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

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

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

Several studies indicate that crystallization, the essential first step for stone formation, starts in the nephron. First a calcium phosphate mineral precipitates in the loop of Henle and this may induce formation of calcium oxalate in the late nephron segments. This study investigated the factors that determine the risk of the first calcium phosphate crystallization step in the loop of Henle. Data from a theoretical model that describes the fluid composition in the different nephron segments are combined with data from nucleation experiments. From this, an assessment was made regarding how changes in plasma and urine composition, tubular functions, and renal anatomy effect the chance of initial crystallization of calcium phosphate in the loop of Henle. The results show that parameters like hypercalciuria and hyperoxaluria do not completely reflect the risk for the initial nucleation step. A combination with data on plasma composition and on tubular function is needed to assess this risk. Renal growth from birth to adulthood and the concomitant increase in renal concentrating capacity are shown to increase the risk for crystallization in the loop of Henle. This coincides with the increasing incidence of calcium oxalate urolithiasis. Treating crystallization and stone formation as a nephron event opens new ways for investigating and understanding the process of urinary stone formation.
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PMID:Risk factors for crystallization in the nephron: the role of renal development. 1054 Dec 65

It is unclear why men have a higher incidence of calcium oxalate nephrolithiasis than women. This study examined the role of sex hormones on urinary oxalate excretion and kidney stone formation in an experimental model of urolithiasis. Adult male and female Sprague Dawley rats with different sex hormone modulations were given 0.75% ethylene glycol for 2 wk to induce hyperoxaluria and kidney calcium oxalate crystal deposition. The study groups were: intact male and female rats; castrated male and female rats; intact male or female rats with opposite sex hormone implants; and castrated male and female rats with either testosterone or estradiol implants. Overall, a significant negative correlation between urinary oxalate and plasma estradiol/testosterone ratio was found. None of the estradiol-implanted rats, whether male or female, intact or castrated, developed kidney crystal deposits. The three groups of testosterone-implanted rats had a 43 to 88% rate of kidney calcium oxalate crystal deposition. These results indicate that androgens increase and estrogens decrease urinary oxalate excretion, plasma oxalate concentration, and kidney calcium oxalate crystal deposition. These findings may partly explain why nephrolithiasis is a predominantly male disease.
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PMID:Role of sex hormones in experimental calcium oxalate nephrolithiasis. 1054 Dec 67

Urolithiasis is uncommon in adolescence and rare in early childhood. In pediatric populations, congenital urinary tract anomalies associated with stasis and infection, idiopathic urolithiasis (adolescents), and nephrocalcinosis (premature infants) account for the majority of urolithiasis patients. Inborn errors of metabolism, such as the primary hyperoxalurias, are rare causes of urolithiasis in childhood. We report six children (mean age at symptom onset 1.3 years; range 0.32-4.1 years) with moderate hyperoxaluria (mean 1.10 +/- 0.58 mmoL/1.73m2 per day; range 0.69-2.19 mmoL/1.73m2 per day). Urolithiasis was present in four. Stones from two children were comprised of calcium oxalate dihydrate. Calcium oxalate crystalluria was seen in two of the patients. Findings included a mean urine calcium concentration of 6.61 +/- 2.28 mg/kg per day, urine citrate of 925.5 +/- 291.29 mg/g of creatinine per day, and mean renal clearance of 99.83 +/- 23.27 mL/min. All children were born full term, none was receiving diuretics, and none had recurrent urinary tract infections. Secondary causes of hyperoxaluria, including dietary oxalate excess, pyridoxine deficiency, and malabsorption, were excluded. Urine glycolate and glycerate were normal in all patients. In one hyperoxaluric member of each sibship, hepatic alanine-glyoxylate aminotransferase and D-glycerate dehydrogenase/glyoxylate reductase activity were normal. The clinical and biochemical features of these children are unlike those in previously recognized hyperoxaluric states. Thus, our description of a separate hyperoxaluric entity, referred to as unclassified hyperoxaluria.
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PMID:Hyperoxaluria and urolithiasis in young children: an atypical presentation. 1060 14

Various endo- and exogenous factors play a role in the urinary stones formation tract. The aim of the study was to define the type and frequency of hyperexcretion of lithogenic substances in school children population and to determine an influence of risk factors on hyperexcretion of crystallizing substances. The study included 220 school children. Preurolithiasis state (PS) was found in 30% children. The most frequently hyperoxaluria, hyperuricosuria and hypercalciuria were diagnosed and it may be connected with abnormal nutritional habits, excessive application of multivitamins, vitamin D and calcium, disturbances in drinking water chemical composition (higher amount of calcium, smaller amount of magnesium, abnormal pH). Urinary tract infections, particularly in children with obstructive uropathy are an important risk factor in the examined population. Positive familial history of urolithiasis in 43.3% children may indicate for the important role of the genetic factor in the pathogenesis of the disease.
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PMID:[The role of environmental factors in the formation of kidney calculi]. 1089 97

Urolithiasis often coexists with recurrent urinary tract infections (RUTI). The aim of the study was to determine the correlation of preurolithiasis state (PS) and recurrent urinary tract infections and to establish an effect of the treatment UTI recurrence incidence. PS was found in 202(21.1%) children, most frequently: hyperoxaluria--in 61/202 (30.2%), hypercalciuria--in 32/202 (15.8%), and hyperuricosuria--in 30/202 (14.9%) children. Complex metabolic abnormality was observed in 62/202 (30.7%) patients. Therapeutic management comprised of: antibacterial prophylaxis, high fluid intake, proper diet, correction of urine pH, and pharmacological treatment if necessary. Disappearance of RUTI and PS in 88/202 (43.6%) children, disappearance of RUTI in spite of persistent PS in 36/202 (17.8%), and decrease of RUTI in 54/202 (26.7%) patients were method. In 110/202 (54.5) children PS disappeared.
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PMID:[Results of the treatment of pre-urolithiasis state in children with recurrent urinary tract infections]. 1089 15

Urolithiasis is a frequent disorder that is characterized by its recurrence following treatment and which can affect between 3-20% of the population, with an incidence that differs from country to country. The aim of the present study was to determine the composition of the calculi, and the remain characteristics of this pathology in Morocco. A series of 80 calculi was therefore analyzed by Fourier transform infrared spectroscopy. The findings showed that calcium monohydrate oxalate was the main lithiasic component, indicating that hyperoxaluria plays a major role in the formation of the calculi. The component identified were as follows: calcium oxalate (58.75%), calcium phosphate and magnesium phosphate (17.5%), uric acid (15%), and urate (8.75%). In 91.25% of cases, the calculi were of mixed composition. Regular patient follow-up is advocated and subjects should be informed of the risk factor involved, as urolithiasic recurrence was observed in 10% of the cases in this series.
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PMID:[Infrared spectrometry and urolithiasis. Report of 80 cases]. 1114 79

Urolithiasis is one of the third most common afflictions found in humans. The efficacy of the two Siddha drugs, Aerva lanata and Vediuppu chunnam as antilithic agents using a urolithic rat model were tested in this study. Hyperoxaluria was induced in rats using 0.75% ethylene glycol in drinking water. Aerva lanata(3.0 mg kg(-1)body weight) and Vediuppu chunnam (3.5 mg kg(-1)body weight) were given orally for 28 days. Urinary risk factors of urolithiasis were monitored at the end of 7th, 14th, 21st and 28th days. Urinary volume was increased in hyperoxaluric as well as drug-treated rats. Increased urinary excretion of calcium, oxalate, uric acid, phosphorus and protein in hyperoxaluric rats was brought down significantly by the administration of A. lanata or Vediuppu chunnam. Decreased magnesium excretion in hyperoxaluric rats was normalized by drug treatment. The drug increases the urine volume, thereby reducing the solubility product with respect to calcium oxalate and other crystallizing salts such as uric acid, which may induce epitaxial deposition of calcium oxalate. Drug alone treated rats did not show any adverse effects. Combination therapy was found to be more effective and this indigenous medicine can be used successfully as an antilithic agent.
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PMID:Effect of A. lanata leaf extract and Vediuppu chunnam on the urinary risk factors of calcium oxalate urolithiasis during experimental hyperoxaluria. 1120 71

To determine whether an "atherogenic" diet (excess of cholesterol and neutral fat) induces pathological calcification in various organs, including the kidney, and abnormal oxalate metabolism, 24 male Sprague-Dawley rats were fed either normal lab chow (controls, n = 12) or the cholesterol- and fat-rich experimental diet (CH-F, n = 12) for 111 +/- 3 days. CH-F rats developed dyslipidemia [high blood levels of triglycerides, total, low-density lipoprotein (LDL)-, very low-density lipoprotein (VLDL)-, high-density lipoprotein (HDL)-bound cholesterol, total phospholipids], elevated serum total alkaline phosphatase and lactate dehydrogenase (LDH) levels, in the absence of changes in overall renal function, extracellular mineral homeostasis [serum protein-corrected total calcium, magnesium, parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (1,25(OH)2D)], plasma glycolate and oxalate levels. There was a redistribution of bone calcium and enhanced exchange of this within the extraosseous space, which was accompanied by significant bone calcium loss, but normal bone histomorphometry. Liver oxalate levels, if expressed per unit of defatted (DF) dry liver, were three times higher than in the controls. Urinary glycolate, oxalate, calcium and total protein excretion levels were elevated, the latter showing an excess of proteins > 100 kD and a deficit of proteins > 30-50 kD. Urinary calcium oxalate supersaturation was increased, and calcium phosphate supersaturation was unchanged. There were dramatically increased (by number, circumference, and area) renal calcium phosphate calcifications in the cortico-medullary region, but calcium oxalate deposits were not detectable. Electron microscopy (EM) and elemental analysis revealed intratubular calcium phosphate, apparently needle-like hydroxyapatite. Immunohistochemistry of renal tissue calcifications revealed co-localization of phospholipids and calcium phosphate. It is concluded that rats fed the CH-F diet exhibited: (1) a spectrum of metabolic abnormalities, the more prominent being dyslipidemia, hyperoxaluria, hypercalciuria, dysproteinuria, loss of bone calcium, and calcium phosphate nephrocalcinosis (NC); and (2) an interaction between calcium phosphate and phospholipids at the kidney level. The biological significance of these findings for the etiology of idiopathic calcium urolithiasis in humans is uncertain, but the presented animal model may be helpful when designing clinical studies.
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PMID:Nephrocalcinosis and hyperlipidemia in rats fed a cholesterol- and fat-rich diet: association with hyperoxaluria, altered kidney and bone minerals, and renal tissue phospholipid-calcium interaction. 1122 20


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