Niloofar Nobakht, Taraneh Mousavi, Pooneh Jabbaripour Sarmadian, Mohammad Kamgar
{"title":"Muscle Health in the Era of Incretin-Based Weight Loss: Implications for Patients with Cardiovascular-Kidney-Metabolic Syndrome.","authors":"Niloofar Nobakht, Taraneh Mousavi, Pooneh Jabbaripour Sarmadian, Mohammad Kamgar","doi":"10.1159/000553166","DOIUrl":"https://doi.org/10.1159/000553166","url":null,"abstract":"<p><p>Background Preserving lean body mass (LBM) is increasingly recognized as a critical determinant of survival and disease progression in individuals with cardiovascular-kidney-metabolic (CKM) syndrome. Sarcopenia is significantly associated with higher risk of all-cause, cardiovascular (CVD), and non-CVD mortality, as well as greater odds of advancing to later CKM stages. While incretin-based therapies, including glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and dual GLP-1/gastric inhibitory polypeptide (GIP) receptor agonists, are now cornerstones of CKM management, emerging evidence suggests a potential association with loss of LBM and skeletal muscle in vulnerable patients. The key gap in knowledge is that most trials and real-world evaluations prioritize weight and cardio-kidney-metabolic endpoints, while muscle mass, strength, functional trajectories, frailty progression, and patient-reported impacts are inconsistently measured, especially in high-risk CKM populations. This review synthesizes clinical trial and real-world evidence to characterize body composition changes with incretin-based therapies and proposes a conceptual, stepwise framework to maintain patient-centered muscle health. PubMed, Scopus, and Web of Science were searched for English-language peer-reviewed studies (January 2004-January 2026) evaluating incretin-based therapies and LBM outcomes; ClinicalTrials.gov and WHO ICTRP were also queried for trials with muscle-related endpoints. Summary Across incretin agents, weight loss is typically fat-predominant; however, available studies suggest approximately 25-39% of total weight loss may reflect LBM reduction over 36-72 weeks. Major evidence gaps include: (1) limited longitudinal data linking LBM loss to strength, mobility, frailty, falls, disability, and patient-reported function; (2) sparse head-to-head comparisons to clarify agent- and dose-specific muscle effects across the CKM continuum; (3) underrepresentation of high-risk CKM subgroups most vulnerable to protein-energy wasting, anabolic resistance, and polypharmacy; and (4) lack of scalable risk prediction and monitoring tools to detect early adverse body-composition trajectories. Key Messages Despite rapid expansion of incretin-based therapies across the CKM continuum, muscle health is rarely measured, yet it strongly shapes survival, frailty, and functional independence. Muscle preservation is a key consideration in benefit-risk assessment and merits explicit tracking in both clinical trials and routine practice. We outline a patient-centered, stepwise roadmap that pairs incretin prescribing with baseline muscle-risk characterization, serial tracking of body composition (e.g., DXA/BIA/BIS where feasible), simple functional measures, and early mitigation strategies (resistance training, nutrition optimization, and, when appropriate, adjunct anabolic/anti-catabolic approaches). Priorities to advance the field include pragmatic long-term studies in high-risk ","PeriodicalId":9584,"journal":{"name":"Cardiorenal Medicine","volume":" ","pages":"1-28"},"PeriodicalIF":3.2,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683364","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}
Cardiorenal MedicinePub Date : 2026-01-01Epub Date: 2026-05-11DOI: 10.1159/000551758
{"title":"Erratum.","authors":"","doi":"10.1159/000551758","DOIUrl":"10.1159/000551758","url":null,"abstract":"<p><p>In the article \"Denosumab Decreases Epicardial Adipose Tissue Attenuation in Dialysis Patients with Secondary Hyperparathyroidism and Low Bone Mass\" [Cardiorenal Med. 2024;14(1):113-122; https://doi.org/10.1159/000535882], the authors identified an error in the labelling of Figure 2b in the originally published version.Fig. 2.Changes in serum phosphate (a) and calcium × phosphate (b) comprising denosumab and calcitriol, compared to the control group. #p < 0.05; *p < 0.01.The labels for the Denosumab group and the Control group were inadvertently interchanged. The underlying data, statistical results, and graphical elements of the figure are correct; only the group labels require reversal. The conclusions of the study remain unchanged.The authors confirmed that the incorrect label arrangement originated from an oversight during the proofchecking stage. The corrected Figure 2b, with the proper labels applied, is reproduced below.</p>","PeriodicalId":9584,"journal":{"name":"Cardiorenal Medicine","volume":"16 1","pages":"153"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147873508","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}
Cardiorenal MedicinePub Date : 2026-01-01Epub Date: 2026-02-09DOI: 10.1159/000550943
María Marques, Alberto Ortiz, Gregorio Romero-González, Javier Díez, Rafael Santamaría, Adriana Puente-García, Roberto Alcázar, Patricia de Sequera, José Luis Górriz, Borja Quiroga
{"title":"Ten Hot Topics in Cardiovascular Risk Management for Chronic Kidney Disease.","authors":"María Marques, Alberto Ortiz, Gregorio Romero-González, Javier Díez, Rafael Santamaría, Adriana Puente-García, Roberto Alcázar, Patricia de Sequera, José Luis Górriz, Borja Quiroga","doi":"10.1159/000550943","DOIUrl":"10.1159/000550943","url":null,"abstract":"<p><strong>Background: </strong>Chronic kidney disease (CKD) is associated with a markedly increased risk of cardiovascular disease (CVD). Despite this, cardiovascular risk in patients with CKD is frequently underestimated and insufficiently treated in routine clinical practice.</p><p><strong>Summary: </strong>In this narrative review, we address ten concise and up-to-date questions focused on cardiovascular risk management in CKD. A panel of ten expert nephrologists provides evidence-based perspectives on key aspects including assessment of the arterial tree, cardiovascular risk estimation, identification of biomarkers for improved risk stratification, and both pharmacological and non-pharmacological interventions proven to reduce cardiovascular risk. Additional topics include blood pressure targets, optimal management of dyslipidemia, and cardiovascular risk management in patients receiving renal replacement therapy. Practical strategies to translate this evidence into everyday clinical care are also discussed.</p><p><strong>Key message: </strong>A comprehensive and structured approach to cardiovascular risk assessment and management are essential in patients with CKD and should be systematically integrated into routine nephrology practice to improve cardiovascular outcomes.</p>","PeriodicalId":9584,"journal":{"name":"Cardiorenal Medicine","volume":" ","pages":"113-133"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13046305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cardiorenal MedicinePub Date : 2026-01-01Epub Date: 2026-04-30DOI: 10.1159/000552030
Jessica B Kendrick, Angelina Magreni Dixon
{"title":"Review of Hyperkalemia Profile for Mineralocorticoid Receptor Antagonist in Patients with Chronic Kidney Disease and Type 2 Diabetes.","authors":"Jessica B Kendrick, Angelina Magreni Dixon","doi":"10.1159/000552030","DOIUrl":"10.1159/000552030","url":null,"abstract":"<p><strong>Background: </strong>Type 2 diabetes (T2D) frequently coexists with chronic kidney disease (CKD), magnifying the risk of both cardiovascular and renal complications. Although therapies targeting the renin-angiotensin-aldosterone system (RAAS) slow CKD progression and reduce cardiovascular events, they also raise the risk of hyperkalemia. Finerenone, a newer nonsteroidal mineralocorticoid receptor antagonist (MRA), offers potent cardiorenal protection with relatively low hyperkalemia risk.</p><p><strong>Summary: </strong>We conducted a narrative review of randomized controlled trials published up to September 2024, which evaluated spironolactone, eplerenone, or finerenone in populations with T2D, CKD, or heart failure. Studies that reported explicit data on hyperkalemia incidence, severity, and management were included. The findings were synthesized narratively with the consideration of heterogeneity in study population and hyperkalemia definition. Evidence from spironolactone and eplerenone trials underscores the survival benefits of steroidal MRAs in heart failure patients but also demonstrates a notable hyperkalemia risk, especially in patients with advanced CKD. Finerenone, studied in FIDELIO-DKD, FIGARO-DKD, and subsequently pooled in FIDELITY, demonstrated robust efficacy in reducing cardiovascular and kidney outcomes. It was associated predominantly with mild-to-moderate hyperkalemia, which stabilized with regular monitoring. The incidence of severe events and therapy discontinuations due to hyperkalemia were low. A risk-prediction model from FIDELITY further stratified patients by hyperkalemia risk, revealing consistent relative hyperkalemia risk of finerenone across all strata.</p><p><strong>Key messages: </strong>Hyperkalemia remains a pivotal challenge when prescribing MRAs in patients with T2D and CKD, often leading to underutilization of these lifesaving agents. However, finerenone's safety profile, combined with diligent potassium surveillance and proactive management strategies (e.g., dietary guidance, potassium binders, use of diuretics), enables sustained cardiorenal benefits. Future research should explore real-world applicability of these trial findings and further refine risk-based treatment algorithms to optimize outcomes in this high-risk population.</p>","PeriodicalId":9584,"journal":{"name":"Cardiorenal Medicine","volume":" ","pages":"312-320"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13322682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cardiorenal MedicinePub Date : 2026-01-01Epub Date: 2026-06-18DOI: 10.1159/000553163
William R Marshall, Rajkumar Chinnadurai, Darren Green, Smeeta Sinha, Philip A Kalra
{"title":"Cardiovascular-Kidney-Metabolic Multimorbidity Burden and Phenotype Differentially Influence Cardiovascular and Renal Risk in Advanced Chronic Kidney Disease.","authors":"William R Marshall, Rajkumar Chinnadurai, Darren Green, Smeeta Sinha, Philip A Kalra","doi":"10.1159/000553163","DOIUrl":"10.1159/000553163","url":null,"abstract":"<p><strong>Introduction: </strong>Chronic kidney disease (CKD) frequently coexists with cardiovascular disease (CVD), diabetes, and obesity through shared biological pathways encompassed within the American Heart Association cardiovascular-kidney-metabolic (CKM) construct. Whether adverse cardiovascular and renal outcomes in CKD are driven predominantly by cumulative multimorbidity burden or by distinct CKM disease phenotypes remains uncertain.</p><p><strong>Methods: </strong>We conducted a retrospective longitudinal cohort study of participants in the Salford Kidney Study with non-dialysis-dependent CKD and at least one other CKM comorbidity. Patients were evaluated according to CKM multimorbidity burden (2, 3, or 4 conditions) and in predefined CKM phenotypes. Co-primary outcomes were major adverse cardiovascular event (MACE: cardiovascular mortality, non-fatal myocardial infarction, non-fatal cerebrovascular accident, or heart failure event), composite kidney endpoint (CKE: ≥40% eGFR decline, eGFR <15 mL/min/1.73 m2, or renal replacement therapy initiation), and all-cause mortality. Associations were evaluated using multivariable time-to-event models.</p><p><strong>Results: </strong>Among 2,003 participants (mean age 68 years; median follow-up 4.7 years), 279 (13.9%) experienced MACE and 1,010 (50.4%) reached the CKE. Compared with 2 CKM conditions, 4 conditions conferred an almost two-fold higher MACE risk (HR 1.93, 95% CI: 1.48-2.53), with the CKD-CVD-diabetes-obesity phenotype demonstrating the highest MACE risk. Diabetes-containing phenotypes were consistently associated with higher CKE risk, whereas increasing multimorbidity burden showed limited discriminatory value for kidney progression. The CKD-diabetes-CVD phenotype had the highest all-cause mortality (27.1 deaths per 100 patient-years).</p><p><strong>Conclusions: </strong>Increasing CKM multimorbidity burden predicted cardiovascular events and mortality in keeping with the American Heart Association staging framework, but kidney progression was more strongly determined by disease phenotype, particularly diabetic kidney disease. This cardiovascular-renal dissociation suggests that phenotypic refinement of the CKM staging model may improve risk stratification in advanced CKD populations with CKM multimorbidity.</p>","PeriodicalId":9584,"journal":{"name":"Cardiorenal Medicine","volume":" ","pages":"409-423"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13446873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148276053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cardiorenal MedicinePub Date : 2026-01-01Epub Date: 2026-03-21DOI: 10.1159/000551617
Jheng-Yan Wu, Keng-Wei Lee, Sheng-Chi Huang, Hsuan-Yuan Chang, Yu-Min Lin
{"title":"Comparative Effectiveness of Ivabradine versus Digoxin in Patients with Heart Failure with Reduced Ejection Fraction and Chronic Kidney Disease: A Real-World Multicenter Cohort Study.","authors":"Jheng-Yan Wu, Keng-Wei Lee, Sheng-Chi Huang, Hsuan-Yuan Chang, Yu-Min Lin","doi":"10.1159/000551617","DOIUrl":"10.1159/000551617","url":null,"abstract":"<p><strong>Introduction: </strong>Heart failure with reduced ejection fraction (HFrEF) commonly coexists with chronic kidney disease (CKD), conferring a markedly increased risk of adverse outcomes. Ivabradine and digoxin are both used for heart rate control in HFrEF, but their comparative effectiveness in patients with CKD remains uncertain. Therefore, this study aimed to compare the risk of major adverse cardiovascular events (MACE), including heart failure exacerbation (HFE) and all-cause mortality, between ivabradine and digoxin in patients with concomitant HFrEF and CKD.</p><p><strong>Methods: </strong>Using the TriNetX global research network, we conducted a retrospective cohort study including adults with HFrEF and CKD between 2015 and 2025. Patients prescribed ivabradine were propensity score-matched 1:1 to those receiving digoxin based on demographic, clinical, laboratory, and medication variables. The primary outcome was MACE (composite of HFE or all-cause mortality). Secondary outcomes included each component separately. Cox proportional hazards models estimated hazard ratios (HRs) with 95% confidence intervals (CIs).</p><p><strong>Results: </strong>After matching, 3,140 patients were included (1,570 per group). Ivabradine use was associated with a significantly lower risk of MACE compared with digoxin (26.8% vs. 31.6%; HR: 0.79, 95% CI: 0.70-0.90; p < 0.001). Ivabradine also reduced the risk of HFE (HR: 0.83, 95% CI: 0.72-0.97; p = 0.015) and all-cause mortality (HR: 0.69, 95% CI: 0.56-0.85; p < 0.001). Subgroup and negative-control analyses yielded consistent results.</p><p><strong>Conclusions: </strong>In this large, real-world cohort of patients with HFrEF and CKD, ivabradine was associated with lower risks of MACE, HFE, and all-cause mortality compared with digoxin. Ivabradine may represent a safer and more effective heart rate-lowering option for this high-risk population.</p>","PeriodicalId":9584,"journal":{"name":"Cardiorenal Medicine","volume":" ","pages":"190-200"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13221172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cardiorenal MedicinePub Date : 2026-01-01Epub Date: 2026-02-11DOI: 10.1159/000550503
Dmitry Abramov, Roy O Mathew, Steve V Fordan
{"title":"Heart Failure and Comorbidities (Chronic Kidney Disease, Diabetes, Obesity) Management: A Multidisciplinary Approach.","authors":"Dmitry Abramov, Roy O Mathew, Steve V Fordan","doi":"10.1159/000550503","DOIUrl":"10.1159/000550503","url":null,"abstract":"<p><strong>Background: </strong>Heart failure (HF) frequently coexists with chronic kidney disease (CKD), type 2 diabetes (T2D), and obesity, creating a complex clinical landscape that requires integrated, multidisciplinary management. The three main HF phenotypes - HF with reduced ejection fraction (EF ≤40%), mildly reduced ejection fraction (EF 41-49%), and preserved ejection fraction (EF ≥50%) - differ in their underlying pathophysiology and therapeutic approaches. Approximately 20-40% of patients with HF have T2D, 30-40% are obese (body mass index ≥30 kg/m2), and 45-63% have CKD. These comorbidities are interrelated through overlapping mechanisms such as insulin resistance, chronic inflammation, neurohormonal activation, and endothelial dysfunction, which amplify morbidity, mortality, and healthcare costs.</p><p><strong>Summary: </strong>The interplay between HF, CKD, T2D, and obesity extends beyond hemodynamic compromise, influencing other frequent conditions such as anemia, sleep apnea, and atrial fibrillation. Addressing these interconnected comorbidities can yield cumulative benefits by improving both HF-specific and overall health outcomes. Data from recent clinical trials and observational studies indicate how these conditions modify risk, affect therapeutic response, and influence guideline-directed medical therapy. Optimal care involves timely recognition, evidence-based management, and coordination across specialties. Key contributors to care include cardiologists, primary care physicians, endocrinologists, nephrologists, pharmacists, dietitians, and mental health professionals.</p><p><strong>Key messages: </strong>The coexistence of HF with CKD, T2D, and obesity constitutes a major clinical challenge with shared pathogenic pathways. Managing these comorbidities requires an integrated, multidisciplinary strategy to improve outcomes and quality of life. Barriers such as clinical inertia, polypharmacy, and socioeconomic disparities continue to impede effective therapy implementation. Enhanced collaboration and patient-centered care models are essential to optimize management in this high-risk population.</p>","PeriodicalId":9584,"journal":{"name":"Cardiorenal Medicine","volume":" ","pages":"95-112"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13106961/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146164063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cardiorenal MedicinePub Date : 2026-01-01Epub Date: 2026-09-08DOI: 10.1159/crm/abtag010
Yitao Li, Jun Wan, Yuanyou Tang, Juan Cao, Qi Peng
{"title":"Comparative Efficacy of Interventions for Vascular Calcification and Stiffness in Dialysis Patients: A Systematic Review and Network Meta-Analysis.","authors":"Yitao Li, Jun Wan, Yuanyou Tang, Juan Cao, Qi Peng","doi":"10.1159/crm/abtag010","DOIUrl":"10.1159/crm/abtag010","url":null,"abstract":"<p><strong>Introduction: </strong>Vascular calcification (VC) and vascular stiffness (VS) significantly increase cardiovascular risks in renal dialysis (RD) patients. Currently, several interventions have been tried to alleviate VC and VS, but they all lack systematic comparison. This study integrated randomized controlled trials (RCTs) of seven interventions to provide evidence-based insights to inform clinical decision-making.</p><p><strong>Methods: </strong>A systematic search was conducted for all RCTs on drug treatments for VS or VC in patients receiving RD published between January 2001 and October 2025 in four databases: PubMed, Web of Science, Embase, and The Cochrane Library. Analyses were conducted in accordance with the PRISMA network meta-analysis (NMA) guidelines and registered in PROSPERO (CRD420251060534). Risk assessment was performed using the Cochrane Risk of Bias 2.0 tool. Bayesian NMA was then conducted using R software and Stata 15.0.</p><p><strong>Results: </strong>Sodium thiosulfate (STS) showed the highest Surface Under the Cumulative Ranking Curve (SUCRA) ranking for improving pulse wave velocity (PWV) (SUCRA = 89.4%), but no statistically significant difference was observed between STS and standard care (mean difference [MD] -1.3, 95% credible interval [95% CrI] -2.8, 0.2). No statistically significant differences were observed across all interventions for PWV improvement. Etidronic acid (EA) ranked first in SUCRA for reducing coronary artery calcification (CAC) volume score (SUCRA = 84.57%), but the difference versus most interventions did not reach statistical significance (MD -1,300, 95% CrI -3,800, 1,100). STS showed statistically significant reduction in CAC volume score compared with standard care, 300 mg SNF472, and 600 mg SNF472 (MD -188.27, 95% CrI -221.68, -154.52; MD -192.55, 95% CrI -245.83, -139.54; MD -182.39, 95% CrI -237.91, -126.55). For coronary artery and aortic Agatston scores, standard care showed superior SUCRA rankings, but EA exhibited a statistically significant difference compared with cinacalcet (aortic Agatston score: MD -1,175.11, 95% CrI -2,220.92, -125.45), indicating partial comparative efficacy among drugs.</p><p><strong>Conclusion: </strong>This study suggests that SUCRA rankings indicate STS has a potential comprehensive advantage in improving VS and delaying calcification progression, making it a reasonable exploratory choice for dialysis patients with concurrent VC and VS. While EA ranks highest in SUCRA for reducing CAC volume score, it has limited impact on VS and requires caution regarding long-term safety. Given the limited sample size, network sparsity for some outcomes, and mostly non-significant between-group comparisons, large-scale, head-to-head RCTs are needed to further validate these findings.</p>","PeriodicalId":9584,"journal":{"name":"Cardiorenal Medicine","volume":" ","pages":"516-535"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911095","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":"Periprocedural Oral Hydration Patterns and Early Renal Function after Coronary Angiography and Intervention: A Prospective Real-World Cohort Study.","authors":"Dan Zhu, Lingling Gao, Nanhui Zhuang, Yuan Ma, Lijing Fan, Haiyan Ma, Yimei Zheng","doi":"10.1159/000550260","DOIUrl":"10.1159/000550260","url":null,"abstract":"<p><strong>Introduction: </strong>Guidelines recommend oral hydration (OH) to prevent contrast-associated acute kidney injury (CA-AKI) after coronary angiography or intervention, but quantitative protocols are lacking, and practice varies. Shorter hospital stays limit opportunities for post-procedure creatinine monitoring, and real-world OH patterns and their early renal effects remain poorly described. This study aimed to characterize periprocedural weight-adjusted OH trajectories and to assess whether trajectory membership was associated with a change in serum creatinine within 24 h.</p><p><strong>Methods: </strong>This single-center prospective cohort study enrolled 192 inpatients undergoing coronary angiography or intervention between November 2024 and May 2025. We recorded weight-adjusted oral intake in four windows: pre-12 h, post-0-6 h, 6-12 h, and 12-24 h. We computed partial-overlap dynamic time warping distances and clustered trajectories using partitioning around medoids. Group comparisons used nonparametric tests. The primary outcome was percent change in serum creatinine, and dose-response was assessed with generalized additive models (GAMs) adjusted for baseline creatinine, estimated glomerular filtration rate, comorbidities, procedural indication, contrast volume, and intravenous hydration.</p><p><strong>Results: </strong>After excluding 18 patients for missing periprocedural oral intake or post-procedure creatinine, 174 patients were analyzed (median age 65.0 years, IQR 57.2 to 72.0; 71.8% male). Median weight-adjusted cumulative oral intake was 10.9, 18.6, 23.9, and 33.3 mL/kg for the pre-12 h, post-0-6 h, 0-12 h, and 0-24 h windows. Time-series clustering produced two stable groups (low-OH n = 85, high-OH n = 89; average silhouette = 0.393; bootstrap adjusted Rand index = 0.845). The largest between-group difference occurred in the 0-6 h window (median 4.12 vs. 2.00 mL/kg/h, p < 0.001). No patient met CA-AKI criteria. In adjusted GAMs, the 0-6 h OH rate was not a significant smooth term (edf = 3.79, p = 0.795), and cluster membership was not associated with creatinine change. However, the high-OH cluster had substantially greater 6-h urine output and a larger positive fluid balance (p < 0.001), while serum potassium was similar between clusters.</p><p><strong>Conclusion: </strong>Periprocedural OH was generally ample and formed two reproducible patterns. Concentrating oral intake in the first 6 h increased early urine output and positive fluid balance but did not show a significant dose-response association with early serum creatinine change. This null result should be interpreted cautiously because the cohort was generally low-risk, follow-up was short, and the study had limited power. Future studies should validate whether early concentrated OH protects renal function using earlier sensitive biomarkers and by targeting high-risk patients.</p>","PeriodicalId":9584,"journal":{"name":"Cardiorenal Medicine","volume":" ","pages":"25-36"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12872192/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cardiorenal MedicinePub Date : 2026-01-01Epub Date: 2026-05-12DOI: 10.1159/000552517
Theresa Nguyen, Lisa Hong, Tomona Iso
{"title":"Preventing Cardiovascular-Kidney-Metabolic Syndrome Progression: Pharmacologic Approaches and Pharmacists' Contributions.","authors":"Theresa Nguyen, Lisa Hong, Tomona Iso","doi":"10.1159/000552517","DOIUrl":"10.1159/000552517","url":null,"abstract":"<p><strong>Background: </strong>Cardiovascular-kidney-metabolic (CKM) syndrome is a condition reflecting the interactions among metabolic dysfunction, chronic kidney disease (CKD), and cardiovascular disease. It is driven by excess adipose tissue, insulin resistance, inflammation, and vascular and kidney dysfunction, which accelerates the development of hypertension, dyslipidemia, type 2 diabetes, and CKD. Early identification and intervention are critical to prevent progression to advanced cardiovascular and kidney disease; however, optimal interdisciplinary approaches to CKM management are not well established. This narrative review summarizes pharmacotherapeutic strategies to prevent CKM progression for individuals with CKM stages 1 and 2 and the expanding role of pharmacists.</p><p><strong>Summary: </strong>Obesity is a primary driver of CKM syndrome, and early assessment with weight-loss interventions is critical to reduce progression of CKM stages. Management emphasizes lifestyle modification, with pharmacotherapy increasingly used as an adjunct. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and dual glucose-dependent insulinotropic polypeptide/GLP-1 RAs promote substantial weight loss and provide cardiovascular benefits. Hypertension is an important modifiable risk factor as it contributes to kidney damage and adverse cardiovascular events. Management includes lifestyle modification and antihypertensive therapy with angiotensin-converting enzyme inhibitors (ACEis), angiotensin receptor blockers (ARBs), calcium channel blockers, or thiazide diuretics. In patients with albuminuria and CKD, ACEis or ARBs should be prioritized due to their kidney-protective effects. Dyslipidemia contributes to endothelial dysfunction, atherosclerosis, and cardiovascular risk. Statins are first-line therapy, with ezetimibe or PCSK9 inhibitors considered when low-density lipoprotein cholesterol remains above goal despite maximally tolerated statin therapy. Type 2 diabetes and CKD substantially increase the risk of progression to advanced CKM stages. Sodium-glucose cotransporter 2 inhibitors and GLP-1 RAs provide additional cardiovascular and kidney-protective benefits, while ACEis or ARBs remain foundational therapy for slowing CKD progression and reducing CKM risk. Pharmacists play a critical role in early CKM management through medication optimization, patient education, access facilitation, and longitudinal follow-up. Pharmacist-led interventions have been shown to improve blood pressure, lipid levels, glycemic control, weight outcomes, and kidney parameters, supporting prevention of progression to advanced disease stages.</p><p><strong>Key messages: </strong>Pharmacotherapy optimization for cardiometabolic and kidney risk factors during CKM stages 1 and 2 is essential to prevent progression to late stage CKM. Although pharmacists are well positioned to participate in comprehensive CKM management, most previous interventions have focused on isolated d","PeriodicalId":9584,"journal":{"name":"Cardiorenal Medicine","volume":" ","pages":"347-356"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13368018/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147926430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}