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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Current treatment options in patients with primary and secondary hyperoxaluria are limited and do not always lead to sufficient reduction in urinary oxalate excretion. Intestinal oxalate degrading bacteria are capable of degrading oxalate to CO(2) and formate, the latter being further metabolized and excreted via the feces. It is speculated, that both endogenously produced, as well as dietary oxalate can be significantly removed via the intestinal tract. Oxalobacter formigenes, an obligate anaerobic microbe normally found in the intestinal tract has one oxalate degrading enzyme, oxalyl-CoA decarboxylase, which is also found in Bifidobacterium lactis. Other bacteria with possible oxalate degrading potency are lactic acid bacteria, as well as Enterococcus faecalis and Eubacterium lentum. However, specific therapeutic studies on humans are scarce and, except for Oxalobacter, data are not congruent. We found the oral application of Oxalobacter successful in patients with primary hyperoxaluria. However, long-term post-treatment follow-up of 1-2 years showed that constant intestinal colonization is not achieved in most patients. In one patient with constant colonization, urinary oxalate excretion normalized over time. Short-term studies with other bacteria such as lactic acid bacteria did not show a specific reduction in urinary oxalate excretion. O. formigenes might be a promising new therapeutic tool in patients with primary and secondary hyperoxaluria.
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PMID:Oxalate degrading bacteria: new treatment option for patients with primary and secondary hyperoxaluria? 1628 77

Oxalic acid is found in dietary sources (such as coffee, tea, and chocolate) or is produced by the intestinal microflora from metabolic precursors, like ascorbic acid. In the human intestine, oxalate may combine with calcium, sodium, magnesium, or potassium to form less soluble salts, which can cause pathological disorders such as hyperoxaluria, urolithiasis, and renal failure in humans. In this study, an operon containing genes homologous to a formyl coenzyme A transferase gene (frc) and an oxalyl coenzyme A decarboxylase gene (oxc) was identified in the genome of the probiotic bacterium Lactobacillus acidophilus. Physiological analysis of a mutant harboring a deleted version of the frc gene confirmed that frc expression specifically improves survival in the presence of oxalic acid at pH 3.5 compared with the survival of the wild-type strain. Moreover, the frc mutant was unable to degrade oxalate. These genes, which have not previously been described in lactobacilli, appear to be responsible for oxalate degradation in this organism. Transcriptional analysis using cDNA microarrays and reverse transcription-quantitative PCR revealed that mildly acidic conditions were a prerequisite for frc and oxc transcription. As a consequence, oxalate-dependent induction of these genes occurred only in cells first adapted to subinhibitory concentrations of oxalate and then exposed to pH 5.5. Where genome information was available, other lactic acid bacteria were screened for frc and oxc genes. With the exception of Lactobacillus gasseri and Bifidobacterium lactis, none of the other strains harbored genes for oxalate utilization.
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PMID:Transcriptional and functional analysis of oxalyl-coenzyme A (CoA) decarboxylase and formyl-CoA transferase genes from Lactobacillus acidophilus. 1651 36

Urinary tract stones are an important clinical problem in human and veterinary medicine. Hyperoxaluria is the single strongest promoter of kidney stone formation. The aims of the present study were to (a) evaluate oxalate degradation by a range of Bifidobacteria species and Lactobacillus species isolated from the canine and feline gastrointestinal tract in vitro and (b) to determine the impact of oxalate degradation by selected strains in vivo. The bacteria were grown in oxalate-containing media and their ability to degrade oxalate in vitro was determined using reverse-phased HPLC. Bifidobacteria species and Lactobacillus species that degraded oxalate in vitro and survived gastric transit were selected for further examination. The selected probiotics were fed to rats for 4 weeks. Urine was collected at week's 0, 2 and 4 and oxalate levels determined by HPLC. In vitro degradation was detected for 11/18 of the Lactobacillus species. In contrast, the capacity to degrade oxalate was not detected for any of the 13 Bifidobacterium species tested. Lactobacillus animalis 223C, Lactobacillus murinus 1222, L. animalis 5323 and L. murinus 3133 were selected for further investigation in a rat model. Urinary oxalate levels were significantly reduced (p<0.05) in animals fed L. animalis 5323 and L. animalis 223C but were unaltered when fed L. murinus 1222, L. murinus 3133 or placebo. Probiotic organisms vary widely in their capacity to degrade oxalate. In vitro degradation does not uniformly translate to an impact in vivo. The results have therapeutic implications and may influence the choice of probiotic, particularly in the setting of enteric hyperoxaluria.
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PMID:Metabolic activity of probiotics-oxalate degradation. 1902 28

It had been suggested that lactic acid bacteria (LAB) may degrade oxalate in the intestinal lumen, reducing urinary oxalate excretion. We aimed to evaluate the effect of a LAB mixture containing Lactobacillus casei (LC) and Bifidobacterium breve (BB) (LC + BB) upon urinary oxalate reduction in stone-forming (SF) patients without hyperoxaluria under conditions of an oxalate-rich diet. After an oxalate restriction period (7 days washout), 14 SF patients consumed an oxalate-rich diet during 4 weeks (200 mg/day) and a lyophilized LC + BB preparation was given t.i.d. after meals during the last 2 weeks. Twenty-four-hour urine samples were collected for determination of oxalate, calcium, magnesium, citrate, sodium, potassium and creatinine at baseline, after 2 weeks (DIET) and 4 weeks (DIET + LC + BB). The mean urinary oxalate excretion was significantly higher after DIET versus baseline (27 +/- 8 vs. 35 +/- 11 mg/24 h), but the mean decrease was not significant between DIET + LC + BB and DIET periods (35 +/- 11 vs. 33 +/- 10 mg/24 h). Seven out of 14 patients presented a reduction in oxaluria after LC + BB versus DIET, being the reduction higher than 25% in 4, and up to 50% in 2 of them. The latter two patients were those who had presented the greatest increase in oxaluria in response to dietary oxalate. In conclusion, this mixture of L. casei and B. breve was shown to possess a variable lowering effect upon urinary oxalate excretion that may be dependent on dietary oxalate intake.
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PMID:Effects of Lactobacillus casei and Bifidobacterium breve on urinary oxalate excretion in nephrolithiasis patients. 1921 93

Humans lack the enzymes needed to metabolize endogenous and dietary oxalate, a toxic compound causing hyperoxaluria and calcium oxalate urolithiasis. Oxalate in humans can be eliminated through (1) excretion in urine, (2) forming insoluble calcium oxalate and elimination in feces, or (3) oxalate degradation by gastrointestinal (GIT) microorganisms. In this article, anaerobic oxalate catabolism in gut bacteria is reviewed, and the possible use of these bacteria as probiotics for treating kidney stone disease is evaluated. Oxalobacter formigenes and Lactobacillus and Bifidobacterium species are the best studied in this regard, with oxalate degradation in the lactic acid bacteria being both species- and strain-specific. The GIT oxalate-degrading bacteria express the catabolic enzymes formyl-CoA transferase (Frc) and oxalyl-CoA decarboxylase (Oxc). The genes encoding these proteins are clustered on the genomes and show strong phylogenetic relationships. Clinical trials investigating reduced hyperoxaluria through administering O. formigenes or its enzymes show a promising trend, but the data need confirmation through larger scale, well-controlled trials. Similar studies using Lactobacillus and Bifidobacterium species also show in vivo oxalate reduction, but these data are still controversial. In particular, further investigations need to determine whether there is a direct link between the lack of oxalate-degrading bacteria and hyperoxaluria and whether their absence is a risk factor. Key experiments linking microbial numbers, functional oxalate degradation, molecular analysis of the regulation of the genes involved, and the ability of the bacteria to survive in the gut are crucial elements in identifying suitable probiotics for treating kidney stone disease.
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PMID:Oxalate-degrading bacteria of the human gut as probiotics in the management of kidney stone disease. 2060 88

Hyperoxaluria significantly increases the risk of calcium oxalate kidney stone formation. Since several bacteria have been shown to metabolize oxalate in vitro, including probiotic bifidobacteria, we focused on the efficiency and possible mechanisms by which bifidobacteria can influence oxalate handling in vivo, especially in the intestines, and compared these results with the reported effects of Oxalobacter formigenes. Bifidobacterium animalis subsp. lactis DSM 10140 and B. adolescentis ATCC 15703 were administered to wild-type (WT) mice and to mice deficient in the hepatic enzyme alanine-glyoxylate aminotransferase (Agxt(-/-), a mouse model of Primary Hyperoxaluria) that were fed an oxalate-supplemented diet. The administration of B. animalis subsp. lactis led to a significant decrease in urinary oxalate excretion in WT and Agxt(-/-) mice when compared to treatment with B. adolescentis. Detection of B. animalis subsp. lactis in feces revealed that 3 weeks after oral gavage with the bacteria 64% of WT mice, but only 37% of Agxt(-/-) mice were colonized. Examining intestinal oxalate fluxes showed there were no significant changes to net oxalate secretion in colonized animals and were therefore not associated with the changes in urinary oxalate excretion. These results indicate that colonization with B. animalis subsp. lactis decreased urinary oxalate excretion by degrading dietary oxalate thus limiting its absorption across the intestine but it did not promote enteric oxalate excretion as reported for O. formigenes. Preventive or therapeutic administration of B. animalis subsp. lactis appears to have some potential to beneficially influence dietary hyperoxaluria in mice.
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PMID:Bifidobacterium animalis subsp. lactis decreases urinary oxalate excretion in a mouse model of primary hyperoxaluria. 2526 40