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 208 REFERENCES
Calcium oxalate urolithiasis in mice lacking anion transporter Slc26a6
TLDR
It is concluded that the anion exchanger SLC26A6 has a major constitutive role in limiting net intestinal absorption of oxalate, thereby preventing hyperoxaluria and calcium oxalates urolithiasis.
The impact of dietary oxalate on kidney stone formation
TLDR
Differences in dietary oxalate intake and in renalOxalate excretion are two other parameters that are likely to receive close scrutiny in the near future, because the research tools required for these investigations are now available.
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.
Oxalate intake and the risk for nephrolithiasis.
TLDR
Oxalate intake and spinach were not associated with risk in younger women, and data do not implicate dietary oxalate as a major risk factor for nephrolithiasis.
[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.
New Insights into the Pathophysiology and Treatment of Nephrolithiasis: New Research Venues
  • F. Coe, J. Parks
  • Medicine
    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
  • 1997
TLDR
Defenses against nephrocalcinosis and stones include regulation of urine pH into an optimal zone, control of urine calcium and citrate concentrations, the addition to tubule fluid of at least six protein and glycosaminoglycan modulators of crystallization, and cellular responses to crystals, which include attachment and internalization.
[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.
...
...