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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study evaluated the ability of the lactic acid bacteria (LAB) component of canine and feline feces to degrade oxalate in vitro. Oxalate degradation by individual canine-origin LAB was also evaluated. The effects of various prebiotics on in vitro oxalate degradation by selected oxalate-degrading canine LAB was also evaluated. Canine fecal samples reduced oxalate levels by 78 +/- 12.2% (mean +/- S.D.; range: 44-97%, median: 81%). Feline results were similar, with oxalate reduction of 69.7 +/- 16.7% (mean +/- S.D.; range: 40-96%, median: 73%). Thirty-seven lactic acid bacteria were isolated from canine fecal samples. Mean oxalate degradation was 17.7 +/- 16.6% (mean +/- S.D.; range: 0-65%, median: 13%). No oxalate degradation was detected for four (11%) isolates, and 10/37 (27%) degraded less than 10% of oxalate. The effects of lactitol, arabinogalactan, guar gum, gum Arabic, inulin, maltodextrin or a commercial fructooligosaccharide (FOS) product on in vitro oxalate degradation by five canine LAB isolates were highly variable, even within the same bacterial species. Overall, in vitro degradation was significantly greater with guar gum compared to arabinogalactan (P < 0.05), gum Arabic (P < 0.05), and lactitol (P < 0.01). This study suggests that manipulation of the LAB component of the canine and feline gastrointestinal microflora may decrease intestinal oxalate, and correspondingly intestinal oxalate absorption and renal excretion, thus potentially reducing oxalate urolithiasis.
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PMID:Oxalate degradation by intestinal lactic acid bacteria in dogs and cats. 1522 20

Previous enzymatic determinations have suggested that serum oxalate concentrations in normal rats, the main animal model used in urolithiasis research, to be 3 to 5 times greater than those in healthy human subjects. In this report we validated this observation using a different method (ion chromatography) on serum samples from healthy rats and human subjects that were prepared and handled similarly. Oxalate recoveries during sample preparation for ion chromatography were strongly and variably affected by ultrafiltration devices employed for sample deproteinization and after Cl(-) removal by means of ion exchange. When oxalate recoveries were accounted for, we found significant differences in serum oxalate (6 human samples, 1.47 +/- 0.15 micromol/L; and 15 rat samples, 9.88 +/- 0.91 micromol/L). We conclude that ion-chromatographic techniques confirm the differences in serum oxalate concentrations between rats and human beings measured enzymatically and that failure to account for oxalate losses during sample preparation for ion chromatography can lead to significant underestimation of serum oxalate in both species.
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PMID:Serum oxalate in human beings and rats as determined with the use of ion chromatography. 1525 7

Oxalate induced renal calculi formation and the associated renal injury is thought to be caused by free radical mediated mechanisms. An in vivo model was used to investigate the effect of phycocyanin (from Spirulina platensis), a known antioxidant, against calcium oxalate urolithiasis. Male Wistar rats were divided into four groups. Hyperoxaluria was induced in two of these groups by intraperitoneal infusion of sodium oxalate (70 mg/kg) and a pretreatment of phycocyanin (100 mg/kg) as a single oral dosage was given, 1h prior to sodium oxalate infusion. An untreated control and drug control (phycocyanin alone) were also included in the study. We observed that phycocyanin significantly controlled the early biochemical changes in calcium oxalate stone formation. The antiurolithic nature of the drug was evaluated by the assessment of urinary risk factors and light microscopic observation of urinary crystals. Renal tubular damage as divulged by urinary marker enzymes (alkaline phosphatase, acid phosphatase and gamma-glutamyl transferase) and histopathological observations such as decreased tubulointerstitial, tubular dilatation and mononuclear inflammatory cells, indicated that renal damage was minimised in drug-pretreated group. Oxalate levels (P < 0.001) and lipid peroxidation (P < 0.001) in kidney tissue were significantly controlled by drug pretreatment, suggesting the ability of phycocyanin to quench the free radicals, thereby preventing the lipid peroxidation mediated tissue damage and oxalate entry. This accounts for the prevention of CaOx stones. Thus, the present analysis revealed the antioxidant and antiurolithic potential of phycocyanin thereby projecting it as a promising therapeutic agent against renal cell injury associated kidney stone formation.
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PMID:Prophylactic role of phycocyanin: a study of oxalate mediated renal cell injury. 1529 40

Calcium oxalate (CaOx) urolithiasis is the most common urinary stone disease (70-75 % of all stones consist of CaOx in countries with western diet). Oxalate is the most lithogenic substance in CaOx crystallisation in urine. Oxalate is either synthesized within the body or absorbed from food. As oxalate is not metabolized in the human body, it appears unchanged in urine. Conventional analysis methods cannot distinguish between endogenous and exogenous oxalate. Our [13C2]oxalate absorption test enabled measurement of intestinal oxalate absorption and quantification of the influence of Ca- and Mg-supplementation on it. The effects of the oral administration of these supplements were compared in order to obtain valid data for recommendations for CaOx urolithiasis patients. A 10 mmol supplement of both ions decreased the oxalate absorption significantly, calcium being more than twice as effective.
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PMID:The effect of oral administration of calcium and magnesium on intestinal oxalate absorption in humans. 1537 Feb 83

It has been suggested that renal tubular cell damage induced by oxalic acid, one of the components of urinary calculi, may be involved in a variety of ways in the development of urolithiasis. During our study on a calculus related protein, renal prothrombin fragment-1 (RPTF-1), we noted that this is an inflammation related substance that mediates an acute inflammatory reaction, one of the original roles of prothrombin. RPTF-1 is a part of prothrombin that is a coagulation factor known to be expressed in the renal tubule. We examined whether oxalic acid may cause cytotoxic effects on tubular epithelial cells and whether such chemical stimulation may promote the translation of RPTF-1 mRNA into RPTF-1 proteins. We used Madin-Darby canine kidney (MDCK) cells derived from the distal tubule of a dog kidney. In this study, the effects of oxalic acid in culture solution at different concentrations on cytotoxicity were assessed using a MTT assay. The location of active oxygen species was identified using dichlorofluorescein diacetate. After the prothrombin sequence of RPTF-1 was confirmed in MDCK cells, RPTF-1 mRNA expression was determined by RT-PCR. The gene sequence of the same promoter area was ligated, and a luciferase sequence was inserted downstream of the vector. The target sequence was transfected into MDCK cells and the relation between oxalic acid and prothrombin promoter was examined. In addition, the variable expression of RPTF-1 mRNA was quantitatively compared depending on oxalic acid concentrations using real-time PCR. When cytotoxicity was investigated, cells were not damaged but, by contrast, were stimulated and activated under oxalic acid below a certain concentration. The relation between cytotoxicity on the cultured MDCK cell membrane and active oxygen species was confirmed. Luminescence in MDCK cells containing the luciferase gene was detected by the addition of oxalic acid, which activated the prothrombin promoter. A part of the prothrombin gene sequence in the MDCK cells was detected and an increase in the expression of RPTF-1 mRNA in MDCK cells by the addition of oxalic acid was confirmed using real-time PCR. Increased expression of prothrombin by adding oxalic acid has already been demonstrated in previous studies. In this study, however, RPTF-1 mRNA was promoted by oxalic acid and a direct association between oxalic acid and RPTF-1 is indicated. This finding shows that increased oxalic acid in urine induces the expression of RPTF-1 in tubular epithelial cells and thereby causes the generation of active oxygen species.
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PMID:Effects of oxalate exposure on Madin-Darby canine kidney cells in culture: renal prothrombin fragment-1 mRNA expression. 1632 15

Of decisive importance for the many research groups all over Europe were the scientific symposia dealing with the theoretical foundations and clinical aspects of urinary stone disease. There were several sources from which today's European Urinary Stone meetings and the "Eurolithiasis Society" itself arose. It was a long way from Leeds in 1968 to Jena 1970, Bonn-Vienna in 1972 and to 11 European meetings from 1989 to 2005. Which developments in urinary stone disease research have been presented at our congresses during the past 40 years? The 1970s and 1980s are the years marked by efforts to measure the important lithogenic substances such as calcium, ionized calcium, uric acid, phosphate, oxalate with reliable methods. Hypercalciuria and specifically mild hyperoxaluria were the topics of numerous investigations in the 1970s, 1980s and 1990s. The calcium-loading test described by Pak has been discussed frequently since its application. It became apparent that oxalic acid is more important in urinary stone formation than hypercalciuria. Of importance were investigations done by Robertson and his colleagues on the influence of diet (in particular, an animal protein-rich diet) on urinary stone formation. Another emphasis of research was investigation of the crystallization process: supersaturation, crystal growth and aggregation are important steps in urinary stone formation. Of great importance in the formation of urinary stones are inhibitors (inhibitory activity): citrate, magnesium, pyrophosphate, macromolecules: GAGs, THP etc. and it became possible in the early 1970s to determine substances such as Tamm-Horsfall protein (THP) and GAGs. Much attention in the 1970s and 1980s was focused on urinary stone analysis (X-ray diffraction, infrared spectroscopy, polarization microscopy) and standardization of these methods. In the mid-1980s, a whole series of epidemiological studies were carried out, with data for the Federal Republic of Germany, East Germany, Czechoslovakia and Austria. The search for "stone-removing" medications, their description and clinical use was the subject of much clinical research and in vitro examinations. A definite advance occurred in the 1980s with the development of new instrumental technologies for the management of urinary stones such as shockwave ("Stosswelle") lithotripsy, percutaneous nephrolithotomy and ureterorenoscopy (" breakthrough innovations"). Since the 8th European Urolithiasis Symposium there have regularly been presentations pertaining to the topic of the molecular basis of inherited lithiasis. The last 10-15 years have shown an increasing turning toward the importance of cellular alterations and supersaturation and their relation to stone formation. In conclusion, I would like to note that it is of decisive importance for the research groups all over Europe to organize scientific symposia dealing with the theoretical foundations and clinical aspects of urinary stone disease under the protection of the European Urolithiasis Society.
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PMID:Thirty-eight years of stone meetings in Europe. 1650 36

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

Detailed knowledge of food oxalate content is of essential importance for dietary treatment of recurrent calcium oxalate urolithiasis. Dietary oxalate can contribute considerably to the amount of urinary oxalate excretion. Because cereal foods play an important role in daily nutrition, the soluble and total oxalate contents of various types of cereal grains, milling products, bread, pastries, and pasta were analyzed using an HPLC-enzyme-reactor method. A high total oxalate content (>50 mg/100 g) was found in whole grain wheat species Triticum durum (76.6 mg/100 g), Triticum sativum (71.2 mg/100 g), and Triticum aestivum (53.3 mg/100 g). Total oxalate content was comparably high in whole grain products of T. aestivum, that is, wheat flakes and flour, as well as in whole grain products of T. durum, that is, couscous, bulgur, and pasta. The highest oxalate content was demonstrated for wheat bran (457.4 mg/100 g). The higher oxalate content in whole grain than in refined grain cereals suggests that oxalic acid is primarily located in the outer layers of cereal grains. Cereals and cereal products contribute to the daily oxalate intake to a considerable extent. Vegetarian diets may contain high amounts of oxalate when whole grain wheat and wheat products are ingested. Recommendations for prevention of recurrence of calcium oxalate stone disease have to take into account the oxalate content of these foodstuffs.
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PMID:Oxalate content of cereals and cereal products. 1660 23

Hyperoxaluria is a risk factor for renal stones. It appears to be sustained by increased dietary load or increased intestinal absorption. The aim of this study was to evaluate whether oral administration of lactobacilli could prevent urolithiasis in stone-forming rats. Oxalate-degrading activities of lactobacilli were evaluated by measuring the oxalate level in a culture medium after inoculation with lactobacilli. Only the strains of Lactobacillus having oxalate-degrading activity were used. Sprague-Dawley rats were fed a powdered standard diet containing 3% sodium oxalate and/or received 100 mg/kg of celecoxib for the first 8 days by gavage, before or after the beginning of this experiment (groups with previous treatment or with co-treatment). Rats were sacrificed after 4 weeks and kidneys were harvested for the assay of crystal formation under a dissecting microscope. Twenty-four-hour urine collections were performed before kidney harvest. Only two strains, Lactobacillus casei HY2743 and L. casei HY7201 out of 31 strains of Lactobacillus were able to degrade oxalate. In both groups of co-treatment and previous treatment with L. casei HY2743 and L. casei HY7201, urine oxalate excretion decreased compared to the group without lactobacilli. The dissecting microscope examination of kidneys in the rats in two previous treatment groups and the co-treatment group with L. casei HY7201 showed less abundant crystals than control groups. Our results show that lactobacilli may be used as a potential therapeutic strategy in the prevention of urinary stones.
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PMID:Prevention of nephrolithiasis by Lactobacillus in stone-forming rats: a preliminary study. 1663 9

Although urolithiasis is common in spinal cord injury patients, it is presumed that the predisposing factors for urinary stones in spinal cord injury patients are immobilization-induced hypercalciuria in the initial period after spinal injury and, in later stages, urine infection by urease-producing micro-organisms, e.g., Proteus sp., which cause struvite stones. We describe a patient who sustained C-7 complete tetraplegia in a road traffic accident in 1970, when he was 16 years old. Left ureterolithotomy was performed in 1971 followed by left nephrectomy in 1972. Probably due to adhesions, this patient developed volvulus of the intestine in 1974. As he had complete tetraplegia, he did not feel pain in the abdomen and there was a delay in the diagnosis of volvulus, which led to ischemia of a large segment of the small bowel. All but 1 ft of jejunum and 1 ft of ileum were resected leaving the large bowel intact. In 1998, suprapubic cystostomy was performed. In 2004, this patient developed calculus in the solitary right kidney. Complete stone clearance was achieved by extracorporeal shock wave lithotripsy. Stone analysis: calcium oxalate 60% and calcium phosphate 40%. Metabolic evaluation revealed hyperoxaluria, hypocitraturia, and hypomagnesiuria. Since this patient had hyperoxaluria, the stool was tested for Oxalobacter formigenes, a specific oxalate-degrading, anerobic bacterium inhabiting the gastrointestinal tracts of humans; absence of this bacterium appears to be a risk factor for development of hyperoxaluria and, subsequently, calcium oxalate kidney stone disease. DNA from the stool was extracted using the QIAamp DNA stool Mini Kit (Qiagen, Chatsworth, CA). The genomic DNA was amplified by polymerase chain reaction using specific primers for oxc gene (developed by Sidhu and associates). The stool sample tested negative for O. formigenes. The patient was prescribed potassium citrate mixture; he was advised to avoid oxalate-rich food, maintain recommended levels of calcium in his diet, and take live bio-yogurt. Two months later, 24-h urinary oxalate decreased from 0.618 to 0.411 mmol/day; 24-h urine citrate increased from 0.58 to 1.10 mmol/day. Six months later, an oxalate absorption test was performed. The patient swallowed a capsule, soluble in gastric juice, containing 50 mg (0.37 mmol) sodium [13C2]oxalate corresponding to 33.8 mg of [13C2]oxalic acid. The amount of labeled oxalate, excreted in urine, was measured by a gas chromatographic-mass spectrometric assay. Oxalate absorption, expressed as the percentage of the labeled dose recovered in the 24-h urine after dosing, was 8.3% (reference range: 2.3-17.5%). In addition to other conventional measures, oral administration of O. formigenes or lactic acid bacteria mixture to promote bacterial degradation of oxalate in the gut, and thus combat hyperoxaluria, may play a role in prevention of calcium oxalate kidney stones.
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PMID:Hyperoxaluria, hypocitraturia, hypomagnesiuria, and lack of intestinal colonization by Oxalobacter formigenes in a cervical spinal cord injury patient with suprapubic cystostomy, short bowel, and nephrolithiasis. 1761 9


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