Dietary Oxalate and Calcium Oxalate Nephrolithiasis

Saeed R. Khan, Patricia A. Glenton, Karen J. Byer

Research output: Contribution to journalArticle

Abstract

Purpose: Patients with calcium oxalate kidney stones are advised to decrease the consumption of foods that contain oxalate. We hypothesized that a cutback in dietary oxalate would lead to a decrease in the urinary excretion of oxalate and decreased stone recurrence. We tested the hypothesis in an animal model of calcium oxalate nephrolithiasis. Materials and Methods: Hydroxy-L-proline (5%), a precursor of oxalate found in collagenous foods, was given with rat chow to male Sprague-Dawley rats. After 42 days rats in group 1 continued on hydroxy-L-proline, while those in group 2 were given chow without added hydroxy-L-proline for the next 21 days. Food and water consumption as well as weight were monitored regularly. Once weekly urine was collected and analyzed for creatinine, calcium, oxalate, lactate dehydrogenase, 8-isoprostane and H2O2. Urinary pH and crystalluria were monitored. Rats were sacrificed at 28, 42 and 63 days, respectively. Renal tissue was examined for crystal deposition by light microscopy. Results: Rats receiving hydroxy-L-proline showed hyperoxaluria, calcium oxalate crystalluria and nephrolithiasis, and by day 42 all contained renal calcium oxalate crystal deposits. Urinary excretion of lactate dehydrogenase, 8-isoprostane and H2O2 increased significantly. After hydroxy-L-proline was discontinued in group 2 there was a significant decrease in urinary oxalate, 8-isoprostane and H2O2. Half of the group 2 rats appeared to be crystal-free. Conclusions: Dietary sources of oxalate can induce hyperoxaluria and crystal deposition in the kidneys with associated degradation in renal biology. Eliminating oxalate from the diet decreases not only urinary oxalate, but also calcium oxalate crystal deposits in the kidneys and improves their function.

Original languageEnglish (US)
Pages (from-to)2191-2196
Number of pages6
JournalJournal of Urology
Volume178
Issue number5
DOIs
StatePublished - Nov 2007
Externally publishedYes

Fingerprint

Dietary Calcium
Oxalates
8-epi-prostaglandin F2alpha
Calcium Oxalate
Proline
Kidney
Hyperoxaluria
L-Lactate Dehydrogenase
Food
Kidney Calculi
Calcium Oxalate Nephrolithiasis
Drinking
Sprague Dawley Rats
Microscopy
Creatinine
Animal Models
Urine
Diet
Light
Weights and Measures

Keywords

  • calcium oxalate
  • diet
  • inflammation
  • kidney
  • nephrolithiasis

ASJC Scopus subject areas

  • Urology

Cite this

Khan, S. R., Glenton, P. A., & Byer, K. J. (2007). Dietary Oxalate and Calcium Oxalate Nephrolithiasis. Journal of Urology, 178(5), 2191-2196. https://doi.org/10.1016/j.juro.2007.06.046

Dietary Oxalate and Calcium Oxalate Nephrolithiasis. / Khan, Saeed R.; Glenton, Patricia A.; Byer, Karen J.

In: Journal of Urology, Vol. 178, No. 5, 11.2007, p. 2191-2196.

Research output: Contribution to journalArticle

Khan, SR, Glenton, PA & Byer, KJ 2007, 'Dietary Oxalate and Calcium Oxalate Nephrolithiasis', Journal of Urology, vol. 178, no. 5, pp. 2191-2196. https://doi.org/10.1016/j.juro.2007.06.046
Khan, Saeed R. ; Glenton, Patricia A. ; Byer, Karen J. / Dietary Oxalate and Calcium Oxalate Nephrolithiasis. In: Journal of Urology. 2007 ; Vol. 178, No. 5. pp. 2191-2196.
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abstract = "Purpose: Patients with calcium oxalate kidney stones are advised to decrease the consumption of foods that contain oxalate. We hypothesized that a cutback in dietary oxalate would lead to a decrease in the urinary excretion of oxalate and decreased stone recurrence. We tested the hypothesis in an animal model of calcium oxalate nephrolithiasis. Materials and Methods: Hydroxy-L-proline (5{\%}), a precursor of oxalate found in collagenous foods, was given with rat chow to male Sprague-Dawley rats. After 42 days rats in group 1 continued on hydroxy-L-proline, while those in group 2 were given chow without added hydroxy-L-proline for the next 21 days. Food and water consumption as well as weight were monitored regularly. Once weekly urine was collected and analyzed for creatinine, calcium, oxalate, lactate dehydrogenase, 8-isoprostane and H2O2. Urinary pH and crystalluria were monitored. Rats were sacrificed at 28, 42 and 63 days, respectively. Renal tissue was examined for crystal deposition by light microscopy. Results: Rats receiving hydroxy-L-proline showed hyperoxaluria, calcium oxalate crystalluria and nephrolithiasis, and by day 42 all contained renal calcium oxalate crystal deposits. Urinary excretion of lactate dehydrogenase, 8-isoprostane and H2O2 increased significantly. After hydroxy-L-proline was discontinued in group 2 there was a significant decrease in urinary oxalate, 8-isoprostane and H2O2. Half of the group 2 rats appeared to be crystal-free. Conclusions: Dietary sources of oxalate can induce hyperoxaluria and crystal deposition in the kidneys with associated degradation in renal biology. Eliminating oxalate from the diet decreases not only urinary oxalate, but also calcium oxalate crystal deposits in the kidneys and improves their function.",
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