With the global increase in chronic diseases, chronic kidney disease (CKD) and stroke have become major public health concerns. This study aims to investigate the relationship between estimated glomerular filtration rate (eGFR), urine albumin-to-creatinine ratio (UACR), and the incidence of stroke in a CKD population.

This cross-sectional study analyzed the relationship between eGFR, UACR, and prevalence of self-reported stroke in 6,037 participants using data from the National Health and Nutrition Examination Survey (NHANES) from 2007 to 2018. Multivariate logistic regression analysis was used to evaluate the association of eGFR, UACR with the incidence of stroke, and smoothing curve fitting was applied to explore the linear relationship between eGFR and stroke. To further explore the effect of eGFR on stroke risk, we performed subgroup analyses of demographic factors.

After adjusting for confounding factors, eGFR was found to be significantly negatively associated with stroke risk. Compared with participants with an eGFR ≥ 90 mL/min/1.73 m2, the risk of stroke was increased in those with an eGFR of 60-90 (OR = 1.78; 95% CI = 1.18-2.69), 30-60 (OR = 2.26; 95% CI = 1.49-3.44), and <30 mL/min/1.73 m2 (OR = 3.14; 95% CI = 1.74-5.65). In the unadjusted model, patients with UACR of 30-300 mg/g had a slightly lower risk of stroke than those with UACR < 30 mg/g (OR = 0.70, 95% CI = 0.57-0.86); however, this association was not seen after adjusting for potential confounders.

This study identified a negative linear correlation between eGFR and stroke in CKD patients.

Both Adropin and Clusterin are associated with cardiovascular and cerebrovascular diseases. Unfortunately, the clinical implications of them in Chronic renal failure (CRF) population remains largely unclear.

We included 356 CRF patients received hemodialysis. Determination of serum concentrations of Adropin and Clusterin were performed by ELISA.The optimal cutoff values of Adropin or Clusterin for cardiovascular and cerebrovascular complications/death were determined by receiver operating characteristics (ROC) curve analysis. The prognostic value of Adropin and Clusterin was evaluated using Kaplan-Meier survival curves, log-rank tests, and Cox proportional hazards models.

Baseline serum Adropin significantly decreased, while serum Clusterin elevated in CRF patients who suffered cardiovascular or cerebrovascular implications during hemodialysis. Both decreased baseline serum Adropin and increased serum Clusterin showed potentials for predicting cardiovascular/cerebrovascular implications during hemodialysis in CRF patients. Reduced baseline serum Adropin indicated poor prognosis in CRF patient during hemodialysis, whereas increased baseline serum Clusterin indicated poor prognosis in CRF patient during hemodialysis. Combining baseline serum Adropin and Clusterin detection achieved better performance for predicting prognosis in CRF patients.

We demonstrated that decreased Adropin, or increased Clusterin could be novel but useful tool for predicting cardiovascular/cerebrovascular complications and overall survival. Importantly, combination of Adropin and Clusterin detection might be help to construct new management system for CRF patients to effectively improve their prognosis in the future.

Triglyceride-glucose (TyG) index is strongly correlated with insulin resistance (IR). A plethora of studies has established the role of TyG index in cerebrovascular diseases. However, the predictive value of TyG index for new-onset ischemic stroke (IS) in maintenance hemodialysis (MHD) patients remains unclear. This study aims to explore the correlation between TyG index and the occurrence of IS in MHD patients.

This study analyzed clinical data and cranial Computed Tomography results of patients undergoing MHD at Baoding First Central Hospital from January 2019 to January 2024. TyG index was calculated using fasting blood glucose and triglyceride levels. Univariate Logistic regression analysis was employed to identify factors associated with IS, incorporating variables with P < 0.05 into multivariate Logistic regression analysis, with results expressed as odds ratio (OR) and 95% confidence interval (95% CI). Receiver operating characteristic (ROC) curve analysis was used to evaluate the predictive value of TyG index for the occurrence of IS.

Triglyceride-glucose index in the IS group was significantly higher than that in the non-IS group, with a statistically significant difference [9.32 (8.87, 9.92) vs 8.59 (8.06, 9.12), P < 0.001]. Variables with P < 0.05 from the univariate Logistic regression analysis, along with clinically relevant variables, were included in the multivariate Logistic regression analysis, indicating that an elevated TyG index is a factor associated with IS in hemodialysis patients (OR = 2.09, 95% CI 1.073-3.781, P < 0.001). ROC curve analysis revealed that the optimal cutoff value of TyG index for diagnosing new-onset IS in MHD patients was 9.2, with an area under the curve of 0.75 (95% CI 0.70-0.79, P < 0.001). Restricted cubic spline analysis demonstrated a non-linear relationship between TyG index and risk (non-linear p = 0.010).

Triglyceride-glucose index is significantly elevated in MHD patients with new-onset IS, serving as a potential risk factor for such events and offering valuable clinical diagnostic reference.

Chronic renal function impairment (RFI) increases the risk of acute ischemic stroke (AIS), greater stroke severity, and post-stroke disability and mortality.

We aimed to assess the three-month functional outcomes of AIS in patients with chronic RFI.

In this prospective study, stroke severity was assessed using the National Institutes of Health Stroke Scale (NIHSS), and functional outcomes were assessed using the modified Rankin Scale (mRS). Outcomes were analyzed based on estimated glomerular filtration rate (eGFR).

Among the 205 patients included (median age: 70 years, IQR: 61-82), 123 (60%) were male. Patients with lower eGFR had higher NIHSS scores (more severe strokes) and higher mRS scores at both baseline and three months (poorer functional outcomes). Based on a logistic regression model adjusted for confounding factors, higher eGFR was significantly associated with good three-month functional outcomes (adjusted OR = 2.634, 95% CI [1.207, 5.748], p = 0.015).

Chronic RFI is associated with more severe strokes and poorer baseline and three-month functional outcomes after AIS. Future research should explore targeted management strategies to improve post-stroke recovery in this population.

The STANDFIRM (Shared Team Approach Between Nurses and Doctors for Improved Risk Factor Management; ANZCTR registration ACTRN12608000166370) trial was designed to test the effectiveness of chronic disease care management for modifying the Framingham risk score (FRS) among patients with stroke or transient ischemic attack. The primary outcome of change in FRS was not met. We determine baseline characteristics that predict reduction in FRS at 12 months and whether future FRS is predetermined at baseline.

We used machine learning regression methods to evaluate 35 variables encompassing demographics, risk factors, psychological, social and education status, and laboratory tests. We determine the optimal machine learning and associated tuning parameters from the following: random forest, extreme gradient boosting, category boosting, support vector regression, multilayer perceptron neural network, and K-nearest neighbor. Training (n=404) and test (n=103) data were evenly matched for age, sex, baseline, and 12-month FRS. The optimal model for predicting FRS at 12 months was category boosting (R2=0.712; root mean square error, 7.32). The 5 variables with highest Shapley values for category boosting were baseline FRS (Shapley additive explanation [SHAP], 8.42 of total of 12.12), age (SHAP, 1.58), systolic blood pressure (SHAP, 0.23), male sex (SHAP, 1.05), and London Handicap (SHAP, 0.18). Machine learning methods were poor at determining change in FRS at 12 months (R2<0.22).

Our findings suggest that change in FRS as an end point in secondary stroke trials may have limited value as it is largely determined at baseline. In this cohort, category boosting was the optimal method to predict future FRS but not change in FRS.

Cognitive impairment is highly prevalent among individuals with chronic kidney disease (CKD). Despite its high prevalence, the contributing factors and mechanisms underlying brain-kidney dysfunction in CKD remain poorly understood. However, advances in neuroscience, including novel imaging techniques and cognitive assessment methods, have begun to clarify this complex relationship. Several factors contribute directly to cognitive decline in people with CKD, including accumulation of uraemic toxins, microvascular damage, malnutrition, chronic inflammation and disruptions in key neuroprotective pathways, such as those involving Klotho and the glymphatic system. These factors are also linked to the accelerated ageing observed in people with CKD, a key contributor to cognitive decline. However, most studies on cognition in people with CKD have been cross-sectional and associative, offering limited insight into causation. Research advances, such as studies on the effect of uraemic toxins on the blood-brain barrier and the role of the endothelial glycocalyx in vascular damage, offer promising new directions. Emerging data from longitudinal cohort studies are also enhancing our understanding of these processes, with potential implications for both the treatment of CKD-related cognitive decline and the broader issue of cognitive dysfunction in ageing populations. Here, we examine key mechanisms linking CKD to cognitive decline and consider potential therapeutic interventions.

Hypertension is a prevalent metabolic disorder in the elderly, with its pathogenesis linked to gut microbiota dysbiosis. Recent studies suggested that oral microbiota may also play a role in hypertension development, yet its relationship with hypertension in the elderly remains underexplored.

This cross-sectional study aimed to examine the structure of the oral microbiota and its association with hypertension in elderly patients, providing insights into hypertension prevention and treatment.

A total of 206 subjects (60-89 years) were categorized into normal (CON) and hypertensive (HTN) groups, based on the Chinese Hypertension Guidelines. Saliva samples were analyzed using 16S rRNA gene sequencing.

Oral microbiota composition was significantly influenced by blood pressure. At the phylum level, Synergistetes and Spirochaetes were more significantly abundant in the HTN group, while at the genus level Treponema and Leptothrix was higher, Actinomyces and Capnocytophaga were lower in HTN. Random Forest analysis identified 15 key microbiota as strong discriminators of HTN (AUC 0.74). Blood pressure was negatively correlated with Actinomycetes and positively correlated with Leptothrix. PICRUST2 analysis revealed elevated chlorinated compound degradation in HTN patients.

This study identified distinct oral microbiota in elderly hypertensive patients, highlighting the role of the oral microbiome in hypertension pathogenesis.

Patients with chronic kidney disease (CKD) are at a significantly increased risk of stroke and experience worse stroke outcomes and higher mortality. CKD exacerbates stroke risk and severity through a complex interplay of systemic inflammation, oxidative stress, and impaired clearance of uremic toxins, leading to neuroinflammation and microglial activation. Current acute ischemic stroke treatments, while effective in the general population, do not adequately address CKD-specific mechanisms, limiting their efficacy in this high-risk population. Prolyl hydroxylase domain (PHD) inhibitors have shown promise in treating anemia associated with CKD and may offer cerebroprotective benefits. However, the effects of PHD2 inhibition on long-term sensorimotor outcomes and the underlying mechanisms in mice with CKD remain largely unknown. Here, we investigated the impact of CKD on stroke severity and assessed the therapeutic potential of desidustat, a PHD inhibitor, in improving stroke outcomes. Using an adenine-induced CKD mouse model, we demonstrated that CKD exacerbated stroke-induced long-term sensorimotor deficits, increased neuroinflammation, and impaired microglial efferocytosis via dysregulation of the ADAM17-MerTK axis. Desidustat treatment in mice with CKD significantly improved long-term sensorimotor functional outcomes and reduced post-stroke neuroinflammation while enhancing microglial efferocytosis by reducing ADAM17 and enhancing microglial MerTK expression. In vitro studies using human-induced microglia-like cells further confirmed the ability of desidustat to enhance efferocytosis of apoptotic neurons by reducing the cleavage of MerTK. These findings suggest that desidustat may serve as a novel therapeutic strategy for improving stroke outcomes in patients with CKD, a population at high risk for stroke and poor functional recovery.

The association between changes in physical functions and stroke incidence remains uncertain.

A total of 7978 participants without stroke from the China Health and Retirement Longitudinal Study (CHARLS) were recruited in 2011-2012 and followed up until 2020. We assessed annual changes in physical functions from 2011 to 2015, including absolute grip strength, relative grip strength, walking speed, chair-rising time and standing balance. The Cox proportional hazards model was applied to assess the longitudinal associations between annual changes in physical functions and stroke. Restricted cubic spline analyses were used to explore the dose-response relationships.

During 71 714 person-years of follow-up, 549 incident stroke cases were reported. For each 1-kg absolute grip strength increment, 0.1-unit relative grip strength increment, or 1-point standing balance test score increment, the hazard of stroke was reduced by 12% [hazard ratio (HR): 0.88; 95% confidence interval (CI): 0.84-0.93], 53% (HR: 0.47; 95% CI: 0.34-0.64), 55% (HR: 0.45; 95% CI: 0.30-0.67), respectively. We found a negative linear dose-response association of the annual change in absolute and relative grip strength with incident stroke, as well as a nonlinear association between the annual change in standing balance and incident stroke. However, neither the annual change in walking speed nor chair-rising time was related to the incident stroke.

A greater improvement in absolute grip strength, relative grip strength or standing balance was suggested to be associated with a lower risk of stroke amongst middle-aged and older people. These objectively measured physical function changes are imperative for high-risk population classification and stroke prevention.

Kidney transplantation remains the best treatment for chronic kidney failure, offering better outcomes and quality of life compared with dialysis. Cardiovascular disease (CVD) is a major cause of morbidity and mortality in kidney transplant recipients and is associated with decreased patient survival and worse graft outcomes. Post-transplant CVD results from a complex interaction between traditional cardiovascular risk factors, such as hypertension and diabetes, and risk factors specific to kidney transplant recipients including chronic kidney disease, immunosuppressive drugs, or vascular access. An accurate assessment of cardiovascular risk is now needed to optimize the management of cardiovascular comorbidities through the detection of risk factors and the screening of hidden pretransplant coronary artery disease. Promising new strategies are emerging, such as GLP-1 receptor agonists and SGLT2 inhibitors, with a high potential to mitigate cardiovascular complications, although further research is needed to determine their role in kidney transplant recipients. Despite this progress, a significant gap remains in understanding the optimal management of post-transplant CVD, especially coronary artery disease, stroke, and peripheral artery disease. Addressing these challenges is essential to improve the short- and long-term outcomes in kidney transplant recipients. This narrative review aims to provide a comprehensive overview of cardiovascular risk assessment and post-transplant CVD management.

The prediction of ischaemic stroke in patients with heart failure with reduced ejection fraction (HFrEF) but without atrial fibrillation (AF) remains challenging. Our aim was to evaluate the performance of machine learning (ML) in identifying the development of ischaemic stroke in this population.

We performed a post-hoc analysis of the WARCEF trial, only including patients without a history of AF. We evaluated the performance of 9 ML models for identifying incident stroke using metrics including area under the curve (AUC) and decision curve analysis. The importance of each feature used in the model was ranked by SAPley Additive exPlanations (SHAP) values.

We included 2213 patients with HFrEF but without AF (mean age 58 ± 11 years; 80% male). Of these, 74 (3.3%) had an ischaemic stroke in sinus rhythm during a mean follow-up of 3.3 ± 1.8 years. Out of the 29 patient-demographics variables, 12 were selected for the ML training. Almost all ML models demonstrated high AUC values, outperforming the CHA2DS2-VASc score (AUC: 0.643, 95% confidence interval [CI]: 0.512-0.767). The Support Vector Machine (SVM) and XGBoost models achieved the highest AUCs, with 0.874 (95% CI: 0.769-0.959) and 0.873 (95% CI: 0.783-0.953), respectively. The SVM and LightGBM consistently provided significant net clinical benefits. Key features consistently identified across these models were creatinine clearance (CrCl), blood urea nitrogen (BUN) and warfarin use.

Machine-learning models can be useful in identifying incident ischaemic strokes in patients with HFrEF but without AF. CrCl, BUN and warfarin use were the key features.

Equations for estimated glomerular filtration rate (eGFR) have previously included a coefficient for African American race. We evaluated and compared risk of incident stroke and dementia between old and new equations of eGFR for African American and non-African American participants.

Prospective observational study.

Baseline values were collected from 6,814 participants in the Multi-Ethnic Study of Atherosclerosis (MESA) cohort between 2000 and 2002. Participants were followed up until 2018. The analytic sample consisted of 6,646 participants (mean [SD] age 62 [10] years; 53% female; 39% White, 27% African American, 12% Chinese American, and 22% Hispanic/Latino).

eGFR equation from 2021 based on serum creatinine and cystatin C levels without race.

Incident stroke and dementia.

Cox proportional regression adjusting for demographic, lifestyle, and clinical variables was performed to estimate associations between different eGFR measures and risk of incident stroke and dementia.

During a median follow-up period of 17 years, 349 (5.3%) participants experienced an incident stroke event, and 574 (8.6%) participants experienced incident dementia. In the fully adjusted model, overall participants with eGFR <60 compared with those >90 mL/min/1.73 m2 were at significantly increased risk of dementia (HR, 95% CI: 1.73, 1.21-2.45). A lower eGFR was not significantly associated with incident stroke (1.30, 0.75-2.24). African American participants tended to be reclassified to a lower group of eGFR in the new equations, whereas non-African American participants were reclassified to a higher group of eGFR. When comparing older versus newer equations of eGFR in African American and non-African American participants in association with incident stroke and dementia, differences were minimal.

Incident dementia was ascertained through International Classification of Diseases (Ninth and Tenth Revisions) codes.

Our findings illustrate participants with 2021 eGFR < 60 compared with those with eGFR > 90 mL/min/1.73 m2 have higher risk of dementia in both African American and non-African American participants, but not of stroke.

Chronic kidney disease (CKD) significantly increases stroke risk and severity, posing challenges in both acute management and long-term outcomes. CKD contributes to cerebrovascular pathology through systemic inflammation, oxidative stress, endothelial dysfunction, vascular calcification, impaired cerebral autoregulation, and a prothrombotic state, all of which exacerbate stroke risk and outcomes.

This review synthesizes evidence from peer-reviewed literature to elucidate the pathophysiological mechanisms linking CKD and stroke. It evaluates the efficacy and safety of acute reperfusion therapies-intravenous thrombolysis and endovascular thrombectomy-in CKD patients with acute ischemic stroke. Considerations, such as renal function, drug dosage adjustments, and the risk of contrast-induced nephropathy, are critically analyzed. Evidence-based recommendations and research priorities are drawn from an analysis of current practices and existing knowledge gaps.

CKD influences stroke outcomes through systemic and local pathophysiological changes, necessitating tailored therapeutic approaches. Reperfusion therapies are effective in CKD patients but require careful monitoring of renal function to mitigate risks, such as contrast-induced nephropathy and thrombolytic complications. The bidirectional relationship between stroke and CKD highlights the need for integrated management strategies to address both conditions. Early detection and optimized management of CKD significantly reduce stroke-related morbidity and mortality.

Optimizing stroke care in CKD patients requires a comprehensive understanding of their pathophysiology and clinical management challenges. This article provides evidence-based recommendations, emphasizing individualized treatment decisions and coordinated care. It underscores the importance of integrating renal considerations into stroke treatment protocols and highlights the need for future research to refine therapeutic strategies, address knowledge gaps, and consider tailored interventions to improve outcomes and quality of life for this high-risk population.

For any physician treating a patient with a medical condition of unclear etiology, the differential diagnosis aims to identify the actual most probable cause among various potential etiologies, in order to tailor treatment options. In patients with embolic stroke of undetermined source (ESUS), this can be challenging due to the frequent presence of multiple potential embolic sources, raising difficulties to identify the most likely cause. Additionally, despite targeted preventive measures for the presumed embolic source, patients may remain at risk for stroke and cardiovascular events due to other unrecognized or underestimated pathologies. The multi-level complexity and multimorbidity typically associated with ESUS, represents a challenge that requires broad knowledge of the cardiovascular pathophysiology, deep expertise of the available diagnostic and therapeutic options, and interdisciplinary approach. At the same time, it is an ideal opportunity to assess thoroughly the overall cardiovascular status of the patient, which in turn can allow us to optimize therapeutic and preventive strategies in a holistic approach, and prevent future strokes, cardiovascular events and disability through different parallel pathways. In this context, rather than narrowing our perspective on identifying the specific embolic source presumed to be the most likely cause of ESUS, it is crucial to shift our focus from the disease to the patient, and evaluate the overall cardiovascular profile by assessing the risk of all cardiovascular comorbidities present, no matter if causally associated with ESUS or not. In order to bring across these points and more, this article is centred around a clinical case that serves as a starting point to illustrate the holistic approach to the management of patients with ESUS. After all, this is the beauty, the magic and the art of Internal Medicine: to treat the patient, not the disease, the system or the organ.

Cognitive impairment is a prevalent and debilitating complication in patients with chronic kidney disease (CKD). This position paper, developed by the Cognitive Decline in Nephro-Neurology: European Cooperative Target network, provides guidance on the epidemiology, risk factors, pathophysiology, diagnosis and clinical management of CKD-related cognitive impairment. Cognitive impairment is significantly more common in CKD patients compared with the general population, particularly those undergoing haemodialysis. The development of cognitive impairment is influenced by a complex interplay of factors, including uraemic neurotoxins, electrolytes and acid-base disorders, anaemia, vascular damage, metabolic disturbances and comorbidities like diabetes and hypertension. Effective screening and diagnostic strategies are essential for early identification of cognitive impairment utilizing cognitive assessment tools, neuroimaging and circulating biomarkers. The impact of various drug classes, including antiplatelet therapy, oral anticoagulants, lipid-lowering treatments and antihypertensive drugs, on cognitive function is evaluated. Management strategies encompass pharmacological and non-pharmacological interventions, with recommendations for optimizing cognitive function while managing CKD-related complications. This guidance highlights the importance of addressing cognitive impairment in CKD patients through early detection, careful medication management and tailored therapeutic strategies to improve patient outcomes.

We employed a meta-analysis to investigate the risk factors associated with sarcopenia in patients undergoing dialysis.

We conducted a search in PubMed, Embase, Cochrane Library, and Web of Science databases. Inclusion criteria included case-control and cohort studies on risk factors for sarcopenia in dialysis patients. The search period spanned from the inception of each database to September 20, 2024. The quality of the included studies was assessed using the Newcastle-Ottawa Scale (NOS). Data analysis was performed using Stata 15.0.

A total of 625 articles were screened, with 610 articles excluded based on predefined eligibility criteria, resulting in 15 articles involving 2904 individuals were included in the final analysis, meta-analysis results indicate that older dialysis patients [SMD = 0.76, 95% CI (0.54, 0.99), I2 = 81%, P = 0.001], those with a lower BMI [SMD = -0.50, 95% CI (-0.80, -0.20), I2% = 87.4%, P = 0.02], a lower SMI [SMD = -2.67, 95% CI (-3.87, -1.47), I2% = 98.2%, P = 0.001], and those with diabetes [OR = 1.43, 95% CI (1.13, 1.82), I2% = 48.8%, P = 0.03] are more likely to develop sarcopenia.

Based on current research, our study found that elderly dialysis patients, those with a lower BMI, lower SMI, and diabetic patients are more likely to develop sarcopenia. These findings highlight the necessity of early intervention for these high-risk groups. However, the study has limitations. Future research should address these limitations and investigate the mechanisms linking these risk factors to sarcopenia to develop targeted prevention and treatment strategies.

Background: Recent evidence supports the protective role of metformin on kidney function in patients with type 2 diabetes mellitus. However, its potential to prevent new-onset chronic kidney disease (CKD) in patients with type 2 diabetes mellitus with normal renal function remains unclear. Therefore, this study aimed to investigate whether metformin could prevent the development of new-onset CKD in such patients. Methods: This retrospective, observational, multicenter cohort study included 316,693 patients with type 2 diabetes mellitus. After matching using the inverse probability of treatment weighting, 9109 metformin users and 1221 nonusers were analyzed. The primary outcomes were an estimated glomerular filtration rate (eGFR) of <60 mL/min/1.73 m2, urinary albumin-to-creatinine ratio of ≥30 mg/g, and a composite outcome defined as new-onset CKD. Results: The multivariable Cox survival model showed that metformin users had significantly better renal outcomes, with a notably lower risk of sustained eGFR of <60 mL/min/1.73 m2 (hazard ratio (HR), 0.71; 95% confidence interval (CI), 0.56-0.90) and new CKD onset (HR, 0.78; 95% CI, 0.65-0.94). Conclusions: Metformin plays a key role in delaying renal events in individuals with type 2 diabetes mellitus and in those with initially normal renal function.

Despite effective secondary prevention, including oral anticoagulant (OAC) therapy, the risk of recurrent stroke (RS) in patients with atrial fibrillation (AF) remains substantial with an annualized risk of 3.2%-6.5% per year. The reasons for this high residual risk are unclear. There is growing need for improved risk prediction tools to identify patients at greatest risk of RS in AF and to find new therapeutic targets for secondary prevention. Our objective was to perform a systematic review to investigate the association of clinical factors and echocardiographic, blood, and neuroimaging biomarkers, with stroke recurrence after AF-related stroke.

We searched Embase/Ovid Medline until August 2023. Studies were included irrespective of OAC use. Risk ratios (RRs) were pooled using random effects. Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were followed.

Of 5,427 records searched, 42 reports from 28 studies including 52,798 patients (5,046 RS events during follow-up) were identified. In addition to the CHA2DS2-Vasc score (RR 1.22, 95% CI 1.15-1.30, per point) and its individual components, the clinical factors associated with recurrence were a qualifying stroke despite OAC (RR 1.55, 1.23-1.94 [vs OAC-naïve]), sustained AF (RR 1.44, 1.19-1.75 [vs paroxysmal]), hyperlipidemia (RR 1.27, 1.05-1.53), chronic kidney disease (RR 1.86, 1.19-2.92), and malignancy (RR 4.36, 1.85-10.78). NIH Stroke Scale scores (RR 0.97, 0.95-0.99) and Asian ethnicity (RR 0.59, 0.36-0.97) were associated with a reduced risk of recurrence. Known AF was not associated with a higher risk of stroke compared with AF detected after stroke (RR 1.20, 0.93-1.55). Neuroimaging markers associated with RS included chronic lacunar (RR 1.91, 1.29-2.84) or embolic-appearing (RR 2.76, 1.32-5.77) infarcts and cerebral microbleeds (RR 1.29, 1.04-1.59). Echocardiographic markers included atrial size (RR 1.40, 1.12-1.75 per cm/m2), intracardiac thrombus (RR 1.99, 1.38-2.87), spontaneous left atrial appendage (LAA) echocardiographic contrast (RR 2.91, 1.21-6.17), or low LAA intensity variation (RR 2.81, 1.48-5.32). Data were limited for blood biomarkers.

We identified several clinical factors associated with recurrence after AF-related stroke, with AF burden and stroke despite OAC of particular clinical relevance. Biomarkers of atrial cardiopathy, small vessel disease, or previous infarction were also associated with RS. Collaborative efforts are needed to identify and validate new risk factors and biomarkers of RS in AF.

Chronic kidney disease (CKD) is a significant risk factor for cerebrovascular disease. However, there is limited research on how successful living donor kidney transplantation (LDKT) affects cerebral blood flow (CBF). This study aims to comprehensively investigate how LDKT influences CBF across various brain levels and regions.

Data from 53 recipients between 2016 and 2020 were obtained from the VINTAGE study conducted at our hospital. CBF was measured by level and region using single-photon emission computed tomography (SPECT), according to the Talairach brain atlas. The primary endpoint was the mean difference in CBF before and 1-year post-LDKT. Subgroup analysis using traditional risk factors assessed the heterogeneity of the effect on CBF in the frontal lobe region.

LDKT improved blood flow in the anterior cerebral artery and middle cerebral artery but had less impact on the posterior cerebral artery. The most consistent improvements were observed in the frontal lobe region {left frontal lobe: -0.12 [95% confidence interval (CI) -0.18 to -0.05], P < .001; right frontal lobe: -0.13 [95% CI -0.21 to -0.05], P = .001}. Subgroup analysis showed a consistent effect of LDKT on frontal lobe CBF improvement, with no qualitative interaction observed.

LDKT contributes to the normalization of CBF, with improvement in anterior circulation and frontal lobe blood flow. To clarify the clinical significance of KT's CBF-improving effect, future studies should investigate the relationship between specific cognitive impairments (e.g. short-term memory, visuospatial ability, executive function) and CBF in each perfusion region.

Transient ischaemic attack (TIA) is characterised by a temporary neurological dysfunction resulting from focal ischaemia in the brain, spinal cord or retina without acute infarction. These episodes typically last less than 24 hours and are significant predictors of subsequent ischaemic strokes. Hypertension is a major risk factor for cerebrovascular events, and primary aldosteronism (PA) is recognised as a common cause of secondary hypertension. This case report presents a male patient with secondary hypertension due to Conn Syndrome, a form of PA, who experienced a TIA manifesting as left leg weakness, underscoring the heightened stroke risk associated with secondary hypertension.

A 78-year-old male with secondary hypertension caused by Conn Syndrome presented with an episode of left leg weakness that resolved within 24 hours. After ruling out other potential causes such as metabolic disturbances, infections, and structural brain lesions, he was diagnosed with TIA and treated with dual antiplatelet therapy. A carotid ultrasound revealed significant stenosis, leading to a referral for carotid endarterectomy. Long-term management included clopidogrel monotherapy and optimising hypertension control.

This case highlights the increased stroke risk in patients with Conn Syndrome-related hypertension, emphasising the importance of early recognition and optimising hypertension management in patients with secondary hypertension to prevent future cerebrovascular events.

This retrospective cohort study aimed to investigate the impact of age-related medical conditions on the incidence of dementia, considering factors such as hypertension, diabetes mellitus, cerebrovascular disease, cardiovascular disease, chronic kidney disease, osteoarthritis, osteoporosis, chronic obstructive pulmonary disease, and hearing difficulties.

Data from 513 640 patients at Keimyung University Dongsan Hospital were analyzed using the Observational Medical Outcomes Partnership Common Data Model. Patients with and without age-related medical conditions were assigned to experimental and control groups, respectively, with propensity score matching. Cox proportional hazards models assessed the association between each condition and dementia incidence.

Hypertension, diabetes mellitus, cerebrovascular disease, cardiovascular disease, chronic kidney disease, osteoarthritis, osteoporosis, and hearing difficulties were associated with increased dementia risk. Chronic obstructive pulmonary disease showed no significant association with increased risk of dementia. Incidence rates ranged from 4.52 to 8.05 per 1000 person-years in the control group and 7.46 to 14.99 per 1000 person-years in the experimental group. Hazard ratios ranged from 1.38 to 2.36.

The study highlights the importance of managing age-related medical conditions to mitigate dementia risk. Understanding these risk factors can inform preventive strategies and improve cognitive health outcomes. Problems with deidentification data analysis and the need for further multicentred studies are among the limitations of this study.

The coexistence of type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD) represents a significant global health challenge, contributing to substantial morbidity, mortality, and economic burden. T2DM is the leading cause of CKD, and CKD exacerbates diabetes-related complications, creating a bidirectional relationship driven by oxidative stress, inflammation, and endothelial dysfunction. Diabetic kidney disease (DKD), affecting some individuals with T2DM, accelerates progression to end-stage renal disease (ESRD) and increases cardiovascular mortality. Microvascular complications, including nephropathy, retinopathy, and neuropathy, and macrovascular complications, such as coronary artery disease and stroke, are prevalent in this population, further diminishing the quality of life. The pathophysiology underlying these complications is multifaceted. Hyperglycemia-induced oxidative stress and inflammation drive kidney damage and systemic vascular complications, while CKD alters glucose metabolism and antidiabetic drug pharmacokinetics. Endothelial dysfunction exacerbates vascular complications through impaired nitric oxide production and heightened thrombogenicity. Emerging insights into genetic and epigenetic mechanisms, including DNA methylation and mitochondrial dysfunction, have highlighted new therapeutic targets. Management strategies emphasize early screening, glycemic control, and a multidisciplinary approach integrating lifestyle modifications, pharmacotherapy, and patient education. Interventions targeting oxidative stress, inflammation, and endothelial dysfunction have shown promise in mitigating disease progression. Current evidence on the interconnected mechanisms driving DKD and associated vascular complications highlights the critical need for proactive, patient-centered management and further research into innovative diagnostic and therapeutic approaches to address this global health challenge.

To investigate the potential mechanism of arachidonic acid deoxyribozyme 15 (ALOX15) in ferroptosis and inflammation induced by cerebral ischemia reperfusion injury.

The mice and cell models of cerebral ischemia-reperfusion injury were constructed. Western Blot was used to detect the protein expression levels of ALOX15, glutathione peroxidase (GPX4), hypoxia-inducible factor-2α (HIF-2α), prolyl hydroxylase (PHD) and inflammatory factors (NLRP3, IL-1β, IL-18) in brain tissues and cells. Cell proliferation activity was detected by CCK-8 method. LDH assay was used to detect the release of lactate dehydrogenase. TTC staining was used to observe cerebral infarction.

In cerebral ischemia-reperfusion mice and cell models, the expression of ALOX15 protein was increased, the expression of GPX4, a key marker of ferroptosis was decreased, and silencing of ALOX15 down-regulated the GPX4 expression. HIF-2α expression was down-regulated in animal and cell models of cerebral ischemia reperfusion, and silencing of ALOX15 increased the HIF-2α expression by inhibiting PHD2 expression. Inhibition of ALOX15 expression reduced inflammatory factors levels (NLRP3, IL-1β, and IL-18) in cerebral ischemia. Inhibitor of PHD2 (IXOC-4) alleviating brain injury and cell death induced by cerebral ischemia reperfusion and stabilize HIF-2α expression in vivo.

The expression of ALOX15 was up-regulated in cerebral ischemia-reperfusion animals and cells model. Inhibition of ALOX15 up-regulated the GPX4 expression, and promoted HIF-2α expression by inhibiting PHD2, thus alleviating ferroptosis and inflammation caused by cerebral ischemia-reperfusion injury.

Asundexian is a reversible and selective inhibitor of activated factor XI. It is currently under investigation for the prevention of secondary stroke in at-risk patients; these patients are often characterised by advanced age, impaired organ function and comorbidities. This article summarises results from three Phase I studies that investigated the effects of age and sex (study 1), chronic kidney disease including end-stage kidney disease (ESKD) on dialysis and dialysis-free days (study 2) and Child-Pugh A and B liver disease (study 3) on the safety, pharmacokinetics and pharmacodynamics of a single oral dose of asundexian 25 mg.

Study 1 was a multicentre, randomised, single-blind, placebo-controlled group-stratification design; study 2 was a single-centre, non-randomised, non-placebo-controlled, non-blinded group-stratification design; and study 3 had a non-randomised, non-blinded, non-placebo-controlled group-stratification design.

Single doses of asundexian 25 mg were generally well tolerated in all three studies, with no asundexian-related bleeding events or treatment-emergent adverse events of special interest. Point estimates (geometric least squares [LS] means) (90% confidence intervals [CIs]) for the total asundexian area under the plasma concentration-time curve (AUC) for participants aged ≥ 65 to < 75 years versus ≥ 18 to < 45 years and ≥ 75 to ≤ 80 years versus ≥ 18 to < 45 years were 1.257 (1.134-1.393) and 1.288 (1.158-1.433), respectively, and for females versus males, it was 1.084 (0.995-1.182). Point estimates (geometric LS means) (90% CIs) for unbound AUC in participants in estimated glomerular filtration rate (eGFR) categories G2 (60-89 mL/min/1.73 m2), G3 (30-59 mL/min/1.73 m2) and G4 (15-29 mL/min/1.73 m2) versus control were 1.003 (0.698-1.443), 0.791 (0.550-1.138) and 0.882 (0.606-1.285), respectively, and in participants with ESKD on dialysis-free day versus control was 0.597 (0.406-0.877). There was no effect of the dialysis procedure on the pharmacokinetics of asundexian. In participants deemed Child-Pugh class A and Child-Pugh class B, geometric LS means (90% CIs) for unbound AUC were 0.834 (0.597-1.164) and 1.143 (0.810-1.612), respectively, when compared to participants with normal liver function. Activated partial thromboplastin time (aPTT) was assessed as a pharmacodynamic variable of interest. Geometric mean maximum aPTT prolongation as a ratio to baseline after administration of asundexian 25 mg ranged from 1.45 to 1.55 in all age and sex groups, 1.49-1.59 in the control and eGFR G2 to G4 groups, 1.38-1.54 in the control and ESKD groups on dialysis and dialysis-free day and 1.38-1.89 in the healthy control and liver impairment groups.

The effects of the investigated intrinsic factors on the exposure of asundexian were small and not considered clinically relevant. The impact of lower exposure in participants with ESKD requires further investigation. Pharmacodynamics were as expected.

EudraCT 2022-000196-38 and 2020-000626-25.

Magnesium ion metabolism disorder is pervasive in the chronic kidney disease population, which is affected by many factors. Magnesium ion plays an important role in maintaining vascular functional integrity.. The Magnesium Depletion Score (MDS), serving as a novel metric for the assessment of magnesium deficiency, has not been thoroughly investigated for its association with stroke in patients with chronic kidney disease (CKD). Therefore, this study aims to explore the relationship between the MDS index and stroke in CKD patients.

We conducted a cross-sectional population-based study using data from the National Health and Nutrition Examination Survey 2009-2016 to explore the impact of MDS on the stroke outcome of CKD patients. The primary outcome was the risk of stroke in CKD patients. Sample-weighted multivariate logistic regression was used in our analysis.

In this study of 3536 CKD patients from the database, we found an 8.6 % prevalence of stroke with higher stroke risk in older individuals and males. Lower dietary magnesium intake and higher MDS scores were significantly associated with stroke risk. Multivariate logistic regression analysis revealed a dose-dependent relationship between MDS scores and stroke likelihood, independent of demographic and clinical factors. Subgroup analysis confirmed these findings, particularly in those with hypertension, diabetes, and obesity, without significant interactions (all p > 0.05).

Magnesium depletion is independently associated with a heightened stroke risk in chronic kidney disease patients.

Chronic kidney disease (CKD) is a risk factor for embolic stroke, and many nonvalvular atrial fibrillation (NVAF) patients have concomitant CKD. Anticoagulation therapy can be challenging in CKD due to increased bleeding risk, and left atrial appendage occlusion (LAAO) may be a promising alternative.

This systematic review aimed to consolidate current evidence on the safety and effectiveness of transcatheter LAAO in patients with CKD and end-stage renal disease (ESRD).

Medline, Cochrane, and Embase databases were searched from inception to September 2, 2022. We conducted a meta-analysis if an outcome was evaluated in at least two similar studies.

We included 15 studies with 77,780 total patients. Of the 15 studies, 11 had a cohort design (five prospective and six retrospective), and four were case series. Patients with CKD were older and had a higher prevalence of comorbidities than non-CKD patients. The two groups did not differ in procedural failure rate, vascular complications, or pericardial tamponade. CKD patients exhibited higher odds of in-hospital acute kidney injury (AKI) and bleeding, longer-term bleeding, and mortality than those without CKD. The risk of in-hospital and longer-term cardioembolic events was similar between CKD and non-CKD populations (odds ratio = 1.01 [95% CI 0.70-1.15] and 1.05 [95% CI 0.55-2.00], respectively). Patients with ESRD had higher odds of in-hospital mortality and cardioembolic events than non-ESRD patients, with no differences in risk of pericardial tamponade.

Based on observational studies, LAAO may be an effective option to prevent cardioembolic events in CKD. However, CKD patients may have higher odds of AKI and in-hospital and long-term bleeding and mortality. The adverse clinical outcomes observed in CKD patients may be attributed to this population's high burden of comorbidities, especially among those with ERSD, rather than the LAAO procedure itself. To ensure maximum clinical benefit, careful patient selection, management, and surveillance involving multidisciplinary teams are essential for CKD patients undergoing LAAO.

Clonal hematopoiesis of indeterminate potential (CHIP) and dementia disproportionately burden patients with chronic kidney disease (CKD). The association between CHIP and cognitive impairment in CKD patients is unknown.

We conducted time-to-event analyses in up to 1452 older adults with CKD from the Chronic Renal Insufficiency Cohort who underwent CHIP gene sequencing. Cognition was assessed using four validated tests in up to 6 years mean follow-up time. Incident cognitive impairment was defined as a test score one standard deviation below the baseline mean.

Compared to non-carriers, CHIP carriers were markedly less likely to experience impairment in attention (adjusted hazard ratio [HR] [95% confidence interval {CI}] = 0.44 [0.26, 0.76], p = 0.003) and executive function (adjusted HR [95% CI] = 0.60 [0.37, 0.97], p = 0.04). There were no significant associations between CHIP and impairment in global cognition or verbal memory.

CHIP was associated with lower risks of impairment in attention and executive function among CKD patients.

Our study is the first to examine the role of CHIP in cognitive decline in CKD. CHIP markedly decreased the risk of impairment in attention and executive function. CHIP was not associated with impairment in global cognition or verbal memory.

The mechanisms that modulate the onset of acute kidney inlury (AKI) after ischemic stroke (IS) and valuable biomarkers to predict the occurrence and prognosis of AKI among patients with IS are missing.

To evaluate the frequency of AKI and the prognostic validity of clinical and laboratory biomarkers in predicting AKI and short-term mortality after the IS.

Ninety-five patients with IS were enrolled. Baseline IS severity was assessed using the National Institutes of Health Stroke Scale (NIHSS) and disability was determined after three-month follow-up using the modified Rankin Scale. Patients with IS were also categorized as survivors and non-survivors after the follow-up. Baseline data and laboratory biomarkers were obtained up to 24 h of the admission.

Fifteen (15.7 %) patients with IS presented AKI. The proportion of patients with vitamin D deficiency and the mortality were higher among those with AKI than those without AKI (p=0.011 and p-0.009, respectively). Patients with AKI showed higher disability and higher increased soluble vascular cellular adhesion molecule-1 (sVCAM-1) than those without AKI (p=0.029 and p=0.023, respectively). Logistic regression analysis showed that only sVCAM-1 was associated with the occurrence of AKI after IS [odds ratio (OR): 2.715, 95 % confidence intereval (CI): 1.12-6.67, p=0.027]. When both AKI and NIHSS were evaluated as explanatory variables, this panel showed an OR of 5.782 (95 % CI: 1.09-30.43, p<0.001) and correctly classified 83.6 % of cases.

In conclusion, sVCAM-1 levels showed a potential useful for prediction of AKI after IS.

Background/Objectives: Efforts have been made toward primary or secondary stroke or transient ischemic attack (TIA) prevention. However, little attention has been paid to recurrent stroke or TIA. This study investigated risk factors for multiple or single recurrent stroke or TIA. Methods: Data from 3646 patients with ischemic stroke or TIA were obtained from the Korea University Ansan Hospital Stroke Center between March 2014 and December 2021, using the prospective institutional database of the Korea University Stroke Registry. The associations between clinical features and recurrent stroke or TIA were assessed using bivariable and multivariable Cox models. Results: Recurrent stroke or TIA was associated with male sex (adjusted hazard ratio (HR) 1.95, 95% confidence interval (CI) 1.42-2.80), hypertension (HR 1.49, 95% CI 1.00-2.23), diabetes mellitus (HR 1.54, 95% CI 1.13-2.13), an etiologic subtype of transient ischemic attack (HR 1.88, 95% CI 1.09-3.16), white matter changes (HR 1.62, 95% CI 1.05-2.38), and cerebral microbleeds (HR 1.79, 95% CI 1.26-2.59). Multiple recurrent stroke or TIA was associated with male sex (HR 3.86, 95% CI 1.94-11.55), diabetes mellitus (HR 2.40, 95% CI 1.31-4.53), and anemia (HR 4,58, 95% CI 2.31-10.44). Conclusions: Given the risk factor profiles for recurrent stroke or TIA, risks differed among patient subgroups and were based on multiple or single recurrences. It may exert an effect as a prognostic indicator in the high risk of recurrences.

Coronavirus disease 2019 (COVID-19) has been shown to increase the risk of stroke. However, the prevalence and risk of recurrent stroke in COVID-19 patients with prior stroke/transient ischemic attack (TIA), as well as its impact on mortality, are not established.

To evaluate the impact of COVID-19 on in-hospital mortality, length of stay, and healthcare costs in patients with recurrent strokes.

We identified admissions of recurrent stroke (current acute ischemic stroke admissions with at least one prior TIA or stroke) in patients with and without COVID-19 using ICD-10-CM codes using the National Inpatient Sample (2020). We analyzed the impact of COVID-19 on mortality following recurrent stroke admissions by subgroups.

Of 97455 admissions with recurrent stroke, 2140 (2.2%) belonged to the COVID-19-positive group. The COVID-19-positive group had a higher prevalence of diabetes and chronic kidney disease vs the COVID-19 negative group (P < 0.001). Among the subgroups, patients aged > 65 years, patients aged 45-64 years, Asians, Hispanics, whites, and blacks in the COVID-19 positive group had higher rates of all-cause mortality than the COVID-19 negative group (P < 0.01). Higher odds of in-hospital mortality were seen in the group aged 45-64 (OR: 8.40, 95%CI: 4.18-16.91) vs the group aged > 65 (OR: 7.04, 95%CI: 5.24-9.44), males (OR: 7.82, 95%CI: 5.38-11.35) compared to females (OR: 6.15, 95%CI: 4.12-9.18), and in Hispanics (OR: 15.47, 95%CI: 7.61-31.44) and Asians/Pacific Islanders (OR: 14.93, 95%CI: 7.22-30.87) compared to blacks (OR: 5.73, 95%CI: 3.08-10.68), and whites (OR: 5.54, 95%CI: 3.79-8.09).

The study highlights the increased risk of all-cause in-hospital mortality in recurrent stroke patients with COVID-19, with a more pronounced increase in middle-aged patients, males, Hispanics, or Asians.

Recent studies have reported an increasing incidence of ischaemic stroke among young adults. However, the strength of the association between traditional vascular risk factors has not been fully established.

We compared 120 patients with a first ischaemic stroke before the age of 55 years admitted to the stroke unit of our centre with 600 healthy non-stroke controls from a population-based cohort study (HERMEX), matched for sex. Risk factors assessed included: hypertension, obesity, auricular fibrillation, current smoking, estimated glomerular filtration rate (eGFR), total cholesterol, low-density lipoprotein cholesterol (LDL-C), triglycerides, high-density lipoprotein cholesterol (HDL-C) and diabetes mellitus. We used logistic regression analysis and calculated population attributable risk. We performed an overall analysis, by sex and aetiological subgroup.

Using logistic regression analysis, we found that overall, the significant risk factors were: hypertension (OR: 1.58; 95%CI: 1.01-2.50), atrial fibrillation (OR: 4.77; 95%CI: 1.20-19.00), low eGFR (OR: 4.74; 95%CI: 1.3-21.94) and low HDL-C (OR: 5.20; 95%CI: 3.29-8.21), as well as smoking for males (OR: 1.86; 95%CI: 1.14-3.03). LDL-C showed an inverse association with stroke. The population attributable risk for HDL-C was 37.8% and for hypertension 21.1%. In terms of aetiological subgroups, only low HDL-C was associated with stroke of undetermined aetiology.

Hypertension, auricular fibrillation, low eGFR, and low HDL-C, plus tobacco use in men, are the main risk factors among patients under 55 years of age with a first ischaemic stroke. We believe that it would be of particular interest to further explore the management of low HDL-C levels as part of preventive strategies in young stroke patients.

Accurately discerning periods of heightened risk of stroke or transient ischemic attack (TIA) recurrence and managing modifiable risk factors are essential for minimizing overall recurrence risk. This study identified differences in the timing of stroke or TIA recurrence based on risk factors and patient characteristics to develop strategies for reducing recurrence in clinical practice.

We retrospectively selected patients with ischemic stroke or TIA at the Korea University Ansan Hospital Stroke Center between March 2014 and December 2021 using the prospective institutional database of the Korea University Stroke Registry. We collected demographic, clinical data, and categorized participants by recurrence timing (early within or late after 3 months). Using multinomial logistic regression analysis, we examined variables associated with early and late recurrent stroke or TIAs.

Among 3,646 patients, 255 experienced a recurrent stroke or TIA and 3,391 experienced their first stroke or TIA. Multinomial logistic regression analysis revealed significant associations between early recurrent stroke or TIA and diabetes mellitus (odds ratio [OR]: 1.98, 95% confidence interval [CI]: 1.25-3.15), other determined etiologies in the Trial of Org 10172 in the Acute Stroke Treatment classification (OR: 3.00, 95% CI: 1.37-6.61), and white matter changes (OR: 1.97, 95% CI: 1.17-3.33). Late recurrence showed a significant correlation with TIA (OR: 2.95, 95% CI: 1.52-5.71) and cerebral microbleeds (OR: 2.22, 95% CI: 1.32-3.75).

Substantial differences in factors contribute to stroke or TIA recurrence based on timing. Managing the risk of recurrence in clinical practice necessitates accurate identification of heightened risk periods and rigorous control of modifiable risk factors.

The serum lipid level is strongly associated with atherosclerosis. However, research on the relationship between lipid-derived indices and acute ischemic stroke (AIS) occurrence in hemodialysis populations is limited. This study aimed to explore the predictive value of lipid-derived indices, including atherogenic index of plasma (AIP), Non- high density lipoprotein cholesterol (Non-HDL-C), Non-HDL-C/HDL-C, and lipoprotein combine index (LCI) in clinical practice for the occurrence and prognosis of AIS in hemodialysis patients.

A total of 451 patients undergoing maintenance hemodialysis were screened and 350 were enrolled in this study. The lipid parameters exhibit a progressive increase across the tertiles, with values rising from Q1 through Q3. Enrolled patients were divided into three groups (Q1, Q2, and Q3) based on tertiles of AIP, Non-HDL-C, Non-HDL-C/HDL-C, and LCI values. Kaplan-Meier curves were performed to investigate the association between the AIP, Non-HDL-C, Non-HDL-C/HDL-C, LCI and AIS-free survival in hemodialysis patients. Chi-square analysis was used to explore the association between the AIP, Non-HDL-C, Non-HDL-C/HDL-C, LCI and AIS outcomes in hemodialysis patients. AIS outcomes were assessed using the modified Rankin Scale (mRS).

Kaplan-Meier analysis revealed that the AIS-free survival rates were significantly higher in the Q1 group compared to Q2 and Q3 groups for AIP, Non-HDL-C, Non-HDL-C/HDL-C, and LCI. Log rank tests showed statistically significant differences between the Q1 group and the Q2 and Q3 groups (p < 0.05 for all). The proportion of patients with a good outcome mRS was higher in the Q1 group compared to the Q2-Q3 groups (AIP: 0.818 vs 0.792; Non- HDL-C: 0.866 vs 0.767; Non- HDL-C/HDL-C: 0.867 vs 0.767; LCI: 0.938 vs 0.750).

The four lipid-derived parameters are effective predictors of AIS in patients undergoing hemodialysis, and AIP has a strongest correlation with the risk of AIS. Hemodialysis patients with elevated levels of the four lipid-derived indices had a higher incidence of AIS and poorer functional outcomes compared to those with lower levels. Our conclusions may require confirmation by further research in the future.