Abstract
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. 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 H(2)O(2). 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. 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 H(2)O(2) increased significantly. After hydroxy-L-proline was discontinued in group 2 there was a significant decrease in urinary oxalate, 8-isoprostane and H(2)O(2). Half of the group 2 rats appeared to be crystal-free. 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.
Highlights
Calcium oxalate (CaOx) is the major constituent of about 75% of all urinary stone and the secondary hyperoxaluria is a primary risk factor
Engineered lactic acid bacteria (LAB) efficiently degraded oxalate under in vitro The recombinant oxalate decarboxylase (OxdC)-secretory L. plantarum WCFS1OxdC harboring the recombinant vector pLdhl0373OxdC size of 4.7 kb and non-secretory L. plantarum NC8OxdC harboring the recombinant plasmid without signal peptide sequence pLdhlOxdC was used to analyze in vivo oxalate degradation in rat model
The specific activity of recombinant OxdC purified from recombinant strain of WCFS1OxdC was found to be 19.1 U/mg and secretion efficiency of the strain WCFS1OxdC shows that 25% of the OxdC produced was secreted into the medium
Summary
Calcium oxalate (CaOx) is the major constituent of about 75% of all urinary stone and the secondary hyperoxaluria is a primary risk factor. Current treatment options for the patients with hyperoxaluria and CaOx stone diseases are limited. The aim of the present study is to examine the in vivo oxalate degrading ability of genetically engineered Lactobacillus plantarum (L. plantarum) that constitutively expressing and secreting heterologous oxalate decarboxylase (OxdC) for prevention of CaOx stone formation in rats. Secondary hyperoxaluria either based on intestinal hyperabsorption of oxalate or high intake of oxalate is considered a crucial risk factor in the pathogenesis of CaOx stone formation [3]. Existing treatments for patients with CaOx urolithiasis are limited and do not always lead to sufficient reduction in UOx excretion. The invasive technologies (shockwave lithotripsy, ureteroscopy, percutaneous stone extractions) exist, these techniques have its own disadvantages like renal injury, recurrent stone formation with a prevalence of 50% over 10 years
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