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

Calcific kidney stones in both humans and mildly hyperoxaluric rats are located on renal papillary surfaces and consist of an organic matrix and crystals of calcium oxalate and/or calcium phosphate. The matrix is intimately associated with the crystals and contains substances that can promote as well as inhibit calcification. Osteopontin, Tamm-Horsfall protein, bikunin, and prothrombin fragment 1 have been identified in matrices of both human and rat stones. Hyperoxaluria can provoke calcium oxalate nephrolithiasis in both humans and rats. Kidney-stone-forming rats are hypomagnesuric and hypocitraturic during nephrolithiasis. Human stone formers may have the same disorders. Males of both species are prone to develop calcium oxalate nephrolithiasis, whereas females tend to form calcium phosphate stones. Oxalate metabolism is considered to be almost identical between rats and humans. Thus, there are many similarities between experimental nephrolithiasis induced in rats and human kidney-stone formation, and a rat model of calcium oxalate nephrolithiasis can be used to investigate the mechanisms involved in human kidney stone formation.
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PMID:Animal models of kidney stone formation: an analysis. 928 52

A total of 19 patients with active nephrolithiasis, 14 patients with non-active nephrolithiasis and 17 healthy subjects were examined under standardized intake of calcium, phosphorus, purine and protein. In patients with both active and non-active renal stone disease the following abnormalities were found: elevated plasma levels of PTH and osteocalcin, increased activity of the bone isozyme of alkaline phosphatase, low plasma levels of phosphate and increased urinary excretion of calcium and oxalic acid. These abnormalities were more marked in patients with active than non-active nephrolithiasis. No correlation was found between plasma PTH levels and parameters of bone turnover as well as calciuria and oxaluria. Results presented in this paper suggest that (a) Smith's criteria of active renal stone disease are of minor pathogenetic and therapeutic value and (b) patients with active nephrolithiasis differ from non-active renal stone formers by more elevated oxaluria and markers of bone turnover and more marked abnormalities in calcium-phosphate metabolism related parameters.
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PMID:Markers of bone turnover in patients with nephrolithiasis. 941 56

Primary hyperoxaluria (PH) is a severe inherited disease induced by an enzymatic deficiency responsible for high endogenous production of oxalate. Oxalate ions are excreted by the kidney where they can form an insoluble salt with calcium ions, thus inducing urinary stones, crystal deposition in the tubular lumen and renal parenchyma leading to nephrocalcinosis and renal failure. Eighty-seven calculi from 63 PH patients with primary hyperoxaluria were analyzed and compared to 24,130 calculi from unselected consecutive stone formers referred to our laboratory between January 1977 and December 1996. All stones were analyzed according to a protocol including morphological examination of both surface and cross-section, and sequential infrared identification of the crystalline phases. A typical aspect of both surface and section corresponding to morphological type Ic according to our proposed classification (Daudon et al. Scanning Microsc 1993, 7:1081-1106) was observed in all patients but two whereas only two type Ic stones were observed among patients without primary hyperoxaluria. The latter two patients suffered from severe inflammatory bowel disease and developed heavy hyperoxaluria following extensive ileal resection. We conclude that evidence of type Ic morphology is a simple, cheap and fast tool to detect diseases with heavy hyperoxaluria such as primary hyperoxaluria.
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PMID:Unusual morphology of calcium oxalate calculi in primary hyperoxaluria. 960 12

Homeostasis of oxalic acid appears to be regulated, in part, by the gut-associated bacterium Oxalobacter formigenes. The loss of this bacterium from the gut flora is associated with an increased susceptibility to hyperoxaluria, a condition which can lead to the formation of calcium oxalate crystalluria and kidney stones. In order to identify and quantify the presence of O. formigenes in clinical specimens, a quantitative-PCR-based assay system utilizing a competitive DNA template as an internal standard was developed. This quantitative competitive-template PCR test allows for the rapid, highly specific, and reproducible quantification of O. formigenes in fecal samples and provides a prototype for development of DNA-based quantitative assays for enteric bacteria.
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PMID:Direct quantification of the enteric bacterium Oxalobacter formigenes in human fecal samples by quantitative competitive-template PCR. 1020 13

Background: Oxalobacter formigenes is a recently discovered anaerobic bacterium residing in the gastrointestinal tracts of most vertebrates, including humans. Evidence suggests that this bacterium plays an important symbiotic relationship with its hosts by regulating oxalic acid homeostasis. Oxalic acid is a ubiquitous toxic by-product of metabolism associated with numerous pathologic conditions, including hyperoxaluia, cardiac myopathy and conductance disorders, kidney stones, and even death. Despite the potential importance of O. formigenes in several major health disorders, the difficulty in culturing, isolating, and identifying this fastidious anaerobe has limited research of its disease associations. Because O. formigenes must use two unique enzymes to catabolize oxalic acid, this bacterium appeared to be a suitable model for DNA-based identification, thereby circumventing the labor-intensive procedures currently used. Methods and Results: In this study, genus- and group-specific oligonucleotide sequences were designed corresponding to homologous regions residing in the oxc gene that enodes for oxalyl-coenzyme A decarboxylase. A polymerase chain reaction (PCR)-based amplification of the 5'end of this gene directly from genomic DNA isolated from various strains of O. formigenes was used to show that the genus- and group-specific oligonucleotide probes could identify and subgroup the bacterium. Field testing of this PCR-based detection system with 100 fecal cultures collected from children aged 0-12 years demonstrated the ease and efficacy with which O. formigenes can now be identified. Furthermore, these latter data provide a profile for the natural colonization of a human population with this intestinal bacterium. Conclusions: Development and use of this PCR-based detection system permit the rapid identification and classification of the gut-associated bacterium O. formigenes, thereby circumventing the need for the more labor-intensive and lengthy method currently used. The first field test of this detection system indicates that humans apparently do not become colonized with O. formigenes until they begin crawling about in the environment. Furthermore, studies investigating the association between several disorders (eg, kidney stones, irritable bowel syndrome, and hyperoxaluria) and the absence of the bacterium from the gut will now prove far easier.
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PMID:Evaluating Children in the Ukraine for Colonization With the Intestinal Bacterium Oxalobacter formigenes, Using a Polymerase Chain Reaction-based Detection System. 1046 96

In up to one-third of patients with calcium oxalate stones, a hyperoxaluria can be detected. Hyperoxaluria can result from increased endogenous production, from excessive oxalate content of the food, or from intestinal hyperabsorption. For a causal therapy, it is important to discriminate between metabolic and hyperabsorptive hyperoxaluria. Our new 13C-oxalate test allows this differentiation. Under standardized conditions, 50 mg of disodium salt of [13C2]oxalic acid was applied. From the amount of labeled oxalate excreted in urine as measured by a gas chromatographic-mass spectrometric assay, the intestinal absorption was calculated. Seventy patients with recurrent calcium oxalate urolithiasis who had no signs of inflammatory bowel disease were tested. Their mean intestinal oxalate absorption was 9.2+/-5.1%. This was significantly higher than the mean absorption of 50 healthy volunteers (6.7+/-3.9%). There was no difference in oxalate absorption between male (n = 25) and female volunteers. Oxalate absorption correlated with the oxalate excretion in the 24-h urine (volunteers: r = 0.46, P < 0.01; patients: r = 0.62, P < 0.001). Oxalate hyperabsorption was defined as an absorption exceeding 10%. According to this definition, 34% of the patients had oxalate hyperabsorption; 20% of the volunteers showed a hyperabsorption, too. The 13C-oxalate absorption test allows reliable determination of intestinal oxalate absorption. Because of the use of a stable isotope, this test may be repeated as often as required. It will allow the control of therapeutic regimens and also help to unravel genetic influences in stone formation.
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PMID:Intestinal hyperabsorption of oxalate in calcium oxalate stone formers: application of a new test with [13C2]oxalate. 1054 Dec 57

The data reviewed in this paper indicate that there is compelling direct and indirect evidence that certain dietary modifications can limit the risk for stone formation. Fluid therapy should be a front-line approach for all stone formers, because it is safe, cheap, and effective. Restricting sodium and animal-protein consumption produces changes in the urinary environment that should benefit the majority of stone formers, including a decrease in calcium and increase in citrate excretion. Minimizing the intake of processed goods limits sodium gluttony. These dietary modifications also reduce cardiovascular risks. Indiscriminant calcium restriction should be avoided, because it could accelerate stone formation and violate skeletal integrity. Oxalate restriction should be considered for calcium oxalate stone formers, especially those with hyperoxaluria. Specific recommendations for modifying the consumption of other nutrients cannot be made at this time because of the limited available information about the resultant effects. The aforementioned goals can be achieved within the context of a nutritionally balanced diet providing adequate sources of fruits and vegetables. There is a definite need for better designed studies of the nutritional effects on stone disease. This would promote a better understanding of the interplay between the genetic and environmental components of this disorder.
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PMID:Role of diet in the therapy of urolithiasis. 1077 68

Hyperoxaluria is the most important risk factor for a formation of calcium oxalate-urinary stones. Usually, the bulk of oxalate will be formed in the human body, but in many patients the oxalate from food plays the decisive role. Conventionally, in urine the endogenous oxalate can not be distinguished from food derived oxalate. We have developed a standardized oxalate-absorption test, applying a physiological dose (50 mg disodium salt of [13C2]oxalic acid) of labelled oxalate. The assay has been published. Now we report on the first extensive applications of this test in 86 volunteers and 135 patients from different groups with calcium oxalate stones or an increased risk of the formation of such stones. In one-third of the patients with calcium oxalate-urinary stones an oxalate hyperabsorption was diagnosed. For these patients, a dietetic stone prophylaxis and/or therapy is indicated.
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PMID:Experience with the [13C2]oxalate absorption test. 1102 22

Proteins are thought to play a major role in stone formation and structurally abnormal proteins have been reported to be present in the urine of stone formers. This study was aimed to determine whether hyperoxaluria modifies the kinetic properties of urinary inhibitory proteins. Hyperoxaluria was induced by feeding 1% ethylene glycol to rats. Oxalate, uric acid and calcium excretion were increased progressively during hyperoxaluria, while magnesium level was decreased. Urinary proteins were separated on a DEAE-cellulose column by eluting with stepwise increasing salt concentration in 0.05 M Tris-HCl buffer (pH 7.0). Each protein fraction was studied for its crystallization inhibitory potential by the spectrophotometric method. The protein eluted in 0.3 M NaCl containing buffer had the maximal nucleation as well as inhibitory activity. The protein had a molecular weight of 45 kD. In hyperoxaluria, the urinary excretion of this protein significantly increased. In the crystal growth assay, the control rat 45-kD protein inhibited nucleation by 75% and aggregation by 100%. In contrast, it is very interesting to note that the protein derived from 28th day hyperoxaluric urine, behaved as a promoter of nucleation (-113%, percentage inhibition) and weak inhibitor of aggregation (28%). A significantly high negative correlation (r = -0.97) between oxalate excretion and the inhibitory activity of the 45-kD protein was observed suggesting a modification of the protein by oxalate.
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PMID:Effect of hyperoxaluria on the inhibitory activity of a 45-kD urinary protein. 1181 6

A 37-year-old patient underwent two successive renal transplantations 7 months apart. He remained dialysis dependent. Early biopsy of both grafts revealed widespread calcium oxalate deposition suggestive of acute oxalate nephropathy. Several causes of oxalate nephropathy, including primary oxalosis and an increased intake of oxalic acid precursors, were excluded. Two years later, the identification of steatorrhea with radiologic signs of chronic pancreatitis led to the hypothesis of enteric hyperoxaluria. Surprisingly, 11 months after the second transplantation, graft function improved progressively allowing interruption of dialysis. Three years later, renal function is stable. The causes and prevention of acute oxalate-induced graft failure are highlighted. Subclinical evidence of enteric hyperoxaluria should be looked for and appropriate therapy instituted as early as possible. The possibility of a late recovery of renal function warrants attentive patience from attending physicians.
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PMID:Enteric hyperoxaluria: a hidden cause of early renal graft failure in two successive transplants: spontaneous late graft recovery. 1208 89


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