Background And Objectives: Estimating equations for calculating glomerular filtration rate (eGFR) occasionally identify patients with elevated eGFR, yet the prognostic significance remains to be determined. This study sought to define the association of an elevated eGFR on the risk for death and cardiovascular outcomes among subjects with atherosclerotic cardiovascular disease.
Design, Setting, Participants, & Measurements: Data from 8941 subjects who had a history of atherosclerotic vascular disease and were enrolled in the Blockade of the Glycoprotein IIb/IIIa Receptor to Avoid Vascular Occlusion trial were analyzed. Time to the composite end point of death, congestive heart failure, myocardial infarction, or stroke was modeled using Cox proportion hazards regression. Glomerular filtration rate was estimated using the Modification of Diet in Renal Disease and Cockcroft-Gault formulas.
Results: Compared with subjects with eGFR of 100 to 125 ml/min per 1.73 m2, subjects with eGFR > or = 125 (n = 462) were younger, female, and nonwhite. In addition, subjects with an elevated eGFR were more likely to have diabetes and congestive heart failure. In adjusted analyses, every 10-ml/min per 1.73 m2 decrease in eGFR < 100 was associated with a 13% increased hazard for the composite end point. In addition, every 10-ml/min per 1.73 m2 increase in eGFR > or = 100 was associated with a 9% increased hazard for the composite end point.
Conclusions: In individuals with a history of vascular disease, the relationship between eGFR and cardiovascular outcomes may be parabolic, with increased risk among patients with both reduced and elevated eGFR.
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http://dx.doi.org/10.2215/CJN.00930207 | DOI Listing |
J Exp Clin Cancer Res
January 2025
School of Medicine, Chinese PLA General Hospital, Nankai University, Beijing, China.
Background: Glioblastoma multiforme (GBM) exhibits a cellular hierarchy with a subpopulation of stem-like cells known as glioblastoma stem cells (GSCs) that drive tumor growth and contribute to treatment resistance. NAD(H) emerges as a crucial factor influencing GSC maintenance through its involvement in diverse biological processes, including mitochondrial fitness and DNA damage repair. However, how GSCs leverage metabolic adaptation to obtain survival advantage remains elusive.
View Article and Find Full Text PDFInt J Biol Sci
January 2025
Department of Medical Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan, China, 610041.
Int J Med Sci
January 2025
Department of Otolaryngology, Head and Neck Surgery, Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan.
Am J Kidney Dis
December 2024
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland; Center for Drug Safety and Effectiveness, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland; Division of General Internal Medicine, Johns Hopkins Medicine, Baltimore, Maryland. Electronic address:
Rationale & Objective: Chronic kidney disease (CKD) populations face an elevated risk of cardiovascular disease (CVD), yet many remain undertreated with statins for primary prevention of CVD despite meeting eligibility criteria. We examined trends in statin use for primary prevention among individuals with CKD before and after the release of the 2013 Kidney Disease: Improving Global Outcomes (KDIGO) guideline recommending statin use for lipid management in selected adults with CKD.
Study Design: Cross-sectional time-trend analysis.
In Vivo
December 2024
Laboratory of Molecular Diagnostics and Therapeutics, Joint Faculty of Veterinary Medicine, Yamaguchi University, Yamaguchi, Japan;
Background/aim: Soft tissue sarcoma (STS) is a mesenchymal tumor affecting multiple organs in dogs. Previous studies identified activation of the phosphatidylinositol-3 kinase (PI3K)/protein kinase B (PKB, AKT) pathway in canine STS cell lines and clinical samples, but the underlying mechanism remains unclear. This study investigated PTEN loss, PIK3CA mutation, and EGFR over-expression as potential drivers of PI3K/AKT pathway activation in STS.
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