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

Oxalobacter formigenes is a specific oxalate-degrading, anaerobic bacterium inhabiting the gastrointestinal tracts of vertebrates, including humans. This bacterium maintains an important symbiotic relationship with its host by regulating oxalate homeostasis, primarily by preventing enteric absorption. Increased absorption of oxalate can lead to multiple complications associated with hyperoxaluria, especially recurrent calcium oxalate urolithiasis. Detection of O. formigenes in the gastrointestinal tract has attracted attention because the absence of this bacterium appears to be a risk factor for development of hyperoxaluria and/or recurrent calcium oxalate kidney stone disease. In the present study, epidemiologic studies with patients at high risk for calcium oxalate urolithiasis showed a direct correlation between the number of recurrent kidney stone episodes and the lack of O. formigenes colonization. As expected, the lack of O. formigenes revealed a clear association with prophylactic antibiotic therapy. To confirm the importance of O. formigenes in regulating hyperoxaluria, laboratory rats known to be noncolonized were colonized with live bacteria or treated with a preparation of oxalate-degrading enzymes derived from O. formigenes to determine any subsequent increased resistance to high oxalate challenge. Rats receiving either bacteria or enzyme replacement therapy excreted far lower levels of oxalate, did not develop the crystalluria observed with control rats, and resisted the formation of calcium oxalate crystals in their nephrons. These observations, taken together, support the concept that O. formigenes is important in maintaining oxalate homeostasis, that its absence from the gut increases the risk for hyperoxaluria and recurrent kidney stone disease, and that replacement therapy is an efficient procedure to prevent hyperoxaluria and its complications.
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PMID:Direct correlation between hyperoxaluria/oxalate stone disease and the absence of the gastrointestinal tract-dwelling bacterium Oxalobacter formigenes: possible prevention by gut recolonization or enzyme replacement therapy. 1054 Dec 58

Oxalate degradation by the anaerobic bacterium Oxalobacter formigenes is important for human health, helping to prevent hyperoxaluria and disorders such as the development of kidney stones. Oxalate-degrading activity cannot be detected in the gut flora of some individuals, possibly because Oxalobacter is susceptible to commonly used antimicrobials. Here, clarithromycin, doxycycline, and some other antibiotics inhibited oxalate degradation by two human strains of O. formigenes. These strains varied in their response to gut environmental factors, including exposure to gastric acidity and bile salts. O. formigenes strains established oxalate breakdown in fermentors which were preinoculated with fecal bacteria from individuals lacking oxalate-degrading activity. Reducing the concentration of oxalate in the medium reduced the numbers of O. formigenes bacteria. Oxalate degradation was established and maintained at dilution rates comparable to colonic transit times in healthy individuals. A single oral ingestion of O. formigenes by adult volunteers was, for the first time, shown to result in (i) reduced urinary oxalate excretion following administration of an oxalate load, (ii) the recovery of oxalate-degrading activity in feces, and (iii) prolonged retention of colonization.
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PMID:Oxalobacter formigenes and its potential role in human health. 1214 79

Kidney stones are increased in patients with bowel disease, particularly those who have had resection of part of their gastrointestinal tract. These stones are usually CaOx, but there is a marked increase in the tendency to form uric acid stones, as well, particularly in patients with colon resection. These patients all share a tendency to chronic volume contraction due to loss of water and salt in diarrheal stool, which leads to decreased urine volumes. They also have decreased absorption, and therefore diminished urinary excretion, of citrate and magnesium, which normally act as inhibitors of CaOx crystallization. Patients with colon resection and ileostomy form uric acid stones, as loss of bicarbonate in the ileostomy effluent leads to formation of an acid urine. This, coupled with low urine volume, decreases the solubility of uric acid, causing crystallization and stone formation. Prevention of stones requires treatment with alkalinizing agents to raise urine pH to about 6.5, and attempts to increase urine volume, which increases the solubility of uric acid and prevents crystallization. Patients with small bowel resection may develop steatorrhea; if the colon is present, they are at risk of hyperoxaluria due to increased permeability of the colon to oxalate in the presence of fatty acids, and increased concentrations of free oxalate in the bowel lumen due to fatty acid binding of luminal calcium. EH leads to supersaturation of urine with respect to CaOx, in conjunction with low volume, hypocitraturia and hypomagnesuria. Therapy involves a low-fat, low-oxalate diet, attempts to increase urine volume, and agents such as calcium given to bind oxalate in the gut lumen. Correction of hypocitraturia and hypomagnesuria are also helpful.
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PMID:Stones from bowel disease. 1247 41

Approximately 4 million Germans suffer from stone disease. In the majority of cases (70-75%) it is calcium oxalate. Its pathophysiology is complex and comprises disorders such as hypercalciuria, hyperoxaluria, hypocitraturia, hyperuricosuria, and hypomagnesuria. These biochemical changes in urine are well known as "classic" risk factors of calcium oxalate stone formation. However, studies in the last decade showed that calcium oxalate stones are strongly related with other diseases or disorders such as overweight, hypertension, or a lack of oxalate-degrading bacteria in the gut. The evidence for these "new" risk factors in the literature is very strong. It is particularly important in regard to effective treatment and aftercare of patients with calcium oxalate stones to be familiar with both the "classic" and the new risk factors.
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PMID:[Calcium oxalate stones and hyperoxaluria. What is certain? What is new?]. 1623 94

An association between small bowel resection and stone disease has been noted, which is primarily due to increased gut oxalate absorption and resulting excretion by the kidney. In order to better understand the factors affecting both oxalate absorption and renal excretion, and the resulting renal lesions, we have developed a rodent model of small bowel resection and hyperoxaluria. Using this model, we have studied the renal histology in animals with hyperoxaluria over time spans from 2 weeks to 7 months. The initial lesion appears to be crystal formation along the brush border of the proximal tubule, with eventual crystal deposition in collecting ducts and papillary interstitium, and eventual tubule obstruction, interstitial inflammation and fibrosis. Crystal formation appears to dissociate from urinary supersaturation. We hypothesize that oxalate transporters in the proximal tubule may increase local saturations, leading to crystal formation at this site initially. Further studies are required to better characterize the causes and consequences of hyperoxaluria in this animal model.
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PMID:A new animal model of hyperoxaluria and nephrolithiasis in rats with small bowel resection. 1628 81

Food and nutrition professionals provide medical nutrition therapy for patients with kidney stones. If the stones contain oxalate or the patient has been diagnosed with hyperoxaluria, reduction of dietary oxalate may be appropriate. Differences in oxalate values for a single food may be due to analytical methods, and/or biological variation from several sources, including cultivar, time of harvest, and growing conditions. Bioavailability of food oxalate and, thus, urine oxalate, will also be affected by salt forms of oxalate, food processing and cooking methods, meal composition, and the presence of Oxalabacter formigenes in the patient's gut. Dietary advice for reducing urinary oxalate should include both reduction of dietary oxalate and simultaneous consumption of calcium-rich food or supplement to reduce oxalate absorption.
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PMID:Food oxalate: factors affecting measurement, biological variation, and bioavailability. 1760 50

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

Intestinal diseases may cause the formation of urinary stones through changes in the metabolism of oxalate, calcium, and uric acid. The oxalate that is excreted into urine comes from the catabolism of ascorbic acid and some amino acids or from intestinal absorption of food oxalate. Calcium is absorbed by the gut after the stimulation of active vitamin D and is excreted by the kidney under the control of the bone/parathyroid hormone axis. Uric acid is generated by the oxidation of exogenous and endogenous purine bases, is excreted by the kidney through glomerular filtration/tubular secretion, and is soluble in alkaline urine. Several data indicate that patients with inflammatory bowel diseases are at high risk of urinary stones containing calcium-oxalate salt or uric acid. Calcium-oxalate stones are caused by colonic oxalate hyperabsorption (secondary to intestinal dysfunction) or by parenteral nutrition. Uric acid stones are typical of patients with severe diarrhea and/or intestinal neostomy, that is, in patients with hyperconcentrated acidic urine. Relationships between malabsorptive intestinal diseases and urinary stones are less well defined. Preventive countermeasures are not the same for all disorders. Hyperoxaluria should be controlled by diets with a low content of lipids and oxalate but supplemented with calcium and probiotics. The presence of hyperconcentrated acidic urine should be controlled by correct hydration and administration of citrate.
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PMID:[Nephrolithiasis in patients with intestinal diseases]. 1826 17

Hyperoxaluria is a major risk factor for the formation of calcium oxalate stones, but dietary restriction of oxalate intake might not be a reliable approach to prevent recurrence of stones. Hence, other approaches to reduce urinary oxalate to manage stone disease have been explored. The gut-dwelling obligate anaerobe Oxalobacter formigenes (OF) has attracted attention for its oxalate-degrading property. In this review we critically evaluate published studies and identify major gaps in knowledge. Recurrent stone-formers are significantly less likely to be colonized with OF than controls, but this appears to be due to antibiotic use. Studies in animals and human subjects show that colonization of the gut with OF can decrease urinary oxalate levels. However, it remains to be determined whether colonization with OF can affect stone disease. Reliable methods are needed to detect and quantify colonization status and to achieve durable colonization. New information about oxalate transport mechanisms raises hope for pharmacological manipulation to decrease urinary oxalate levels. In addition, probiotic use of lactic acid bacteria that metabolize oxalate might provide a valid alternative to OF.
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PMID:A critical analysis of the role of gut Oxalobacter formigenes in oxalate stone disease. 1902 5

We report 3 cases of primary oxalosis with nephrocalcinosis and severe renal failure. Extrarenal involvement was noted in bones in 3 cases, the heart in 2 cases, the central nervous system in 2 cases, the skin in 1 case and the eye in 1 case. The 3 patients presented with acute digestive disorders. Ultrasonography and CT scans showed digestive wall calcifications in addition to the classic appearance of primary oxalosis such as nephrocalcinosis or bone involvement. Primary hyperoxaluria is characterized by a calcium deposit in different tissues, mainly in kidneys. Digestive wall involvement has never been reported in the literature. Primary oxaluria should be considered in the presence of such a deposit in the gut wall.
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PMID:[Exceptional digestive location of crystal deposits in primary hyperoxaluria]. 1974 2


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