Kidney & blood pressure research最新文献

{"title":"ACOT4 and ACOT6 activate Akt-mTOR pathway and inhibit calcium oxalate-induced renal tubular cell injury.","authors":"Shenghan Wang, Zhentao Lei, Wei Liu, Yuqiang Shi, Sherryn Sherryn, Qiang Gao, Bao Zhang","doi":"10.1159/000546897","DOIUrl":"https://doi.org/10.1159/000546897","url":null,"abstract":"<p><strong>Introduction: </strong>Kidney stones caused by calcium oxalate (CaOx) is a chronic kidney disease. Acyl coenzyme A thioesterases (ACOTs) serve as the key regulators of fatty acids metabolism. However, ACOTs' effect on CaOx kidney stone formation remains to be explored. Here, we aimed to investigate the effect of ACOTs on CaOx kidney stone formation.</p><p><strong>Methods: </strong>HK-2 and M-1 cells were cultured in DMEM/F12 medium supplemented with 10% FBS. Cells were treated with varying concentrations of calcium oxalate (CaC2O4) and transfected with siRNA or plasmid vectors targeting ACOT4 and ACOT6 using Lipofectamine RNAiMAX or Lipofectamine 3000. RT-qPCR and Western blotting were used to analyze gene and protein expression. Cell viability was assessed with CCK-8, and cell apoptosis was measured by flow cytometry. Crystal adhesion was visualized under a microscope. Lactate dehydrogenase (LDH) release was measured using a cytotoxicity assay kit. A kidney stone mouse model was established by injecting glyoxylic acid to induce kidney stones, and tissues were analyzed by Western blotting.</p><p><strong>Results: </strong>The mRNA and protein levels of several ACOT family members were upregulated in HK-2 cells treated with CaOx (inducing cell injury). Knockdown of ACOT4 and ACOT6 significantly suppressed the activity of CaOx-pretreated HK-2 and M-1 cells, and promoted the crystal formation and LDH release, whereas overexpression of ACOT4 and ACOT6 reduced CaOx crystal-induced kidney cell injury. Furthermore, the levels of p-AKT and p-S6 decreased after ACOT4 and ACOT6 knockdown and increased following ACOT4 and ACOT6 overexpression, suggesting that both ACOT4 and ACOT6 activated Akt/mTOR signaling pathway in HK-2 cells. We also observed that knockdown of ACOT4 and ACOT6 induced the apoptosis of HK-2 cells after CaOx treatment. Inhibition of apoptosis using Z-VAD-FMK reversed the enhanced cell injury caused by CaOx treatment and ACOT4/6 knockdown, suggesting that knockdown of ACOT4 and ACOT6 promoted cell injury via inducing cell apoptosis.</p><p><strong>Conclusions: </strong>ACOT4 and ACOT6 could be protecting factors for kidney cell injury induced by CaOx via reducing apoptosis and activating Akt/mTOR signaling pathway. The study of the role of ACOT4 and ACOT6 in kidney cell injury provides a new insight into the cause of CaOx kidney stone formation. Its in-depth study may provide new targets for stone treatment.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-16"},"PeriodicalIF":2.3,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368959","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":"Acute Kidney Injury in Endocrine Emergencies.","authors":"Nadezda Petejova, Josef Zadrazil, David Karasek, Arnost Martinek, Vladimir Teplan, Marianna Bystrianska, Marcela Kanova","doi":"10.1159/000547081","DOIUrl":"https://doi.org/10.1159/000547081","url":null,"abstract":"<p><strong>Background: </strong>Acute kidney injury (AKI) is a serious condition in clinical medicine that significantly increases morbidity and mortality, particularly in critically ill patients. Rapid and accurate identification of the underlying causes of AKI is crucial for determining appropriate therapeutic management and potentially saving the patient's life. Although endocrine emergencies are a less common cause of AKI in critically ill patients, recognizing when they occur is vital to comprehensive care.</p><p><strong>Summary: </strong>AKI can impair the endocrine system and result in critical conditions for patients, particularly in cases of sepsis. In addition, several factors can contribute to severe conditions associated with AKI, including thyrotoxicosis, adrenal crisis, severe hypothyroidism, complications related to diabetes mellitus, panhypopituitarism, diabetes insipidus with acute hypernatremia, severe hypercalcemia, neuroendocrine tumors, and ovarian hyperstimulation syndrome.</p><p><strong>Key message: </strong>The early recognition of endocrine emergencies and the impact of AKI on the endocrine system in critically ill patients is essential to intensive and comprehensive care.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-33"},"PeriodicalIF":2.3,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368968","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":"Construction of a PANoptosis-Related Gene Signature for Diabetic Nephropathy.","authors":"Li Geng, Yingying Liu, Yunwei Sun, Yan Chen","doi":"10.1159/000546764","DOIUrl":"https://doi.org/10.1159/000546764","url":null,"abstract":"<p><strong>Introduction: </strong>Diabetic nephropathy (DN) is a serious complication of diabetes. In this study, we aimed to develop a diagnostic model for DN based on PANoptosis-related genes.</p><p><strong>Methods: </strong>PANoptosis-related DEGs associated with DN were identified in the GSE96804 and GSE142025 datasets. Pairwise correlations among these genes were assessed via Pearson correlation analysis. Immune cell abundance in DN patients versus controls was compared in GSE96804. Feature genes for DN preiction were selected with machine learning, and a diagnostic model was constructed using LASSO regression. High-risk and low-risk groups were established based on risk scores, with GSEA used to explore enriched biological processes and pathways. The association between risk scores and immune cell infiltration was examined using CIBERSORT. Potential therapeutic drugs were investigated via the DGIdb database.</p><p><strong>Results: </strong>Six PANoptosis-related DEGs were found. Immune cell analysis showed significant differences in dendritic cells, macrophages, mast cells, and neutrophils between DN patients and controls. A diagnostic model using three genes (PDK4, YWHAH, PRKX) achieved high accuracy (AUC = 0.8-1.0) across datasets, with a reliable nomogram for DN prediction. Risk stratification linked higher risk scores to distinct immune infiltration patterns and enriched cellular transport and metabolic pathways in high-risk DN patients. PPI network and correlation analyses revealed complex gene interactions. Potential therapeutic targets (PRKX, PDK4) and drugs were identified, and qPCR validated YWHAH upregulation in patient plasma samples.</p><p><strong>Conclusion: </strong>The integration of PANoptosis-related genes PDK4, YWHAH, and PRKX offers a promising diagnostic model for DN, with YWHAH potentially involved in the pathological progression of DN.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-21"},"PeriodicalIF":2.3,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144285060","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":"A META ANALYSIS OF THE RELATIONSHIP BETWEEN STROKE AND ALZHEIMER'S DISEASE: THERAPEUTIC AND PROGNOSTIC IMPLICATIONS.","authors":"Olalla Saiz Vazquez, Silvia Ubillos-Landa, Alicia Puente Martínez","doi":"10.1159/000546395","DOIUrl":"https://doi.org/10.1159/000546395","url":null,"abstract":"<p><strong>Background: </strong>Several population-based studies have highlighted the association between stroke and dementia. Alzheimer's disease (AD) related dementia and vascular dementia are the most common causes of dementia, with clearer pathophysiological mechanisms for the latter. Given the ongoing debate surrounding the link between stroke and Alzheimer's disease, to determine their relationship and the possible influence of some moderators (sex, age, and region), a systematic meta-analysis was performed.</p><p><strong>Methods: </strong>We searched five databases (ISI Web of Science, Scopus, PubMed, Elsevier Science Direct, and Google Scholar) with no initial publication date restriction, with the last search conducted in 2022. We included longitudinal population-based studies assessing the stroke-AD association, selecting those with reported effect sizes, standardized AD diagnosis, and an AMSTAR score ≥9. Case reports, reviews, animal studies, and non-English publications were excluded. The meta-analysis, conducted using Comprehensive Meta-Analysis 3.1, presented pooled log odds ratios (LogOR) with 95% confidence intervals, heterogeneity analysis (Cochran's Q, I²), and moderator analyses by age, gender, and region.</p><p><strong>Results: </strong>The meta-analysis included three meta-analyses and twelve primary studies, comprising a total of 14,207 stroke cases and 1,952 AD cases. Our analysis found a significant association between ischemic stroke (IS), hemorrhagic stroke (HS), and microinfarcts (MI) with the risk of AD. Despite some heterogeneity across studies, no significant differences were observed in the stroke-AD association based on age, sex, or region.</p><p><strong>Conclusion: </strong>Our study describes the risk of AD in patients with episodes of stroke (IS, HS and MI), and suggests that the risk of AD may be higher in patients that suffer stroke when compared to matched controls without incidence of stroke. Moreover, moderator analysis supports the robustness of our results. The link between stroke and Alzheimer's suggests that stroke may speed up cognitive decline. This calls for tighter vascular control and points to a worse prognosis in dementia progression.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-31"},"PeriodicalIF":2.3,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234474","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":"Endothelial MicroRNA-214 Confers Angiotensin II Hypertension by Targeting eNOS in mice.","authors":"Shuzhen Li, Bing Liu, Shuang Kang, Bingyu Yang, Yue Zhang, Songming Huang, Aihua Zhang, Zhanjun Jia","doi":"10.1159/000546674","DOIUrl":"https://doi.org/10.1159/000546674","url":null,"abstract":"<p><p>MicroRNAs have been increasingly recognized for their roles in cardiovascular diseases. Among these microRNAs, miR-214 was reported to be involved in hypertension. However, the role of endothelial miR-214 in hypertension is still unknown. The aim of this study was to determine the role of cell-specific miR-214 on regulating blood pressure, as well as the potential mechanisms. miR-214 levels in hypertensive mice and cultured mouse aortic endothelial cells (MAECs) were detected and its role in Ang II-induced hypertension was examined. In mice and MAECs, Ang II significantly enhanced miR-214 levels, and anti-miR-214 markedly attenuated Ang II hypertension in line with enhanced eNOS/p-eNOS in aorta. Then we generated vascular endothelial cell-specific miR-214 knockout mice and found an anti-hypertensive phenotype in endothelial miR-214 conditional knock-out mice after Ang II treatment. In normotensive animals and MAECs, exogenous miR-214 administration reduced eNOS expression at protein and mRNA levels, in contrast, anti-miR-214 played an opposite role in regulating eNOS. By luciferase assay, our results confirmed that eNOS was a direct target gene for miR-214 in endothelial cells. However, smooth muscle cell-specific or renal tubular cell-specific deletion of miR-214 did not alter Ang II-induced hypertension. Thus, our findings suggested that endothelial miR-214 promoted Ang II hypertension by targeting eNOS in mice, which increased the understanding on the pathogenic mechanism of hypertension.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-21"},"PeriodicalIF":2.3,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199555","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":"Hydronephrosis-Associated Renal Fibrosis: Clinical Validation of Spp1 as a Biomarker and Therapeutic Target.","authors":"Xiao Wang, Jie-Hao Zhou, Guang Chen, Ji-Dong Chen, Hui Li, Wei-Min Shan, Wei-Xiao Li","doi":"10.1159/000546465","DOIUrl":"https://doi.org/10.1159/000546465","url":null,"abstract":"<p><strong>Background: </strong>Renal fibrosis is a key driver of chronic kidney disease (CKD), often leading to end-stage renal disease (ESRD). Secreted Phosphoprotein 1 (Spp1) is implicated in fibrotic processes, but its specific role in renal fibrosis, particularly associated with hydronephrosis, remains underexplored. This study investigates Spp1's involvement using transcriptomic analysis, machine learning, and clinical data integration.</p><p><strong>Methods: </strong>Renal tissues from sham-operated and UUO7 (unilateral ureteral obstruction) mice were analyzed via transcriptome sequencing to identify differentially expressed genes (DEGs). Hub genes were identified through Weighted Gene Co-expression Network Analysis (WGCNA) and pathway enrichment. LASSO regression pinpointed potential biomarkers, with Spp1 validated in mouse and human samples through RT-PCR and immunohistochemistry. Clinical correlations were drawn from hydronephrosis patient data.</p><p><strong>Results: </strong>Transcriptomic analysis revealed 5,219 DEGs, highlighting key pathways including IL-17, TNF, and PI3K/AKT. Spp1 emerged as a significant biomarker, strongly associated with tubular injury and fibrosis markers such as neutrophil gelatinase-associated lipocalin (NGAL). Logistic regression and ROC analyses confirmed Spp1 and urinary transferrin (U-TRF) as predictors of severe hydronephrosis, with high diagnostic accuracy (AUC: 0.898 for Spp1; 0.938 for U-TRF).</p><p><strong>Conclusions: </strong>Spp1 is a critical mediator in renal fibrosis and a promising biomarker for assessing hydronephrosis severity. Its diagnostic value, particularly when combined with U-TRF, underscores the need for further research into Spp1-targeted therapies in renal fibrosis.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-26"},"PeriodicalIF":2.3,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174290","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":"CFHR5 nephropathy case report: a novel variant characterized by tubulointerstitial kidney disease.","authors":"Rita Santarsiere, Giulia Florio, Annalisa Gonnella, Pierluigi D'Angiò, Simona Laurino, Miriam Zacchia, Francesca Del Vecchio Blanco, Alessandra F Perna, Francesco Trepiccione, Giuseppe Gigliotti","doi":"10.1159/000546321","DOIUrl":"https://doi.org/10.1159/000546321","url":null,"abstract":"<p><p>CFHR5 nephropathy is considered a subtype of C3 glomerulopathy. It was originally described in Greek Cypriot families and it is characterized by the time with the development of microscopic hematuria and proteinuria associated with a fast progression towards ESKD especially in men. These symptoms present an autosomal dominant inheritance pattern and are associated with the exon 2 to 3 duplication of the CFHR5 gene. Here, we describe a novel clinical phenotype associated with a variant of the CFHR5. The affected subjects present the clinical features of Autosomal Dominant Tubulo-interstitial Kidney Disease. They present with CKD of unknown origin with no hematuria nor proteinuria. Like the classical CFHR5 nephropathy, males have a worse prognosis than females, with a fast progression towards ESKD in the second-third decade of life. Kidney pathology shows severe tubular atrophy and interstitial fibrosis and infiltrate. Arteries involvement is characterized by thickening of the intima layer, while no major alterations are described at the glomerular level. Electron Microscopy confirms no interstitial or glomerular filtration barrier alterations.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-10"},"PeriodicalIF":2.3,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142946","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":"Rethinking models of CKD care: a narrative review.","authors":"Hannah Wallace, J Oliver Daly, Min Jun, Craig Nelson","doi":"10.1159/000546562","DOIUrl":"https://doi.org/10.1159/000546562","url":null,"abstract":"<p><strong>Background: </strong>Chronic kidney disease (CKD) affects over 850 million people worldwide and is associated with significant morbidity and mortality. There has been recent expansion in treatment options to reduce CKD progression and cardiovascular risk, and it is essential that this translates into clinical practice.</p><p><strong>Summary: </strong>The primary objectives of this review were to outline current CKD care models and associated care gaps, and review the literature for alternative care models, with a focus on the early detection and management of CKD. Several care models have been proposed to improve CKD management including nurse-led, pharmacy-led, integrated care models and digital interventions, with mixed results.</p><p><strong>Key messages: </strong>There is a need for ongoing health systems and implementation research to improve translation of evidence into practice in the management of chronic kidney disease.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-17"},"PeriodicalIF":2.3,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142950","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":"Relation of Serum Creatinine Twitches and Outcomes among STEMI Patients.","authors":"Shir Frydman, Ophir Freund, Lior Zornitzki, Nevo Barel, Shmuel Banai, Yacov Shacham","doi":"10.1159/000545523","DOIUrl":"https://doi.org/10.1159/000545523","url":null,"abstract":"<p><strong>Background: </strong>Acute kidney injury (AKI) is notoriously associated with adverse outcomes and mortality in patients with acute coronary syndrome. However, using the general cutoff of 0.3 mg/dL increase from baseline for AKI definition and neglecting smaller changes could result in late diagnosis and impaired prognostication. We aimed to assess the prognostic utility of minor creatinine changes (\"twitches\") in a large cohort of ST-segment-elevation myocardial infraction (STEMI) patients and determine an optimal cutoff value for future use.</p><p><strong>Methods: </strong>This retrospective analysis of a prospective database included 2933 consecutive patients admitted with STEMI between 2008-2022 to the cardiac intensive care unit of a large tertiary medical center. Renal function was assessed upon admission and at-least once daily thereafter. Creatinine twitches were defined as a change from baseline to peak creatinine level of between 0.1 to 0.3 mg/dl. 30-day and 1-year mortality were the main outcomes.</p><p><strong>Results: </strong>From the study cohort (mean age 62 ±13, 19% female, 16% with prior MI), 551 (19%) subjects presented creatinine twitches and 254 (9%) developed AKI. Compared to subjects with stable creatinine, those with creatinine twitches had higher rates of 30-day (1% vs. 2.5%, p<0.001) and 1-year (1.6% vs. 4.4%, p<0.001) mortality. In cox multivariate analysis, creatinine twitches had a higher hazard for 1-year mortality (HR 1.87, 95% CI 1.1-3.2) and only a trend for 30-day mortality (HR 1.52, 95% CI 0.96-2.96). Creatinine rise had an area under the curve of 0.780 (95% CI 0.73-0.83) for 1-year mortality prediction, and 0.12 mg/dl was the optimal cutoff for prediction, with a sensitivity of 71%, specificity of 79%. In sub-group multivariate analysis, only twitches that did not resolve during hospitalization had higher hazard for mortality (HR 3.42, 95% CI 1.65-7.05).</p><p><strong>Conclusion: </strong>Serum creatinine twitches are common among STEMI patients and correlate with elevated 30 days and 1-year mortality. These seemingly minor changes should prompt renal protective strategies for early detection and treatment.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-20"},"PeriodicalIF":2.3,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143764235","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":"Impact of renal artery stenosis on renovascular hypertension and the therapeutic role of renal artery stenting: a comprehensive review.","authors":"Changgang Shao, Guoqing Chi, Fang Li, Hongcheng Ren, Liyan Zhang, Jinming Yang, Bin Wang, Mingchao Ding","doi":"10.1159/000545135","DOIUrl":"https://doi.org/10.1159/000545135","url":null,"abstract":"<p><p>Background Renal artery stenosis (RAS) is characterized by reduced renal perfusion, activating the renin-angiotensin-aldosterone system (RAAS), which can lead to secondary hypertension, ischemic nephropathy, and cardiac destabilization syndrome. These conditions have significant healthcare implications. Renovascular hypertension (RVH) in RAS patients can be managed through medical therapy and revascularization, either endovascular or surgical. While renal artery stenting (RAS) was once viewed as the most effective treatment for atherosclerotic renovascular disease, recent trials suggest no significant difference in RVH management between medical therapy alone and combined with renal artery stenting. However, certain subgroups have exhibited favorable outcomes in blood pressure control post-stenting. Summary This comprehensive review synthesizes data, including findings from the HERCULES trial, which showed a reduction in blood pressure from 162.3±18.5/77.7±11.5 mmHg to 145.7±20.7/75.4±11.0 mmHg over 36 months (P<0.0001). Additionally, the ASPIRE-2 study demonstrated significant decreases in blood pressures from 168±25/82±13 mmHg to 149±25/77±12 mmHg at 24 months (P<0.001). The review delves into the prevalence, pathophysiology, clinical manifestations, diagnosis, and treatment of RAS-related RVH, specifically analyzing the efficacy and safety of renal artery stenting. Key Messages The analysis indicates that renal artery stenting may be particularly advantageous for certain patient subgroups, enhancing blood pressure outcomes and overall clinical status. Nevertheless, the criteria for selecting candidates for this intervention remain under debate. Future research should focus on high-risk RAS patients to explore long-term benefits and refine the utilization of renal artery stents, ultimately improving RVH management.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-15"},"PeriodicalIF":2.3,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143597343","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}