ients with AF across the spectrum of non-dialysis-dependent CKD using large, routinely collected data. Methods: We combined findings from 5 retrospective cohorts (2013-2018) across Australia and Canada. Adults with AF, new dispensation of apixaban or warfarin, and a recorded eGFR grouped as ≥60, 45-59, 30-44 and <30mL/min/1.73m2 were included. Patients on dialysis or kidney transplant recipients were excluded. We assessed outcomes within one year of initiating either therapy: (1) composite of all-cause death, ischemic stroke or transient ischemic attack and (2) first hospitalization for major bleeding (intracranial, gastrointestinal or other). Cox models estimated hazard ratios (HRs; 95% confidence intervals [CIs]) for outcomes across eGFR categories, after 1:1 matching using propensity scores. We summarized center-level data using random effects meta-analysis. Results: Among 38,598 matched apixaban and warfarin users, there were 4130 (10.7%) ischemic and 697 (1.8%) bleeding events wit

physical dysfunction. Factors such as uremia, systemic inflammation, oxidative stress, and inappropriate activation of the renin-angiotensin-aldosterone system may play are role on mitochondrial dysfunction. On the other hand, the accumulation of ectopic adipose tissue in skeletal muscle, also known as intermuscular adipose tissue (IMAT), is a newly recognized factor in muscle function and physical performance. IMAT is a marker of muscle quality, adversely affecting local muscle function, and is associated with insulin resistance and systemic inflammation, conditions commonly observed in CKD. Nevertheless, the exact composition of IMAT and its relationship with mitochondria and muscle energetics in CKD is not fully understood. Evaluating the relationship between IMAT accumulation and mitochondrial dysfunction in CKD may unveil potential interventions to improve physical function and the quality of life of patients with CKD. Patients with chronic kidney disease (CKD) often experience lo