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<p>For decades, the clinical management of urolithiasis has emphasized dietary oxalate restriction. However, this review synthesizes over 40 years of research demonstrating that endogenous production, driven by specific metabolic precursors, plays the dominant role in oxalogenesis. Utilizing acute and chronic rat models, we quantified the conversion of glyoxylate, glycolate, ethylene glycol, hydroxypyruvate, and hydroxyproline into urinary oxalate. These studies establish a clear hierarchy of lithogenicity, with glyoxylate and glycolate emerging as the most potent precursors. Importantly, we identify Vitamin B6 (pyridoxine) deficiency as a critical metabolic “gatekeeper” that markedly amplifies oxalate synthesis. Deficiency states were found to increase precursor-to-oxalate conversion rates by up to 25-fold by suppressing hepatic alanine-glyoxylate aminotransferase (AGT) activity. Collectively, these findings support a paradigm shift in stone prevention: moving beyond dietary oxalate restriction toward managing precursor load and optimizing Vitamin B6 status.</p>

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Metabolic origins of hyperoxaluria: the critical role of precursors and vitamin B6 status in rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月26日

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  • Yoshihide Ogawa

摘要

For decades, the clinical management of urolithiasis has emphasized dietary oxalate restriction. However, this review synthesizes over 40 years of research demonstrating that endogenous production, driven by specific metabolic precursors, plays the dominant role in oxalogenesis. Utilizing acute and chronic rat models, we quantified the conversion of glyoxylate, glycolate, ethylene glycol, hydroxypyruvate, and hydroxyproline into urinary oxalate. These studies establish a clear hierarchy of lithogenicity, with glyoxylate and glycolate emerging as the most potent precursors. Importantly, we identify Vitamin B6 (pyridoxine) deficiency as a critical metabolic “gatekeeper” that markedly amplifies oxalate synthesis. Deficiency states were found to increase precursor-to-oxalate conversion rates by up to 25-fold by suppressing hepatic alanine-glyoxylate aminotransferase (AGT) activity. Collectively, these findings support a paradigm shift in stone prevention: moving beyond dietary oxalate restriction toward managing precursor load and optimizing Vitamin B6 status.