Abstract
Kidney stone disease is increasing in prevalence, and the most common stone composition is calcium oxalate. Dietary oxalate intake and endogenous production of oxalate are important in the pathophysiology of calcium oxalate stone disease. The impact of dietary oxalate intake on urinary oxalate excretion and kidney stone disease risk has been assessed through large cohort studies as well as smaller studies with dietary control. Net gastrointestinal oxalate absorption influences urinary oxalate excretion. Oxalate-degrading bacteria in the gut microbiome, especially Oxalobacter formigenes, may mitigate stone risk through reducing net oxalate absorption. Ascorbic acid (vitamin C) is the main dietary precursor for endogenous production of oxalate with several other compounds playing a lesser role. Renal handling of oxalate and, potentially, renal synthesis of oxalate may contribute to stone formation. In this review, we discuss dietary oxalate and precursors of oxalate, their pertinent physiology in humans, and what is known about their role in kidney stone disease.
Highlights
Kidney stone disease affects approximately 10% of the population [1] and calcium oxalate (CaOx) is the most common stone composition [2]
This study found that individuals colonized with O. formigenes excreted significantly lower levels of fecal oxalate compared with those individuals not colonized with O. formigenes, highlighting the importance of a specialist oxalotroph on overall gut oxalate degradation
This study showed that the metabolism of hydroxyproline contributed to at least 15% of endogenous oxalate synthesis in healthy subjects and played a greater role in patients with
Summary
Kidney stone disease affects approximately 10% of the population [1] and calcium oxalate (CaOx) is the most common stone composition [2]. Urinary calcium and urinary oxalate were found to contribute to supersaturation of CaOx [6]. Urinary oxalate is derived from dietary oxalate intake and endogenous oxalate synthesis [7]. The diet-derived portion depends primarily on three factors: the amount of oxalate consumed, the amount of calcium and other divalent cations consumed, and oxalate handling by the intestine. This is further complicated by the degradation of some of the ingested oxalate by intestinal bacteria [8] and differences in oxalate absorption in different regions of the intestinal tract [9]. We review sources of dietary oxalate and oxalate precursors, their impact on the urinary oxalate pool, and their influence on kidney stone risk
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