Abstract: TH-PO1072

Crystalluria and Monocyte Responses in Healthy Subjects Following a Single Dietary Oxalate Load

Session Information

Category: Mineral Disease

  • 1204 Mineral Disease: Nephrolithiasis

Authors

  • Mitchell, Tanecia, University of Alabama at Birmingham, Birmingham, Alabama, United States
  • Patel, Mikita, University of Alabama at Birmingham, Birmingham, Alabama, United States
  • Yarlagadda, Vidhush, University of Alabama at Birmingham, Birmingham, Alabama, United States
  • Ambrosetti, Adam D, University of Alabama at Birmingham, Birmingham, Alabama, United States
  • Knight, John, University of Alabama at Birmingham, Birmingham, Alabama, United States
  • Assimos, Dean G, University of Alabama at Birmingham, Birmingham, Alabama, United States
  • Holmes, Ross P., University of Alabama at Birmingham, Birmingham, Alabama, United States
Background

Dietary oxalate has been suggested to play an important role in the risk and progression of stone formation in patients with calcium oxalate (CaOx) kidney stone disease. Oxalate has also been associated with crystal formation and inflammation in renal cells. We have previously determined that monocyte mitochondrial function is altered in patients with CaOx kidney stone disease. The purpose of this study was to determine whether dietary oxalate causes crystal formation in the urine and alters monocyte mitochondrial responses in the circulation of healthy subjects.

Methods

Twenty healthy subjects (29.1 ± 1.7 years old) with an average BMI of 25.5 ± 0.8 kg/m2 were enrolled in the study. Participants consumed a low oxalate diet for 3 days prior to consuming a single high dietary oxalate load (spinach smoothie; 8 mmoles). Urine and peripheral blood was collected prior to the load and five hours later. Crystalluria was quantified by measuring oxalate levels using ion-chromatography mass spectrometry (IC/MS) and a Nanosight nanoparticle counter. Monocyte mitochondrial responses were assessed using the Seahorse XF96 Analyzer.

Results

A single high dietary oxalate load in healthy subjects significantly increased total urinary oxalate levels (pre-oxalate 2.36 ± 0.6 vs. post-oxalate 35.35 ± 4.8 mg; p<0.0001). In addition, urinary crystals were observed following the load and determined to be approximately 180 nm in diameter via the Nanosight nanoparticle counter. The effect of the high dietary oxalate load on monocyte mitochondrial responses was variable among participants. Eleven of the healthy subjects (55%) had decreased monocyte mitochondrial function; whereas, 3 (15%) were not affected by the load and 6 (30%) had increased mitochondrial function following the load compared to pre-oxalate samples.

Conclusion

These findings suggest that a single high dietary oxalate load causes crystal formation and changes in monocyte mitochondrial responses in healthy subjects. Understanding these mechanisms further may aid in designing dietary recommendations to mitigate crystal formation in patients with CaOx kidney stone disease.

Funding

  • NIDDK Support