Abstract: TH-PO1251
Sarcopenic Obesity and Gut-Derived Glycylvaline in Relation to Myocardial Fibrosis in Patients with ESRD on Maintenance Dialysis
Session Information
- Late-Breaking Research Posters
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Dialysis
- 801 Dialysis: Hemodialysis and Frequent Dialysis
Authors
- Liu, Shang, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital, Shanghai, China
- Cai, Hong, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital, Shanghai, China
- Liu, Youqi, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital, Shanghai, China
- Mou, Shan, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital, Shanghai, China
Background
Patients with end-stage renal disease (ESRD) exhibit markedly elevated cardiovascular risk, among which myocardial fibrosis constitutes the key pathological substrate for heart failure with preserved ejection fraction (HFpEF). This study is the first to systematically investigate the association between "sarcopenic obesity" (co-existence of muscle loss and fat accumulation) and myocardial fibrosis, as well as the underlying gut-heart-axis mechanism in ESRD patients.
Methods
Using a cross-sectional design, we enrolled 122 maintenance dialysis patients. Body composition was assessed by a Body Composition Monitor (BCM); native T1 mapping (gT1) from cardiac magnetic resonance was applied to quantify myocardial fibrosis; and faecal samples were analysed via targeted metabolomics using liquid chromatography mass spectrometry (LC-MS).
Results
The results demonstrated that the gT1 value was significantly higher in the sarcopenic-obesity group (n=30) than in the non-sarcopenic-obesity group (1361.30 vs 1332.35 ms, P=0.01). Multivariate regression confirmed that sarcopenic-obesity independently increased the risk of myocardial fibrosis (OR=3.58, P=0.013). Eighteen differential metabolites were screened by metabolomics. Among them, the dipeptide glycylvaline was negatively associated with the risk of myocardial fibrosis (OR=0.93, P=0.044), and its concentration was significantly reduced in the sarcopenic-obesity group (6623.60 vs 9089.59, P=0.029). Notably, although the elevated T2 value in the sarcopenic-obesity group indicated myocardial oedema (53.93 vs 51.46 ms, P=0.016), no inter group differences were observed in left ventricular functional and structural parameters, highlighting the advantage of gT1 in detecting early micro lesions.
Conclusion
This study reveals a pathological chain whereby sarcopenic obesity synergistically promotes myocardial fibrosis through the malnutritioninflammation atherosclerosis syndrome (MICS) and intestinal metabolic disturbance. It provides novel potential targets for the early intervention of cardiovascular complications in ESRD patients, including body composition management and glycylvaline supplementation. Longitudinal studies are required in the future to verify causal relationships and further explore the specific mechanism by which glycylvaline inhibits oxidative stress via the glutathione synthesis pathway.