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Abstract: TH-PO431

Use of Urinary Metabolomics to Identify Potential Pathways Associated with Hyperuricemia in Hispanic Children: The Viva La Familia Study

Session Information

Category: Nutrition, Inflammation, and Metabolism

  • 1401 Nutrition, Inflammation, Metabolism


  • Voruganti, V. Saroja, University of North Carolina at Chapel Hill, Kannapolis, North Carolina, United States
  • Vazquez-Vidal, Itzel, Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, North Carolina, United States
  • Mohney, Robert P., Metabolon, Inc. , Durham, North Carolina, United States
  • Mehta, Nitesh R., Baylor College of Medicine, Houston, Texas, United States
  • Comuzzie, Anthony Gean, Texas Biomedical Research Institute, San Antonio, Texas, United States
  • Cole, Shelley A., Texas Biomedical Research Institute, San Antonio, Texas, United States
  • Butte, Nancy F., Baylor Coll Medicine, Houston, Texas, United States

Hyperuricemia (elevated serum uric acid) is associated with increased risk for gout, cardiovascular and kidney disease. Studies have shown hyperuricemia in children to be predictive of hypertension in adulthood. Our aim in this study was to identify urinary metabolites and pathways associated with hyperuricemia in a cross-sectional study of 260 Hispanic children from the Viva La Familia Study.


Urinary metabolomics profiling was conducted in 130 hyperuricemic and 130 normouricemic children using ultrahigh performance liquid chromatography mass spectroscopy. Hyperuricemia was characterized using upper most quartile of serum uric acid.


A total of 703 urinary metabolites were identified, of which 377 metabolites were significantly different between the two groups. Key differences were found in amino acid, steroids and xenobiotics metabolic pathways, with 262 metabolites being higher in hyperuricemic than normouricemic group. Metabolites that were significantly higher in hyperuricemia group belonged to histidine (formimimoglutamate and methylhistidine), methionine (S-adenosylhomocysteine (SAH)), nicotinate and nicotinamide (nicotinamide N-oxide and 1-metylnicotinamide), steroid (epiandrosterone glucuronide and cortisol glucuronide) and purine (1,3 dimethylurate and xanthosine) metabolic pathways. The metabolites that were significantly lower in hyperuricemia group were derivatives of glycine, serine, threonine, N-acetylglycine, N-acetylserine, glutamate and gamma-aminobutyrate, and xenobiotics (ferulate, caffeine acid sulfate, vanillate, saccharin, etc). Interestingly, xanthine oxidase, a key enzyme that catalyzes the conversion of xanthine to uric acid and nicotinamide N-oxide to nicotinamide, is also a major enzyme in xenobiotics metabolism. Elevated levels of formimimoglutamate indicate folate deficiency whereas folate is thought to inhibit xanthine oxidase.


Our global urinary metabolomics profiling not only revealed different pathways in hyperuricemic and normouricemic children, but also demonstrated a link between xanthine oxidase, xenobiotics and folate in hyperuricemia


  • NIDDK Support