Abstract
Oxalate is both a plant-derived molecule and a terminal toxic metabolite with no known physiological function in humans. It is predominantly eliminated by the kidneys through glomerular filtration and tubular secretion. Regardless of the cause, the increased load of dietary oxalate presented to the kidneys has been linked to different kidney-related conditions and injuries, including calcium oxalate nephrolithiasis, acute and chronic kidney disease. In this paper, we review the current literature on the association between dietary oxalate intake and kidney outcomes.
Highlights
Oxalate is both a plant-derived molecule and a terminal toxic metabolite with no known physiological function in humans
There are six different SLC26 transporter proteins found along the gastrointestinal tract (GI) tract, with SLC26A3 and SLC26A6 being the most defined in their roles in oxalate handling [22]
We suggest that excess oxalate has deleterious effects on kidney function
Summary
Oxalate is both a plant-derived molecule and a terminal toxic metabolite with no known physiological function in humans. It is predominantly eliminated by the kidneys through glomerular filtration and tubular secretion. Intestinal secretion of oxalate contributes to its elimination, but to a much lesser extent [1,2,3,4,5]. The normal intestinal absorption of oxalate is around 10–15% [8], but varies depending on diet. For instance, have been linked to an increased absorption of oxalate [9]. In individuals with small bowel malabsorption syndrome, oxalate uptake is increased because of a reduction in free intestinal ionized calcium [10]. Gut microbiome dysbiosis might affect intestinal oxalate availability and its urinary excretion [11]
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