Polycystic kidney disease (PKD) is a common hereditary kidney disorder with an insidious onset and complex mechanisms, making early diagnosis challenging. Current diagnostic methods, including imaging and genetic testing, have limitations. Imaging detects cysts only once formed, and genetic testing is costly, labour-intensive, and unable to guarantee complete diagnostic accuracy or predict onset and progression. Metabolomics may offer an approach to uncover PKD mechanisms by detecting metabolic alterations that precede clinical manifestations, enabling identification of disease-specific biomarkers and providing earlier and more practical detection than imaging or genetic testing. This review synthesizes existing metabolomics studies of human PKD and renal cystic disease with significant metabolites extracted, and pathway enrichment analyses conducted at the levels of overall cystic kidney disease and the ADPKD/Pkd1/non-Pkd1 subsets to identify significant pathways and their associated metabolic features. Overall, the top-ranked pathways were arginine biosynthesis; alanine, aspartate and glutamate metabolism; glycine, serine and threonine metabolism, and the citrate cycle, with glycine, serine and threonine metabolism only associated with ADPKD/Pkd1 mouse models. These pathways indicate marked activation of amino acid metabolism accompanied by relative suppression of carbohydrate-related energy metabolism, suggesting a shift in metabolic substrate utilization rather than a complete loss of energy supply. This study provides a foundation for applying metabolomics to early diagnosis and mechanistic investigation of cystic kidney disease.
Liyan Chen, David I. Broadhurst, A. Shafaei et al.· AJP - Renal Physiology· 0 citations
Aim: The cardiovascular-kidney-metabolic (CKM) syndrome highlights the interplay among cardiovascular, renal, and metabolic disorders. However, its relationship with the trabecular bone score (TBS) and bone mineral density (BMD) remains unclear. We aimed to evaluate the association between the CKM syndrome stage and bone health-related indicators.
Methods: Data from the 2005-2008 National Health and Nutrition Examination Survey were analyzed for 4,364 adults aged 30-79 years (median age 51 years; 51.9% male, 48.1% female). Bone health was assessed using TBS, femoral neck (FN) BMD, and lumbar spine (LS) BMD. Multivariate and segmented regression models were used to examine associations between CKM stages and TBS, FN BMD, and LS BMD.
Results: Multivariate linear regression revealed a significant inverse correlation between CKM syndrome stage and TBS, which was predominantly observed across the early stages (0-2), while positive correlations were observed with FN BMD and LS BMD. No significant associations were found between CKM syndrome stage and osteoporosis or prior fractures.
Conclusion: This study revealed a previously unrecognized dissociation in CKM syndrome, in which advanced stages were associated with a lower overall TBS despite higher FN BMD and LS BMD. This discordant pattern parallels the well-established diabetic bone paradox, underscoring the insufficiency of BMD alone for fracture risk assessment in patients with CKM syndrome. A comprehensive evaluation incorporating the TBS is essential to accurately assess bone fragility. Concurrent TBS assessment during routine BMD testing is recommended for patients with early-stage CKM to enable early detection of microarchitectural deficits.
Jiashuang Lin, Weifeng Chen, Xiaoyu Hong et al.· Metabolism and Target Organ...· 0 citations
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