Clinical and Experimental Hypertension最新文献

{"title":"Hypertension and Alzheimer's disease: Pathological interplay, comorbidity risks, and new strategies for synergistic management.","authors":"Xinyu Wei, Lili Li, Guohua Zhao, Yani Luan, Qian Wang, Wenjing Ning","doi":"10.1080/10641963.2025.2595154","DOIUrl":"https://doi.org/10.1080/10641963.2025.2595154","url":null,"abstract":"<p><p>Hypertension and Alzheimer's disease (AD) are common comorbidities that seriously damage the health of the elderly. This review lays out the complex bidirectional association between hypertension and AD. From a pathological perspective, hypertension can not only indirectly increase the risk of AD through inducing cerebrovascular lesions such as atherosclerosis and stroke but also directly accelerate the core pathological progression of AD, including promoting the accumulation of amyloid-β (Aβ) proteins and the hyperphosphorylation of tau protein. Additionally, various shared modifiable risk factors, such as obesity, sleep disturbances, diet patterns, psychosocial factors etc., are summarized in detail, and their shared pathophysiological pathways, including chronic inflammation, oxidative stress and intestinal dysbiosis, are revealed. This article focuses on exploring the potential of synergistic management: on the one hand, some antihypertensive drugs, such as angiotensin II receptor blockers (ARBs), exhibit neuroprotective effects beyond blood pressure reduction. On the other hand, DASH, Mediterranean and MIND dietary patterns, along with regular physical exercise and positive psychological interventions, have all been proven to reduce the incidence risk of both diseases simultaneously. Digital health technology, such as the LETHE App provides a new paradigm for realizing dynamic monitoring and personalized management of risk factors. This review emphasizes that integrating hypertension prevention and control into the primary prevention strategy for AD and adopting a synergistic management plan that combines lifestyle interventions, medications, and digital technologies is crucial for achieving healthy aging.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2595154"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145687092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The causal relationship between aspartate aminotransferase and hypertension: A bidirectional Mendelian randomization study.","authors":"Hongyan Song, Jun Li, Lizhen Lan, Huaxing Meng","doi":"10.1080/10641963.2025.2564298","DOIUrl":"https://doi.org/10.1080/10641963.2025.2564298","url":null,"abstract":"<p><strong>Background: </strong>Hypertension is a major contributor to the global burden of disease and increased mortality in the general population. Currently, the etiology and pathogenesis of hypertension are not fully understood. Emerging evidence suggests an association between aspartate aminotransferase (AST) and hypertension, but whether this relationship is causal remains unclear.</p><p><strong>Methods: </strong>A two-sample MR analysis was conducted using GWAS summary data. Five MR methods - MR-Egger, weighted median, inverse variance weighted (IVW), simple mode, and weighted mode - were applied, with IVW as the primary approach. Sensitivity analyses, including heterogeneity and pleiotropy assessments, as well as leave-one-out (LOO) analysis, were performed. Functional annotation of non-coding SNPs was conducted using the 3DSNP database, while GeneMania and enrichment analysis explored gene interactions and biological pathways.</p><p><strong>Results: </strong>Forward MR analysis using the IVW method indicated a significant causal effect of AST on hypertension (<i>β</i> = 0.0003, Standard Error (SE) = 6.93E-05, <i>P</i> = 0.0002). However, reverse MR analysis found no significant causal relationship between hypertension and AST (<i>β</i> = 15.7148, SE = 12.7551 <i>P</i> = 0.2179). The results of MR-Egger regression, Weighted Median, and Weighted Mode methods were consistent with those of the IVW method. These findings were robust across several reliability analyses. Finally, network and functional enrichment analyses showed that, under the influence of IVs, the SNP-hosted genes and AST promote disease progression through involvement in aspartic acid family metabolism and hexose biosynthesis.</p><p><strong>Conclusion: </strong>The present study reports the potential role of AST in the development of hypertension. The link between AST and hypertension may be due to regulation of substance and energy metabolism. These findings offer new insights into the pathophysiology of hypertension and suggest that AST could serve as a potential biomarker or therapeutic target for hypertension management.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2564298"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gastrin signaling in cardiovascular pathophysiology: From molecular crosstalk to clinical implications.","authors":"Chunmei Xu, Zhuxin Li, Yongchun Zeng, Hao Luo, Xuewei Xia","doi":"10.1080/10641963.2025.2584566","DOIUrl":"https://doi.org/10.1080/10641963.2025.2584566","url":null,"abstract":"<p><p>As a gastrointestinal hormone, gastrin stimulates gastric acid secretion and intestinal mucosal nutrition. Evidence links it closely to coronary heart disease, ischemia‒reperfusion injury and hypertension. The relevant literature was systematically retrieved from PubMed, Web of Science, China National Knowledge Infrastructure (CNKI), and other scientific databases, as well as other sources. Gastrin is a polypeptide hormone that is synthesized mainly by G cells in the antrum and proximal small intestine. Its secretion is controlled by neural regulation and humoral regulation. Gastrin is significantly associated with coronary heart disease, cardiac ischemia-reperfusion injury, hypertension and other cardiovascular diseases. The risk of coronary heart disease in patients with high serum gastrin levels is greater than that in the general population, and the serum gastrin level is higher in patients with myocardial infarction, which further suggests that hypergastrinemia may be an important risk factor for CHD. Myocardial cells express CCKBR, and intracoronary gastrin administration improves myocardial contractility through CCKBR. Several studies have shown that gastrin can also protect the myocardium against ischemia-reperfusion injury through the STAT3 signaling pathway. Gastrin may regulate blood pressure through the central nervous system or directly dilate blood vessels. Gastrin can promote the secretion of gastric acid and nutrition of intestinal mucosa. Gastrin exerts cardioprotective effects and regulates the occurrence of hypertension.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2584566"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145556230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the PHD2/HIF-1α/HO-1 pathway: A key role of trimetazidine in hypertensive nephropathy.","authors":"Daqian Gu, Meixian Chen, Yuhui Yang, Chen Lu, Chao Li, Yi Lin","doi":"10.1080/10641963.2025.2563033","DOIUrl":"https://doi.org/10.1080/10641963.2025.2563033","url":null,"abstract":"<p><strong>Objective: </strong>This study seeks to unravel the effects of trimetazidine (TMZ) on hypertensive nephropathy (HN) in mice and its underlying mechanisms.</p><p><strong>Methods: </strong>Sixty male 129 mice (8-10 weeks old) were randomly categorized into six groups (<i>n</i> = 10 per group): control, model, TMZ, TMZ + small interfering RNA targeting prolyl hydroxylase domain protein 2 (si-PHD2), TMZ + zinc protoporphyrin [ZnPP, a heme oxygenase-1 (HO-1) inhibitor], and TMZ + KC7F2 [a hypoxia-inducible factor-1 alpha (HIF-1α) inhibitor]. All groups except the control group received angiotensin II to induce HN models. TMZ was administered by gavage for 28 days, while the other TMZ-based groups received additional si-PHD2, ZnPP, or KC7F2. Blood pressure, renal function, proinflammatory cytokines, and kidney pathology were measured. Protein/mRNA levels of PHD2, HO-1, HIF-1α, and Collagen I were analyzed via reverse transcription quantitative polymerase chain reaction/Western blot.</p><p><strong>Results: </strong>The model group showed increased blood pressure, renal injury, fibrosis, and elevated levels of PHD2, HIF-1α, HO-1, Collagen I, and inflammatory markers compared to the control group (<i>P</i> < 0.05). TMZ treatment alleviated renal damage and downregulated PHD2, while upregulating HIF-1α and HO-1. These effects were further enhanced by PHD2 knockdown (TMZ + si-PHD2), but reversed by the inhibition of HO-1 or HIF-1α (TMZ + ZnPP, TMZ + KC7F2).</p><p><strong>Conclusion: </strong>TMZ improves HN in mice by modulating the PHD2/HIF-1α/HO-1 pathway.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2563033"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145273949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Iron status mediates the causal effects of high-altitude adaptation signals in the HIF-PHD axis on pulmonary vascular and right-heart outcomes.","authors":"Youqian Zhang, Chang Liu, Jiejun Zhou, Wenrui Li, Mingwei Chen","doi":"10.1080/10641963.2025.2595152","DOIUrl":"https://doi.org/10.1080/10641963.2025.2595152","url":null,"abstract":"<p><strong>Background: </strong>The high-altitude adaptation genes EPAS1 (HIF-2α) and EGLN1 (PHD2) in the HIF-PHD oxygen-sensing pathway regulate erythropoiesis and iron homeostasis and are implicated in hypoxia-related pulmonary vascular disease, yet causal roles are unclear.</p><p><strong>Methods: </strong>This study applied a drug-target Mendelian randomization (DTMR) framework. Cis-eQTLs were used to instrument EPAS1/EGLN1 expression; gene-restricted erythroid instruments were built from genome-wide significant variants within ± 100 kb for hemoglobin (HGB), hematocrit (HCT), and red blood cell count (RBC). Primary analyses used inverse-variance weighted (IVW) and summary-data-based Mendelian randomization (SMR) with eight sensitivity approaches. Outcomes included pulmonary embolism (PE), pulmonary arterial hypertension (PAH), pulmonary-artery structural indices, and right-heart MRI traits. Two-step mediation MR evaluated iron-status traits.</p><p><strong>Results: </strong>In SMR-DTMR, higher EPAS1 expression associated with lower PE risk (OR = 0.861; 95% CI, 0.758-0.979). In IVW-DTMR, EGLN1-mediated increases in HGB/HCT/RBC raised PE risk (HGB: OR 2.55; HCT: OR 2.45; RBC: OR 1.91) and were associated with lower systolic pulmonary artery-to-aorta ratio (PA/Ao) (HGB β-0.322; HCT β-0.282; RBC β-0.425). EPAS1-mediated HGB/HCT/RBC were associated with reduced right ventricular peak filling rate (RVP-FR; β-33.8 to -28.1). Mediation indicated serum iron partially mediated the EGLN1→(HGB/HCT)→PE pathway (3.6-3.8%), with a potential effect for RBC; ferritin potentially mediated the EPAS1→RBC→PA/Ao pathway. Multiple sensitivity analyses supported robustness.</p><p><strong>Conclusions: </strong>EGLN1-driven erythropoietic upregulation increases PE risk and adversely affects pulmonary artery structure, whereas higher EPAS1 expression reduces PE risk. These genetic findings support targeted modulation of HIF-2α and iron metabolism.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2595152"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145699957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypertension accelerates aging: Evidence from NHANES database and Mendelian randomization analyses.","authors":"Zhaobin Sun, Gaoying Dai, Nanhu Quan","doi":"10.1080/10641963.2025.2559743","DOIUrl":"https://doi.org/10.1080/10641963.2025.2559743","url":null,"abstract":"<p><strong>Background: </strong>Hypertension is thought to accelerate biological aging. However, evidence of a causal effect is lacking. This study aimed to provide evidence of a relationship between hypertension and biological aging by analyzing data from the 2005-2010 National Health and Nutrition Examination Survey (NHANES) and by Mendelian randomization (MR).</p><p><strong>Methods: </strong>The association of hypertension with PhenoAge and PhenoAge acceleration was assessed by weighted multivariable-adjusted linear regression using the NHANES data. Two-sample MR was then performed using summary data from genome-wide association studies to determine causal associations of hypertension with accelerated DNA methylation (DNAm) and proxies of age, including telomere length, frailty index, and facial aging. Inverse variance weighting and complementary MR methods were used to confirm the causal relationship between hypertension and biological aging. The robustness of the results was confirmed by sensitivity analyses.</p><p><strong>Results: </strong>Data for 6102 NHANES participants were analyzed. Weighted multivariable-adjusted linear regression analyses showed that hypertension increased PhenoAge (<i>β</i> = 12, 95% CI: 11-13, <i>p </i>< 0.001) and was positively associated with PhenoAge acceleration (<i>β</i> = 0.56, 95% CI: 0.15-0.98, <i>p</i> = 0.009). The MR results also suggested a potential causal association of hypertension with DNAm PhenoAge acceleration (OR 1.31, 95% CI: 1.07-1.60, <i>p </i>< 0.05), DNAm GrimAge acceleration (OR 1.33, 95% CI: 1.13-1.57, <i>p </i>< 0.05), and the frailty index (OR 1.09, 95% CI: 1.07-1.11, <i>p </i>< 0.05). Sensitivity analyses confirmed the robustness and reliability of these findings.</p><p><strong>Conclusion: </strong>Hypertension increases PhenoAge and is correlated with PhenoAge acceleration. The potential causal association between hypertension and multiple biological indicators of aging provides clues to the relationship between hypertension and epigenetic aging.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2559743"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective peptide OL-FS13 attenuates cardiac apoptosis and myocardial infarction injury through Nrf2/HO-1 pathway.","authors":"Hao Wang, Ke Zhou, Xiaoling Chen, Yao Tong, Qiuyan Jiang, Qiang She, Jun Xiao","doi":"10.1080/10641963.2025.2556422","DOIUrl":"https://doi.org/10.1080/10641963.2025.2556422","url":null,"abstract":"<p><p>Myocardial infarction (MI) is a leading cause of morbidity and mortality globally, primarily due to oxidative stress-induced cardiomyocyte apoptosis and adverse cardiac remodeling. OL-FS13, a neuroprotective peptide derived from Odorrana livida, has previously shown anti-apoptotic effects in cerebral ischemia models. However, its role in myocardial protection remains unclear. In this study, we investigated the cardioprotective effects of OL-FS13 in both in vitro and in vivo models of MI. Hydrogen peroxide (H₂O₂) was used to induce oxidative stress in primary neonatal rat cardiomyocytes, while permanent ligation of the left anterior descending (LAD) coronary artery was employed to establish a murine MI model. OL-FS13 treatment significantly attenuated cardiomyocyte apoptosis, reduced ROS accumulation, improved left ventricular function, and decreased infarct size. Mechanistically, OL-FS13 activated the Nrf2/HO-1 signaling pathway, restoring antioxidant protein levels and suppressing oxidative stress-induced apoptosis. Pharmacological inhibition of Nrf2 with ML385 abrogated the antioxidant and anti-apoptotic effects of OL-FS13 both in vitro and in vivo, confirming the central role of this pathway. These findings demonstrate that OL-FS13 exerts potent cardioprotective effects via Nrf2/HO-1 pathway activation and ROS suppression, suggesting its potential as a novel therapeutic agent for the treatment of myocardial infarction.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2556422"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcatheter hybrid closure of a large muscular ventricular septal defect with severe pulmonary hypertension using a duct occluder.","authors":"Shibiao Zhang, Mi Tang, Qin Wu, Huayi Tan, Zhirong Wang, Jinfu Yang, Sijie Wu","doi":"10.1080/10641963.2025.2586068","DOIUrl":"10.1080/10641963.2025.2586068","url":null,"abstract":"<p><strong>Background: </strong>Apical muscular ventricular septal defects (mVSDs) are surgically challenging because of their location. Although transcatheter device closure is effective in many patients, large apical defects in infants present specific technical limitations and risks.</p><p><strong>Case presentation: </strong>A 6-month-old infant (4.5 kg, 62 cm) with severe pulmonary hypertension and marked feeding and respiratory difficulties was found to have a 10 mm apical mVSD.</p><p><strong>Intervention: </strong>The defect was closed using a 10-12 mm arterial duct occluder (PushMed, China) via a hybrid transcatheter approach.</p><p><strong>Outcome: </strong>The procedure achieved complete defect closure without immediate complications. At 3 months' follow-up the infant demonstrated significant weight gain and clinical improvement.</p><p><strong>Conclusions: </strong>Hybrid transcatheter closure with an arterial duct occluder can be a feasible and effective option for large apical mVSDs in select infants. Careful patient selection and close follow-up remain essential.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2586068"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145562933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interdisciplinary collaborative care model combined with family empowerment in patients with comorbid hypertension and diabetes: A study on blood pressure/glucose control and psychosocial adaptation based on the COM-B model.","authors":"Junxia Wu, Xiaofen Zhu, Qiqi Wu, Fang Xiao","doi":"10.1080/10641963.2025.2570212","DOIUrl":"10.1080/10641963.2025.2570212","url":null,"abstract":"<p><strong>Background: </strong>To evaluate the efficacy of an interdisciplinary care model with family empowerment (ICCM-FE) on clinical and psychosocial outcomes in patients with hypertension and diabetes.</p><p><strong>Methods: </strong>This prospective randomized controlled trial (RCT) enrolled 187 patients with comorbid hypertension and diabetes from January 2023 to March 2024. Patients were randomly assigned to a control group (<i>n</i> = 93) receiving routine care and an intervention group (<i>n</i> = 94) receiving ICCM-FE intervention. Follow-up was conducted over 6 months to assess blood pressure (SBP and DBP), glucose levels (FPG and HbA1c), quality of life (SF-36 scale), psychosocial adaptation (PAIS-SR scale), and nursing satisfaction (NSNS scale) pre- and post-intervention.</p><p><strong>Results: </strong>After 6 months, both groups exhibited significant improvements in SBP, DBP, FPG, and HbA1c (<i>p</i> < 0.05), with the intervention group achieving better outcomes than the control group (<i>p</i> < 0.05). The intervention group also demonstrated higher scores on the SF-36, General Self-Efficacy Scale (GSES), and NSNS scale, while lower scores on the PAIS-SR scale compared to the control group (<i>p</i> < 0.05).</p><p><strong>Conclusion: </strong>Compared with routine care, the ICCM-FE intervention, which incorporates the COM-B model and structured family engagement, significantly improved clinical outcomes and psychosocial adaptation in patients with comorbid hypertension and diabetes. These findings highlight the model's effectiveness in promoting better health behavior, emotional coping, and care satisfaction, supporting its potential for broader clinical application.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2570212"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145291199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between serum albumin to serum creatinine ratio and incident heart failure in patients with chronic kidney disease.","authors":"Weiwei Zhang, Youyou Liang, Peishan Xue, Chunlan Ma, Jing Zeng, Yali Qu, Yuting Zeng, Yingying Huang, Linhui He, Yuanyuan Jiang","doi":"10.1080/10641963.2025.2561908","DOIUrl":"https://doi.org/10.1080/10641963.2025.2561908","url":null,"abstract":"<p><p>This prospective cohort study investigated the association between the albumin to serum creatinine ratio (sACR) and heart failure (HF) incidence in 150 chronic kidney disease (CKD) patients. Over a median 23-month follow-up, 114 HF events occurred. Multivariate Cox regression revealed a higher HF risk in the lowest versus highest sACR tertile (adjusted HR=1.742, 95% CI=1.341-2.002, p=0.023). Lower sACR correlated with worsened cardiac structure/function. The predictive AUC for HF was 0.64 for sACR alone and improved to 0.79 when combined with clinical covariates. We conclude that low sACR is independently associated with increased HF incidence in CKD patients.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2561908"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}