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High oxalate diets stimulate crystalluria in healthy subjects and kidney stone patients

 

Vivek Verma Phd, Christine Wright Phd, Mary Doamekpor Bs, Sirisha Swamigari, Ms, Parveen Kumar Phd, Dean Assimos Md, And Tanecia Mitchell Phd

 

Affiliation(s):

University Of Alabama At Birmingham

 

 

Introduction: Kidney stones (KS) occur in one out of ten people in the United States. The predominant KS type is comprised of calcium oxalate (CaOx). Oxalate is a small molecule found in many plant-derived foods such as spinach, nuts, and select fruits. Excess oxalate in the body can be eliminated in soluble and crystalline forms. We developed a novel technique to quantify nanosized crystals in human urine. Using this method, we determined that a single oxalate load increases urinary nanocrystal formation in healthy subjects

Objectives: The objectives of this study were to investigate whether consumption of controlled low or high oxalate diets increase urinary oxalate levels and nanocrystalluria in humans. In addition, we tested whether oxalate diets could impact urinary microcrystal growth ex vivo. 

Methodology: Adult healthy subjects (n=20) and patients with CaOx KS (n=10) were randomized to consume a low (50 mg/day) or high oxalate diet (250 mg/day) for 4 days. Participants were then asked to consume self-selected diets for 10 days (wash-out period) before consuming the opposite oxalate diet. Twenty-four hour urine collections were made on Days 3 and 4 of both dietary oxalate phases. Urinary oxalate levels were measured using ion-chromatography-mass spectrometry. Nanocrystalluria was assessed using nanoparticle tracking analysis. Microscopy and a plate-based crystal growth assay were used to evaluate micron-sized crystal morphology and growth, respectively.  

Findings: Patients with CaOx KS and healthy subjects had significantly higher urinary oxalate levels on high oxalate diets compared to when they consumed low oxalate diets. Patients with CaOx KS had a significant increase in nanocrystalluria with high oxalate intake and also excreted larger size crystals compared to healthy subjects. In contrast, healthy subjects on oxalate rich diets had smaller sized crystals that were heterogeneous. These findings highlight distinct size‑specific crystal phenotypes across cohorts in response to dietary oxalate. In addition, urinary crystal morphology was confirmed using microscopy. Lastly, urinary micron-sized crystal growth was elevated in both cohorts ex vivo.

Significance: Consuming meals rich in oxalate can promote crystalluria and increase a patient’s risk for CaOx KS. Future research will focus on further characterizing crystalluria and crystal growth in a larger sample size across both cohorts. This research could help identify patient-specific phenotypes and guide dietary recommendations and clinical treatment.

 

 

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