascular mortality in HD patients and compared it with NLR.& para;& para;Methods: Patients who had been on a HD treatment for at least 6 months were enrolled. MLR was calculated by dividing the monocyte count by the lymphocyte count. Survival outcomes were estimated using the Kaplan-Meier method and compared by the log-rank test. Univariate and multivariate analyses were performed to evaluate the prognostic impact of MLR and other clinical factors on all-cause and cardiovascular mortality.& para;& para;Results: Mortality rates for the lowest, middle, and highest MLR textile group were 3.65, 7.02, and 11.15, respectively per 100 patient-years. The Kaplan-Meier analysis revealed that survival rates were significantly different among three MLR groups (P < 0.001). In multivariate Cox regression analyses, MLR was independently associated with all-cause mortality (HR 4.842; 95% CI, 2.091-11.214; P< 0.001) and cardiovascular mortality (HR 6.985, 95% CI 1.943-25.115, P = 0.003) as continuous variables. NLR was not an independent predictor of all-cause nor cardiovascular mortality after adjusted with MLR.& para;& para;Conclusions: The main finding of the study suggest that higher MLR was a strong and independent predictor of all-cause and cardiovascular mortality and overwhelmed NLR among HD patients.

Indoxyl sulfate (IS), a typical uremic toxin, is of great importance in the development of chronic kidney disease. In addition to its nephrotoxicity, previous studies have provided increasing evidence for its cardiovascular toxicity. The mechanism underlying IS‑induced cardiovascular toxicity has been elusive to date. The present study aimed to evaluate whether IS treatment could induce apoptosis of H9C2 cells, and used the endoplasmic reticulum (ER) stress‑modulator 4‑phenylbutyric acid (4‑PBA) to evaluate whether IS‑induced apoptosis is indeed associated with ERS. To evaluate whether IS induces apoptosis in H9C2 cardiomyocytes, cells were exposed to increasing concentrations of IS (500, 1,000, and 2,000 µM) for 24 h, and apoptosis was detected by flow cytometry. To determine whether IS‑induced apoptosis is associated with ERS, cells were divided into 4 groups: control group, PBA group, IS group and PBA+IS group. IS dose‑dependently induced apoptosis, and increased the expression of ER chaperones in H9C2 cells. Additionally, 4‑PBA treatment decreased IS‑induced apoptosis, and reduced ERS‑associated protein expression induced by IS. Therefore, the mechanism may be associated with the CCAAT‑enhancer‑binding protein homologous protein and c‑Jun N‑terminal kinase signaling pathways.

Objective To explore the risk factors of pulmonary artery hypertension (PAH) and the its relationship with T cell subsets to provide a foundation for the prevention and treatment of PAH.Methods 154 maintained hemodialysis (MHD) patients in our dialysis center were recruited according to the criterion and divided into two groups subsequently:PAH group (pulmonary artery systolic pressure,PASP ＞ 35 mmHg) and non-PAH group (PASP≤35 mmHg).The related clinical,biochemical and ultrasonic cardiogram data were collected and peripheral blood was acquired to detect the expressions of the surface antigen CD3,CD4,CD8 and CD69 with flow cytometry.Logistic regression analysis was used to find out the relationship between PAH and T cell subsets.Results There was no significant difference between 56 cases of PAH and 98 cases of non-PAH as regards gender,age,mean systolic and diastolic pressure,dialysis durations,morbidities of hypertension and diabetes,smoking rate,and left ventricular diameter.Compared with the non-PAH group,the PAH group demonstrated a lower percent of CD8 T cells and CD8 CD69 T cells,but a much higher left atrial diameter (LAD),Interventricular septum thickness,left ventricular posterior wall thickness,and NT-proBNP.The percentage of T cells,CD4 T cells and CD4 CD69 T cells showed no difference between the two groups.Multivariate analysis confirmed that PAH was negatively independently associated with the percentage of CD8 T cells and CD8CD69 T cells.Conclusions The decreased percentage of CD8 T cells and CD8CD69 T cells in the peripheral blood is a risk factor of PAH in maintained hemodialysis patients,and CD8 T cells may play an important role in the genesis of PAH.

Background: CD4 T-cell abnormality, influencing the outcome of the maintained hemodialysis (MHD), is common in patients on dialysis. We try to find out factors associated with the activated CD4 T cells, CD4CD69 T cells, to improve the dialysis quality.Methods: A cross-sectional study was conducted to evaluate the change of CD4CD69 in MHD patients and healthy controls in our hospital from September 2015 to May 2016. A total of 164 MHD patients and 24 healthy controls were included according to the criteria. Univariate and multivariate logistic regression models after correlation analysis were executed to discover the related factors of CD4CD69 T-cell posterior to the division of the CD4CD69 T cell according to its median.Results: The lymphocytes were lower, but the percentage of CD4CD69 T cells was higher in MHD patients compared with healthy controls, even after the propensity score matching based on age and sex. The percentage of CD4 T cells showed no significant difference between the two groups. Further multivariate logistic regression models revealed that CD4CD69 T cell was independently associated with serum total protein (OR 95% CI: 0.830[0.696, 0.990], p =.038), transferrin (OR 95% CI: 3.072[1.131, 8.342], p =.028) and magnesium (OR 95% CI: 16.960[1.030, 279.275], p =.048).Conclusion: The percentage of CD4CD69 T cells, activated CD4 T cells, elevated in hemodialysis patients despite the decrease in lymphocytes. The elevated CD4CD69 T cells were independently associated with serum total protein negatively, but transferrin and magnesium positively. Strengthening nutrition, reducing the concentration of transferrin and magnesium might be beneficial to reduce the activation of CD4 T cells and improve the outcome of MHD patients.

Chronic kidney disease (CKD) is an increasingly recognized disease with high global incidence and mortality. Yet, the existing diagnostic tools are not sufficient enough to predict prognosis of CKD and CKD comorbidities. Indoxyl sulfate, a typical uremic toxin, is of great importance in the development of CKD with its nephrotoxicity, cardiovascular toxicity, and bone toxicity. Some reports suggest that indoxyl sulfate directly associate with renal function loss and mortality in CKD patients. This review discusses the diagnostic value of indoxyl sulfate from its biological characteristics, pathophysiological effects, related therapies, and its diagnostic value in clinical studies.

Cerebrovascular complications, including ischemic stroke, account for poor outcomes in patients on hemodialysis. T cell responses may be involved in the pathogenesis of ischemic stroke. We aimed to evaluate the role of naïve T cells in development of ischemic stroke in patients on hemodialysis.

Objective To analyze the relationship between serum high-sensitivity cardiac troponin T (hs-cTnT) and cardiovascular disease (CVD) among non-dialysis chronic kidney disease (CKD) patients, and to further explore its value of evaluating and predicting CVD in this population. Methods Five hundred and fifty-seven non-dialysis CKD patients were involved in this cross-sectional study. The relationship between serum hs-cTnT and CVD was analyzed using comparison between groups and regression analysis, and its value on assessing cardiac structure and function was evaluated by ROC curves. Results Median level of hs-cTnT was 13 (7-29) ng/L, with 1.7% undetectable, 46.4% greater than 99th percentile of the general population. Multivariate analysis suggested that compared with the lowest quartile of hs-cTnT, the highest quartile was approximately six times as likely to develop into LVH (OR, 6.515; 95% CI, 3.478-12.206, p < 0.05) and 18 times as likely to progress to left ventricular diastolic dysfunction(OR, 18.741; 95% CI, 2.422-145.017, p < 0.05). And Ln cTnT level had a more modest association with LVEF (OR, -1.117; 95% CI, -5.839 to -0.594; p < 0.05). When evaluated as a screening test, the area under the curve of ROC curves for hs-cTnT was 0.718, 0.788 and 0.736, respectively (p < 0.05). With a specificity of 90% as a diagnostic criterion, the value of hs-cTnT to evaluate LVH, LVEF < 50%, left ventricular diastolic dysfunction increased across CKD stages, from CKD 1 stage to CKD 5 stage. Conclusions In CKD non-dialysis population, hs-cTnT and NT-proBNP were valuable for evaluating LVH, left ventricular systolic dysfunction and left ventricular diastolic dysfunction.

Objective To investigate the relationship between indoxyl sulfate (IS) and left ventricular hypertrophy (LVH) in hemodialysis patients.Methods For the eligible patients (age ≥ 18 years,dialysis duration ＞ 6 months,without history of congestive heart failure within 3 months and comorbidity of cardiac aneurysm),clinical data were collected,biochemical measurements were completed,and echocardiographic examinations were performed.Plasma IS concentration was determined by high performance liquid chromatography electrospray tandem spectrometry (HPLC-ESI-MS/MS).Linear and Logistic regression models were employed to assess the associations of plasma IS and left ventricular mass index (LVMI) and LVH,respectively.Results Two hundred and ten hemodialysis patients (117 males) with mean age of(57.2 ± 14.3)years were enrolled.The prevalence of LVH was up to 64.0％.Univariate linear regression showed that plasma IS was positively correlated with LVMI (β=7.09,P=0.02).The result persisted after adjustment for all kinds of risk factors (β=4.16,P=0.03).Patients were categorized into two groups:LVH and non-LVH group.Logistic regression modelswere employed to assess the relationship of plasma IS and LVH.The result showed that plasma IS was independently associated with LVH after adjustment for other confounding risk factors (β=6.54,OR=1.13,95％CI 1.09-1.44,P=0.03).Conclusions LVH is prevalent in hemodialysis patients.Plasma IS is significantly correlated with LVMI and the independent risk factor for LVH.