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Effects of finerenone on arterial stiffness and cardiorenal biomarkers in patients with type 2 diabetes and chronic kidney disease: a randomised placebo-controlled mechanistic trial (FIVE-STAR)

9Citations signalées, ce qui n’est pas une note de qualité
21Institutions déclarées
2Pays d’affiliation déclarés

Rattachement africain : jp, us. Niveau de preuve : code pays fourni par la source.

Le résumé fourni par la source

Abstract Background The mechanisms underlying cardiorenal benefits of finerenone remain unclear. This mechanistic trial aimed to evaluate the effects of finerenone on vascular stiffness, as assessed using the cardio-ankle vascular index (CAVI), and cardiorenal biomarkers in patients with type 2 diabetes (T2D) and chronic kidney disease (CKD). Methods Eligible patients with T2D and CKD (estimated glomerular filtration rate [eGFR], 25 to < 90 mL/min/1.73 m 2 ; urinary albumin-to-creatinine ratio [UACR], 30 to < 3500 mg/g Cr) were randomly allocated to receive either dose-adjusted finerenone or matching placebo. The primary endpoint was the change in CAVI at week 24. The key secondary endpoint was the proportional change in UACR from baseline over 24 weeks. As an exploratory analysis, changes in circulating proteins were measured by using the Olink® Target 96 Cardiovascular III and Inflammation panels. Results This investigator-initiated, multicentre, prospective, two-arm parallel, placebo-controlled, double-blind, randomised clinical trial was conducted at 13 sites in Japan. Among 102 patients randomised, 101 (66.3% men; median age, 73 years; eGFR, 56.2 mL/min/1.73 m 2 ; and UACR, 193.8 mg/g Cr) were analysed. Changes in CAVI at week 24 were − 0.023 (95% confidence interval [CI], − 0.299 to 0.254) for finerenone and 0.011 (95% CI, − 0.245 to 0.267) for placebo. The group difference was − 0.057 (95% CI, − 0.428 to 0.314; P = 0.760). Compared with placebo, finerenone led to a 29% reduction in UACR levels at weeks 12 (group ratio 0.706 [95% CI, 0.504 to 0.989; P = 0.043]) and 24 (0.709 [95% CI, 0.506 to 0.994; P = 0.046]). Finerenone also resulted in an early and sustained eGFR decline over 24 weeks, without increasing levels of urinary biomarkers of acute tubular injury. Finerenone, compared with placebo, was associated with nominal changes in the expression of 11 proteins among the 181 circulating proteins tested. Conclusions Finerenone did not affect changes in vascular stiffness but led to a significant and sustained reduction in albuminuria in patients with T2D and CKD. The clinical benefits of finerenone may result from lowering intraglomerular pressure rather than from its effect on vascular stiffness. Registration ClinicalTrial.gov (NCT05887817) and Japan Registry of Clinical Trials (jRCTs021230011). Graphical abstract This mechanistic clinical trial involving patients with T2D and CKD found that 24-week finerenone therapy did not significantly reduce CAVI from baseline compared with placebo (−0.057; 95% CI, −0.428 to 0.314), led to a 29% reduction (group ratio [finerenone vs. placebo] of 0.71) in UACR levels, and was associated with nominal changes in 11 circulating proteins (six upregulated and five downregulated) over 24 weeks. CAVI, cardio-ankle vascular index; CI, confidence interval; CKD, chronic kidney disease; eGFR, estimated glomerular filtration rate; T2D, type 2 diabetes; UACR, urinary albumin-to-creatinine ratio.

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Le contrôle bibliographique ouvert

DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.

Titre Crossref
Effects of finerenone on arterial stiffness and cardiorenal biomarkers in patients with type 2 diabetes and chronic kidney disease: a randomised placebo-controlled mechanistic trial (FIVE-STAR)
Date Crossref
05/12/2025
Éditeur
Springer Science and Business Media LLC
Type
journal-article

Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.

Où se fait cette recherche

  • Saga University Department of Cardiovascular Medicine pays non établi dans la notice
    Université ou école supérieure
  • Brigham and Women's Hospital Division of Cardiovascular Medicine pays non établi dans la notice
    Établissement de santé
  • Harvard University pays non établi dans la notice
    Université ou école supérieure
  • Kobe University Hospital Clinical and Translational Research Center pays non établi dans la notice
    Établissement de santé
  • Japan Clinical Cancer Research Organization pays non établi dans la notice
    Structure de recherche
  • University of Occupational and Environmental Health Japan First Department of Internal Medicine pays non établi dans la notice
    Université ou école supérieure
  • Juntendo University Shizuoka Hospital Department of Cardiology pays non établi dans la notice
    Établissement de santé
  • Hiroshima General Hospital pays non établi dans la notice
    Établissement de santé
  • Oita University pays non établi dans la notice
    Université ou école supérieure
  • Fukushima Medical University Department of Diabetes pays non établi dans la notice
    Université ou école supérieure
  • Toho University Division of Cardiovascular Medicine pays non établi dans la notice
    Université ou école supérieure
  • Toho University Ohashi Medical Center pays non établi dans la notice
    Établissement de santé

Department of Cardiovascular Medicine — Saga University, Division of Cardiovascular Medicine — Brigham and Women's Hospital et Harvard University, avec 9 autres affiliations.

Une affiliation ne permet pas de déduire la nationalité d’un auteur.

Les sujets associés

Hormonal Regulation and HypertensionCardiovascular Health and Disease PreventionEicosanoids and Hypertension Pharmacology

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