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Cross-sectional study uncovers urinary metabolic shifts in adults with chronic kidney disease and left ventricular hypertrophy, highlighting mitochondrial and lipid metabolism disruptions.
Although left ventricular hypertrophy (LVH) is common in people with chronic kidney disease (CKD); its mechanisms are not well understood. Metabolomic profiling may reveal novel mechanistic pathways linked to cardiac remodelling in CKD patients. In this single-centre cross-sectional study, fifty-three adults with CKD stages G2–G4 were divided into two groups based on echocardiography: LVH ( n = 31) and non-LVH ( n = 22). Urine samples were analyzed using untargeted gas chromatography–mass spectrometry (GC–MS). Data were evaluated using fold change analysis, t-tests with false discovery rate correction, principal component analysis, and orthogonal partial least squares–discriminant analysis. Metabolites were ranked by importance, and pathway enrichment was done using the Small Molecule Pathway Database. CKD patients with LVH had lower urinary citrate levels, as well as higher levels of myristic acid, and glycerol monoesters while those without LVH had higher 2-bromosebacic acid. Pathway analysis suggested that changes in the tricarboxylic acid (TCA) cycle, pyruvate metabolism, gluconeogenesis, fatty acid oxidation, and amino acid metabolism were implicated in LVH. Urinary metabolomic profiling identified potential metabolic alterations associated with LVH in CKD, mainly affecting mitochondrial energy and lipid metabolism. Larger studies are needed to confirm these findings.
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Chandrakar et al. (2026) studied this question.
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