Objective: Patients with atherosclerotic cardiovascular disease (ASCVD) following percutaneous coronary intervention (PCI) are classified as very-high-risk individuals in cardiovascular disease (CVD) risk stratification. The distribution pattern of traditional Chinese medicine (TCM) syndromes in this patient population, as well as its association with blood lipid profiles and clinical prognosis, remains unclear. The present prospective cohort study aims to investigate these correlations, thereby providing insights to enrich the research fields. Methods: We enrolled consecutive patients with ASCVD who underwent PCI at the Integrated Cardiology Unit of China-Japan Friendship Hospital between September 1, 2020 and December 31, 2022. Demographics and clinical characteristics, signs and symptoms defining each TCM syndrome, and fasting venous blood samples were collected at baseline and follow up or upon major adverse cardiovascular events (MACEs). We analyzed the correlation between TCM syndromes, blood lipid profiles, and MACEs, and developed a new joint prognostic model incorporating both TCM syndromes and blood lipids using logistic regression. The analyses were based on detailed baseline and one-year follow-up data. Results: A per-protocol analysis was performed on 586 patients with complete data ultimately. During the one-year follow-up, 174 patients (29.69%) experienced a MACE. We performed statistical analyses on comorbidities, medication, and biochemical indicators across groups defined by TCM syndrome differentiation. When comparing different TCM syndromes, no significant differences were found in age, body mass index (BMI), history of revascularization, comorbidities, family history of CVD, smoking or drinking, or statin intensity (P > 0.05). Patients with intertwined phlegm and blood stasis syndrome exhibited significantly higher levels of total cholesterol (TC, 5.27 ± 1.18 mmol/L, P < 0.001), triglyceride (TG, 1.96 ± 1.33 mmol/L, P = 0.008), low-density lipoprotein cholesterol (LDL-C, 3.35 ± 0.79 mmol/L, P < 0.001), and high-density lipoprotein cholesterol (HDL-C, 1.24 ± 0.81 mmol/L, P < 0.001) compared with those with other TCM syndromes combined. A multivariable logistic regression model was constructed to predict MACEs. The model included TCM syndrome type [with intertwined phlegm and blood stasis as a predictor, adjusted odds ratio (OR) = 1.413, 95% confidence interval (CI): 0.517 – 3.864, P = 0.501], age (adjusted OR = 0.97, 95% CI: 0.955 – 1.001, P = 0.057), male gender (adjusted OR = 0.698, 95% CI: 0.416 – 1.170, P = 0.173), TC (adjusted OR = 1.004, 95% CI: 0.513 – 1.965, P = 0.990), and LDL-C (adjusted OR = 5.825, 95% CI: 2.214 – 15.326, P < 0.001). This model demonstrated good discriminatory ability for MACEs in post-PCI ASCVD patients [the area under the receiver operating characteristic (ROC) curve (AUC) = 0.865, 95% CI: 0.816 – 0.914]. Conclusion The intertwined phlegm and blood stasis TCM syndrome is associated with a distinct atherogenic lipid profile characterized by elevated levels of TC and LDL-C. The prognostic model that incorporates this TCM syndrome type along with conventional lipid parameters (TC and LDL-C) shows good discriminatory ability for predicting MACEs in ASCVD patients after PCI, underscoring the potential clinical utility of integrating TCM syndrome differentiation into CVD risk assessment.

Objective: To analyze the school tuberculosis (TB) outbreaks and preventive treatment in Hefei from 2022 to 2024, so as to provide reference for TB prevention and control in schools. Methods: Data were collected on all school based TB outbreaks occurring during 2022-2024 in Hefei, defined as ≥2 epidemiologically linked TB cases within the same school during a single semester. Statistical analyses were performed using the Chi square test. Results: Close contacts exhibited significantly higher TB incidence (2.88%) and latent mycobacterium tuberculosis infection (LTBI) rates (13.80%) in the school TB outbreaks, compared to non close contacts (0.12% and 2.63%, respectively). Among close contacts, secondary school students showed lower TB incidence (0.48%) and LTBI prevalence (3.42%) than both primary school or younger children (0.68%, 6.95%) and college students ( 0.78% , 6.50%), with statistically significant differences ( χ 2=360.91, 6.37; 791.71, 102.03, all P <0.05). The proportion of LTBI individuals recommended for preventive therapy was higher in primary school or younger groups (98.59%) than in secondary (95.25%) or college students (86.34%) ( χ 2=25.86, P <0.01). However, among those recommended, close contacts had higher uptake (85.82%) and completion rates (87.25%) of preventive therapy than non close contacts (69.63% and 70.57%); similarly, secondary school students demonstrated higher uptake (91.21%) and completion rates (86.45%) compared to primary school or younger (88.57%, 83.87%) and college students (57.28%, 64.08%) ( χ 2=30.52, 26.72; 125.17, 38.84, all P <0.01). Subsequent TB incidence among LTBI close contacts (13.30%) and among those who did not complete preventive therapy (22.73%) were significantly higher than among non close contacts (2.80%, 2.41%), respectively ( χ 2=32.19, 13.87, both P <0.05). Conclusions In school TB outbreaks, close contacts face higher LTBI prevalence and subsequent TB risk than non close contacts. College students show notably low adherence to preventive therapy. It is necessary to take targeted measures to improve the compliance of preventive measures among students.

Acute lung injury （ALI） is a critical respiratory emergency caused by various non-cardiogenic factors， including severe pulmonary and extrapulmonary infections， lung contusion， and sepsis. Its pathological features are centered on alveolar-capillary barrier dysfunction， uncontrolled inflammatory responses， and impaired alveolar fluid clearance， manifesting as refractory hypoxemia and respiratory distress， with a poor clinical prognosis. Modern studies have revealed that mitochondrial dysfunction and glucose metabolic reprogramming in macrophages， characterized by hyperactivated glycolysis， drive pro-inflammatory polarization and represent a key mechanism leading to excessive inflammatory responses and disease progression in ALI. Therefore， targeting macrophage glycolysis may be a potential therapeutic strategy for ALI. The Plain Questions： Special Discussion on Channels and Vessels in Huangdi's Internal Classic states that "The spleen disseminates essence upward to the lungs". When the spleen fails in transport and transformation， the distribution of refined nutrients becomes disordered， resulting in the endogenous generation of turbid pathogens that obstruct the pulmonary collaterals， causing failure of lung dispersion and descent and leading to dyspneic reversal. This forms the dynamic pathological pattern of ''deficiency in the root with excess in the manifestation''， thereby proposing the core pathogenesis of ALI as ''spleen deficiency with transport dysfunction and turbid pathogens obstructing the lungs''. This process is intrinsically associated with the inflammatory cascade triggered by disordered macrophage glucose metabolism. Taking the theory of ''spleen failing to disperse essence'' as the entry point， the present study systematically elucidates the progressive pathological mechanism of "energy metabolism disorder-cytokine storm'' in ALI from the perspectives of the ''spleen deficiency-turbid obstruction'' pathogenesis and macrophage glycolysis-pro-inflammatory polarization. In addition， we summarize Chinese medicine compound formulas and monomeric components that ''restore spleen transport and eliminate turbid pathogens''， and explore their potential mechanisms in the treatment of ALI by regulating macrophage metabolic phenotypes to improve the state of ''spleen failing to disperse essence''. This provides a molecular basis for elucidating the ''spleen-lung'' energy metabolism dialogue， deepens understanding of the multi-target regulatory mechanisms of herbal prescriptions， and promotes the deep integration of classical theory with modern medicine.

ObjectiveTo investigate the therapeutic effect of paeoniflorin on metabolic dysfunction-associated fatty liver disease （MASLD） combined with insulin resistance （IR）， and to elucidate its regulatory mechanisms on the Toll-like receptor 4 （TLR4）/nuclear transcription factor （NF）-κB-insulin receptor substrate 1 （IRS1） inflammation-insulin signaling axis. MethodsMASLD mouse model was established using a 60% high-fat diet. Mice were randomly assigned to a normal control group， a MASLD model group， and paeoniflorin groups （low dose： 25 mg·kg^-1·d^-1， medium dose： 50 mg·kg^-1·d^-1， high dose： 100 mg·kg^-1·d^-1）， receiving intragastric administration for consecutive 12 weeks. Concurrently， a palmitic acid/oleic acid （PA/OA）-induced lipid deposition model was established in HepG2 cells. Cell counting kit-8 （CCK-8） assay was performed to determine the optimal concentrations of PA/OA and paeoniflorin for intervention. Mice body weight， liver index， and serum levels of alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， triglycerides （TG）， and total cholesterol （TC） were measured. Fasting blood glucose （FBG） and fasting insulin （FINS） levels were measured， and the homeostatic model assessment of insulin resistance （HOMA-IR） was calculated， while an oral glucose tolerance test （OGTT） was performed to evaluate glucose metabolism. Hematoxylin and eosin （HE） staining was used to observe pathological changes and inflammatory cell infiltration in liver tissue， and oil red O staining was used to evaluate lipid droplet deposition in liver tissue and HepG2 cells. Potential targets were screened using network pharmacology and molecular docking. Western blot analysis was performed to detect the expression of HSP90AA1， TLR4， p-NF-κB p65， p-IRS1， and p-Akt proteins in liver tissue and HepG2 cells. ResultsCompared with the normal control group， mice in the MASLD model group exhibited significantly increased body weight， liver index， and serum levels of ALT， AST， TG， and TC， as well as markedly elevated FBG， FINS， and HOMA-IR， and impaired glucose tolerance （P<0.01）. HE staining revealed marked hepatic steatosis and inflammatory cell infiltration， while oil red O staining showed a significant increase in lipid droplet deposition. Compared with the MASLD model group， after intervention with various doses of paeoniflorin， the increase in body weight and liver index was reduced， serum ALT， AST， TG， and TC levels decreased， and FBG， FINS， and HOMA-IR were significantly lowered， with glucose tolerance markedly improved （P<0.05， P<0.01）， showing a certain dose-dependent trend. HE and oil red O staining results showed a marked reduction in hepatic steatosis and lipid deposition. In vitro experiments demonstrated that， compared with the control group， PA/OA treatment significantly induced increased lipid deposition in HepG2 cells. Compared with the model group， paeoniflorin intervention significantly reduced intracellular lipid droplets， and lipid deposition showed a dose-dependent decreasing trend. Mechanism studies indicated that， compared with the normal control group， the MASLD model group exhibited significantly elevated expression of TLR4， HSP90AA1， and p-NF-κB p65， while p-IRS1 （Ser307） expression was elevated and p-Akt （Ser473） expression was reduced （P<0.01）. Compared with the model group， the expression of the aforementioned proteins was significantly reversed in all treatment groups following intervention （P<0.05， P<0.01）. ConclusionPaeoniflorin significantly alleviates lipid deposition and insulin resistance in MASLD mice. Its mechanism of action may involve targeting HSP90AA1， TLR4， and NF-κB1 to regulate the TLR4/NF-κB-IRS1 inflammation-insulin signaling axis. This regulation suppresses inflammatory responses and restores insulin signaling， thereby ameliorating abnormalities in glucose and lipid metabolism.

With the rising incidence of colon cancer, several studies have indicated that aquaporin 1 (AQP1) expression is associated with the development of colon cancer. This study aims to elucidate the potential molecular mechanisms between them. Methods: We screened data from The Cancer Genome Atlas (TCGA) database and retrospectively examined AQP1 protein expression in 127 colon cancer patients to analyze the relationship between AQP1 expression and pathological stages, prognosis. We created stable colon cancer cell lines with differential AQP1 expression, the effect of AQP1 expression on the proliferation and migration of colon cancer cells was assessed by in vitro and in vivo studies, and explored potential molecular mechanisms through Western blotting. Results: High AQP1 expression was associated with poorer survival (overall survival [OS], p = .028) in colon cancer patients from the TCGA database. Similarly, retrospective clinical data indicated that high AQP1 expression was associated with reduced disease-free survival and OS (p = .036 and p = .017, respectively). The low-expressing AQP1 colon cancer cells exhibited a decrease in proliferation and migration ability of colon cancer cells compared to the overexpressing AQP1 group (p < .05) in vitro and in vivo. Immunohistochemistry and western blotting experiments validated heightened expression of N-cadherin, vimentin, and claudin- 1 in the tumor tissues of the overexpressing AQP1 group. Conversely, reduced AQP1 expression resulted in decreased expression of claudin- 1. Conclusions: AQP1 correlates with unfavorable prognosis in colon cancer and potentially enhances the proliferation and migration of colon cancer by up-regulating claudin-1 expression.

ObjectiveTo investigate the therapeutic effect of paeoniflorin on metabolic dysfunction-associated fatty liver disease （MASLD） combined with insulin resistance （IR）， and to elucidate its regulatory mechanisms on the Toll-like receptor 4 （TLR4）/nuclear transcription factor （NF）-κB-insulin receptor substrate 1 （IRS1） inflammation-insulin signaling axis. MethodsMASLD mouse model was established using a 60% high-fat diet. Mice were randomly assigned to a normal control group， a MASLD model group， and paeoniflorin groups （low dose： 25 mg·kg^-1·d^-1， medium dose： 50 mg·kg^-1·d^-1， high dose： 100 mg·kg^-1·d^-1）， receiving intragastric administration for consecutive 12 weeks. Concurrently， a palmitic acid/oleic acid （PA/OA）-induced lipid deposition model was established in HepG2 cells. Cell counting kit-8 （CCK-8） assay was performed to determine the optimal concentrations of PA/OA and paeoniflorin for intervention. Mice body weight， liver index， and serum levels of alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， triglycerides （TG）， and total cholesterol （TC） were measured. Fasting blood glucose （FBG） and fasting insulin （FINS） levels were measured， and the homeostatic model assessment of insulin resistance （HOMA-IR） was calculated， while an oral glucose tolerance test （OGTT） was performed to evaluate glucose metabolism. Hematoxylin and eosin （HE） staining was used to observe pathological changes and inflammatory cell infiltration in liver tissue， and oil red O staining was used to evaluate lipid droplet deposition in liver tissue and HepG2 cells. Potential targets were screened using network pharmacology and molecular docking. Western blot analysis was performed to detect the expression of HSP90AA1， TLR4， p-NF-κB p65， p-IRS1， and p-Akt proteins in liver tissue and HepG2 cells. ResultsCompared with the normal control group， mice in the MASLD model group exhibited significantly increased body weight， liver index， and serum levels of ALT， AST， TG， and TC， as well as markedly elevated FBG， FINS， and HOMA-IR， and impaired glucose tolerance （P<0.01）. HE staining revealed marked hepatic steatosis and inflammatory cell infiltration， while oil red O staining showed a significant increase in lipid droplet deposition. Compared with the MASLD model group， after intervention with various doses of paeoniflorin， the increase in body weight and liver index was reduced， serum ALT， AST， TG， and TC levels decreased， and FBG， FINS， and HOMA-IR were significantly lowered， with glucose tolerance markedly improved （P<0.05， P<0.01）， showing a certain dose-dependent trend. HE and oil red O staining results showed a marked reduction in hepatic steatosis and lipid deposition. In vitro experiments demonstrated that， compared with the control group， PA/OA treatment significantly induced increased lipid deposition in HepG2 cells. Compared with the model group， paeoniflorin intervention significantly reduced intracellular lipid droplets， and lipid deposition showed a dose-dependent decreasing trend. Mechanism studies indicated that， compared with the normal control group， the MASLD model group exhibited significantly elevated expression of TLR4， HSP90AA1， and p-NF-κB p65， while p-IRS1 （Ser307） expression was elevated and p-Akt （Ser473） expression was reduced （P<0.01）. Compared with the model group， the expression of the aforementioned proteins was significantly reversed in all treatment groups following intervention （P<0.05， P<0.01）. ConclusionPaeoniflorin significantly alleviates lipid deposition and insulin resistance in MASLD mice. Its mechanism of action may involve targeting HSP90AA1， TLR4， and NF-κB1 to regulate the TLR4/NF-κB-IRS1 inflammation-insulin signaling axis. This regulation suppresses inflammatory responses and restores insulin signaling， thereby ameliorating abnormalities in glucose and lipid metabolism.

Renal fibrosis is the common pathological endpoint of many forms of chronic kidney disease (CKD), yet the mechanisms determining effective repair versus persistent fibrotic remodeling remain incompletely understood. Peritubular capillaries (PTCs) are not merely passive targets of fibrotic injury, but form a dynamic vascular microenvironment linking regional perfusion, oxygen delivery, tubular metabolism, endothelial barrier integrity, pericyte support, immune-cell trafficking, and extracellular matrix (ECM) remodeling. We propose that PTC abnormalities should not be interpreted simply as reduced capillary density, but as a multidimensional disturbance of microvascular structure and function. Structural vascular preservation does not necessarily indicate effective microcirculation: anatomically detectable capillaries may still exhibit impaired perfusion, barrier dysfunction, abnormal endothelial-pericyte interactions, disturbed oxygen metabolism, or reduced network connectivity. Conversely, increased angiogenesis does not necessarily signify successful vascular repair if vessels remain immature, poorly perfused, or inadequately integrated into the existing network. To organize these abnormalities, we conceptualize PTC remodeling into four predominant but nonexclusive states: endothelial barrier disruption with inflammatory adhesion; endothelial-pericyte uncoupling with no-reflow; dysregulated angiogenesis with network simplification; and capillary rarefaction with fibrotic matrix locking. These states are not sequential stages of CKD. They may coexist within the same kidney, overlap within the same anatomical region, and vary with disease etiology, injury phase, vascular compartment, and treatment exposure. We further propose six dimensions for evaluating PTC status—structural presence, functional perfusion, barrier integrity, pericyte coupling, oxygen metabolism, and network connectivity—so that vascular quantity, function, and reparative capacity are assessed separately rather than inferred from a single endothelial marker or capillary-density measurement. Mechanistically, these states converge on a bidirectional microvascular-fibrotic feedback loop. Barrier disruption facilitates leukocyte recruitment and alters vascular paracrine signaling. Endothelial-pericyte uncoupling compromises capillary stability, whereas abnormal pericyte contraction may increase local vascular resistance and contribute to no-reflow before overt capillary loss. Dysregulated angiogenesis may generate vessels that fail to mature or connect to an effective perfusion network. Progressive capillary rarefaction compromises oxygen delivery, while sustained tubular transport demand and mitochondrial dysfunction may aggravate regional oxygen supply-demand mismatch. Injured tubules, immune cells, endothelial cells, pericytes, and fibroblasts communicate through soluble mediators, extracellular vesicles, direct cell contact, and cell-matrix signaling. Importantly, fibrosis is not merely a downstream consequence of microvascular injury. Altered ECM may increase diffusion distance, modify mechanotransduction, impair endothelial survival and migration, and restrict capillary reopening and regeneration. We use the term matrix locking to describe this sustained constraint on vascular repair, while emphasizing that current evidence does not establish irreversible disease in humans. This framework also has therapeutic implications. PTC-directed treatment should not be reduced to increasing vessel number or uniformly promoting angiogenesis. Instead, intervention should be matched to the dominant and potentially reversible abnormality: preserving endothelial barrier function; restoring endothelial-pericyte stability and reducing pathological microvascular resistance; normalizing angiogenesis so that vascular growth is accompanied by maturation, barrier competence, network integration, and effective perfusion; and, in advanced rarefaction, relieving matrix-related constraints while supporting vascular regeneration. The context- and time-dependent effects of signaling through VEGF, Tie2, PDGF-B/PDGFRβ, eNOS/NO, and related pathways indicate that the same molecular signal may exert different effects depending on disease context and timing. Therapeutic efficacy should therefore be evaluated by restoration of effective microcirculation and tissue function rather than by isolated molecular changes or capillary counts alone. Despite increasing mechanistic evidence, the translational basis for this framework remains limited. Most causal and interventional data derive from animal or cell models, whereas human evidence is largely limited to pathological observations, patient-sample associations, and prognostic studies. Currently available circulating and urinary candidate biomarkers generally lack sufficient specificity for PTC injury or state assignment, and no standardized quantitative thresholds have been externally validated. The four-state model should therefore be regarded as a hypothesis-generating analytical framework rather than a clinicopathological classification system. Future studies should integrate spatially resolved tissue phenotyping, blood and urine biomarkers, and dynamic microcirculatory assessment in longitudinal cohorts. They should test reproducibility, assess prognostic value beyond conventional pathology, estimated glomerular filtration rate, and proteinuria, and determine whether changes in PTC status precede or mediate therapeutic benefit. Linking reproducible microvascular phenotypes to defined mechanisms, treatment response, and long-term renal outcomes will be essential to determine whether state-directed assessment and restoration of the PTC microenvironment can ultimately inform patient stratification and therapeutic decision-making.

Objective:To investigate the correlation between peri-coronary fat attenuation index (FAI) and plaque formation in patients with myocardial bridge (MB) of the left anterior descending artery (LAD) using coronary computed tomography angiography (CCTA) and to develop an optimal predictive model to explore the potential application of FAI in the primary prevention of MB related atherosclerosis.Methods:In this retrospective study, prediction models associated with perivascular fat inflammation were developed and validated using both logistic regression and machine learning (ML) algorithm. A training dataset was collected from 253 patients who underwent ≥2 coronary computed tomography angiography (CCTA) with ≥3 months intervals from one tertiary hospital from January 2007 to April 2021 and had baseline CCTA showing no plaques in LAD MB. The median follow-up time was 3.2 years. According to the same criteria, a total of 75 LAD MB patients from four other hospitals were included to form an independent external validation dataset, with a median follow-up time of 1.8 years. Receiver operating characteristic (ROC) curve analysis with integrated discrimination improvement (IDI) and category net reclassification index (NRI) were used to compare the performance of the predictive models.Results:62 patients (24.5%) in the training dataset had proximal plaque formation in LAD MB, while 22 patients (29.3%) in the external validation dataset had plaque formation during the follow-up period. Baseline FAI within the longitudinal distance equal to 30 mm proximal to the MB entrance was an independent predictor ( OR=1.068, P=0.046). According to the model results, ROC curves were plotted. The AUC of Model 1 was 0.822, and the AUCs of Model 2 and 1 were 0.821 and 0.591 in the training dataset. After the DeLong test, the AUC of Model 1 was superior to that of Model 2 ( Z=2.839, P=0.005) and Model 1 ( Z=6.124, P<0.001). These findings were further validated in the external validation dataset, where ML-model 3 yielded the best predictive performance, outperforming the logistic regression-based Model 2 (categorical NRI=0.359, P=0.048; IDI=0.108, P=0.046). Conclusion:FAI measured within the 30 mm proximal to the entrance of MBs due to its prone to plaque development is an independent predictor for atherosclerotic plaque formation. The ML-prediction model based on a decision tree algorithm combines FAI, MB anatomical features, and patient risk factors, which is beneficial for patients undergoing routine CCTA examination to identify inflamed coronary arteries in advance and guide the clinical adoption of more targeted preventive treatment, including anti-inflammatory treatment.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

This study was a single-center cross-sectional investigation aimed at identifying risk factors for cognitive dysfunction in patients undergoing maintenance hemodialysis (MHD), with the goal of providing a basis for improving patient prognosis. Patients receiving MHD in the Blood Purification Center of Hainan Provincial People's Hospital from June 1 to June 30, 2023, were enrolled. Cognitive function was assessed using the Mini-Mental State Examination (MMSE), and potential risk factors for cognitive impairment were analyzed by using Logistic regression. A total of 278 patients were included, 69 patients (24.8%) of whom had cognitive impairment. Multivariate Logistic regression analysis indicated that the history of cerebrovascular disease ( OR=3.109, 95% CI 1.310-7.378, P=0.010), old age ( OR=1.077, 95% CI 1.040-1.115, P<0.001), low dialysis frequency ( OR=0.270, 95% CI 0.120-0.606, P=0.001), low academic qualification (using college/university as the control group: primary school group OR=26.960, 95% CI 7.519-96.673, P<0.001; Junior high school/technical secondary school group OR=4.264, 95% CI 1.330-13.650, P=0.015; High school group OR=9.554, 95% CI 2.861-31.904, P<0.001), high β2-microglobulin ( OR=1.609, 95% CI 1.044-2.480, P=0.031) and high C-reactive protein/albumin ( OR=2.672, 95% CI 1.226-5.826, P=0.013) were independent risk factors for cognitive impairment in MHD patients.