Oxalate: From the Environment to Kidney Stones

@inproceedings{Brzica2013OxalateFT,
  title={Oxalate: From the Environment to Kidney Stones},
  author={Hrvoje Brzica and Davorka Breljak and Birgitta Christina Burckhardt and Gerhard Burckhardt and Ivan Saboli{\'c}},
  booktitle={Arhiv za higijenu rada i toksikologiju},
  year={2013}
}
Abstract Oxalate urolithiasis (nephrolithiasis) is the most frequent type of kidney stone disease. Epidemiological research has shown that urolithiasis is approximately twice as common in men as in women, but the underlying mechanism of this sex-related prevalence is unclear. Oxalate in the organism partially originate from food (exogenous oxalate) and largely as a metabolic end-product from numerous precursors generated mainly in the liver (endogenous oxalate). Oxalate concentrations in plasma… 

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References

SHOWING 1-10 OF 207 REFERENCES
Oxalobacter formigenes may reduce the risk of calcium oxalate kidney stones.
TLDR
Colonization with O. formigenes is associated with a 70% reduction in the risk for being a recurrent calcium oxalate stone former, and the inverse association was consistently present within strata of age, gender, race/ethnicity, region, and antibiotic use.
Hyperoxaluria: a gut-kidney axis?
TLDR
A good understanding of how oxalate is absorbed and transported throughout the body, together with a better insight in the regulatory mechanisms, is crucial in the setting of future treatment strategies of this disorder.
[14C]Oxalate absorption by normal persons, calcium oxalate stone formers, and patients with surgically disturbed intestinal function.
TLDR
There was no significant difference in the amount of isotope excreted by normal subjects and idiopathic stone formers and the patients with resection or bypass showed a quite different pattern of isotopes excretion.
Extrarenal clearance of oxalate increases with progression of renal failure in the rat.
TLDR
The extrarenal clearance of oxalate in control rats and in 5/6 nephrectomized rats with renal insufficiency was investigated, finding that the total 14C recovered in urine, feces, and CO2 combined was similar in both groups.
[Citrate and kidney stones].
  • P. Osther
  • Medicine, Biology
    Ugeskrift for laeger
  • 1993
TLDR
Citrate-calcium ratio in urine proved to be a reliable index in discriminating stone formers from healthy subjects and factors other than urinary citrate excretion must be of importance in the pathophysiology of calcium stone formation.
Contribution of dietary oxalate to urinary oxalate excretion.
TLDR
It is suggested that dietary oxalate makes a much greater contribution to urinaryOxalate excretion than previously recognized, that dietary calcium influences the bioavailability of ingested oxalATE, and that the absorption of dietary oxAlate may be an important factor in calcium oxalates stone formation.
Intestinal excretion of oxalate in chronic renal failure.
TLDR
It is demonstrated that intestinal transport systems for oxalate are altered in experimental chronic renal failure, and the distal colon is identified as the primary site for this adaptive response.
Ileal oxalate absorption and urinary oxalate excretion are enhanced in Slc26a6 null mice.
TLDR
It is concluded that PAT1 is DIDS sensitive and mediates a significant fraction of oxalate efflux across the apical membrane in exchange for Cl(-); as such, PAT1 represents a major apical membranes pathway mediating J(sm)(Ox).
Hypocitraturia in calcium nephrolithiasis.
TLDR
The data suggest that in adult men, hypocitraturia may be a common predisposing factor for calcific nephrolithiasis.
...
...