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

To better understand the pathogenesis of nephrolithiasis, we developed a new animal model that closely mimics human calcium oxalate stone disease. Rats were treated with a regimen that combines moderate hyperoxaluria (produced by 10 days of feeding with 3% ammonium oxalate) with mild proximal tubular injury/dysfunction (produced by 8 daily injections of gentamicin sulfate -40 mg./kg.). This combined treatment caused a marked increase in the incidence of calcium oxalate crystals and stones over that seen in animals treated with oxalate or gentamicin alone. Using a semiquantitative scoring system for estimating the abundance of crystals in coronal sections of kidneys, we found that 63% of animals receiving gentamicin plus oxalate showed "moderate" numbers of crystal, as compared to 8% of animals receiving oxalate alone; and the majority of the crystals occurred in the papilla, a pattern similar to that seen in human stone disease. Untreated rats and rats treated with gentamicin alone did not exhibit calcium oxalate crystals or stones. Despite the abundance of crystals and stones, animals receiving gentamicin plus oxalate retained relatively normal renal function as judged by creatinine clearance. Thus, the model has several advantages over preexisting models of nephrolithiasis. Crystal and stone deposition develop rapidly (within 14 days). The pattern of deposition resembles that seen in human stone disease and renal function remains relatively normal. These findings indicate that this model of nephrolithiasis may prove useful for studies of the pathogenesis of stone disease. Moreover, they suggest that renal tubular injury and/or dysfunction may produce conditions conducive to the formation and growth of calcium oxalate stones.
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PMID:A new model of nephrolithiasis involving tubular dysfunction/injury. 194 7

Nephrolithiasis is a heterogeneous disorder, with varying chemical composition and pathophysiologic background. Although kidney stones are generally composed of calcium oxalate or calcium phosphate, they may also consist of uric acid, magnesium-ammonium phosphate, or cystine. Stones develop from a wide variety of metabolic or environmental disturbances, including varying forms of hypercalciuria, hypocitraturia, undue urinary acidity, hyperuricosuria, hyperoxaluria, infection with urease-producing organisms, and cystinuria. The cause of stone formation may be ascertained in most patients using the reliable diagnostic protocols that are available for the identification of these disturbances. Effective medical treatments, capable of correcting underlying derangements, have been formulated. They include sodium cellulose phosphate, thiazide, and orthophosphate for hypercalciuric nephrolithiasis; potassium citrate for hypocitraturic calcium nephrolithiasis; acetohydroxamic acid for infection stones; and D-penicillamine and alpha-mercaptopropionylglycine for cystinuria. Using these treatments, new stone formation can now be prevented in most patients.
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PMID:Etiology and treatment of urolithiasis. 196 46

Male Sprague-Dawley rats were challenged with various hyperoxaluric agents including ammonium oxalate, hydroxy-L-proline, and ethylene glycol. All treatments resulted in increased urinary oxalate. Associated with hyperoxaluria was an increase in urinary levels of renal enzymes, gamma-glutamyl transpeptidase, N-acetyl-beta-glucosaminidase, and alkaline phosphatase. Most of the rats did not demonstrate any significant change in urinary levels of beta-galactosidase. There was a highly significant positive correlation between urinary oxalate and N-acetyl-beta-glucosaminidase.
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PMID:Urinary enzymes and calcium oxalate urolithiasis. 257 Jan 67

An 8-year-old boy who had suffered from recurrent stone formation since the age of 4 years, was admitted as an emergency due to anuria for a half day on November 20, 1986. Kidney-ureter-bladder film showed that the urethra was obstructed by a stone, and emergent cystoscopy was performed to remove it. He is the product of consanguinous marriage, his parents being first cousins. There was no family history of renal stone. Laboratory investigations showed hypokalemic, hyperchloremic metabolic acidosis. The ammonium chloride loading test revealed inability to acidify the urine and a markedly decreased excretion of titrable hydrogen ion and ammonium ion in the urine. These results indicate that this is a case of Type I renal tubular acidosis. His 24-hour urinary excretion of oxalate and glyoxylate were also markedly increased. There were no underlying causes leading to the development of secondary hyperoxaluria. These results also establish the diagnosis of Type I primary hyperoxaluria. The patient then received regimens of Polycitra 1ml/kg/day and Vitamin B6 50mg/day for 4 months. However, urinary stone developed again in this patient 4 months later. To our knowledge, Type I primary hyperoxaluria in association with Type I renal tubular acidosis has not been previously reported.
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PMID:Type I primary hyperoxaluria associated with type I renal tubular acidosis. 344 74

The increasing incidence of urolithiasis makes it important to report about 34 children with urolithiasis seen between 1976 and 1986 at the Department of Pediatrics, University Medical School Vienna. At the time of the first diagnosis 59 percent of the patients were less than 7 years of age; 62 percent of our patients were males. Recurrent chronic urinary tract infection in 32 percent, metabolic disorder (secondary hyperoxaluria 5, idiopathic hypercalciuria 3, cystinuria 2, hyperuricuria 2) in 27 percent were evaluated; in 13 patients the origin of calculi was idiopathic. Most infectious stones contained magnesium ammonium phosphate, most idiopathic stones calcium oxalate. In 21 patients (62%) surgical treatment, in one patient extracorporal shock wave lithotripsie was realized. Adequate metaphylaxis (general, dietetic, medicementous) can lower the rate of occurrence of stone formation.
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PMID:[Urolithiasis in pediatrics: analysis of 34 patients]. 368 52

Fifty-two cases of urinary tract calculus disease were investigated for dietary habits, routine chemical and microscopic urinalysis, bacterial culture, quantitative analysis of 24 h urine sample and qualitative analysis of the stones. 54 out of the 56 stones analysed were of mixed type. Magnesium ammonium phosphate was present in 78.2% stones. Dietary habits revealed principal dependence on cereals, lack of animal proteins, consumption of oxalate rich vegetables and widespread consumption of tea. Urinary tract infection was present in 63.7% of the cases. Significant calcium oxalate crystalluria (2+ to 4+) was present in 34.6% of the cases. Hyperoxaluria, hypercalciuria associated with hyperoxaluria-lower excretion of magnesium and citric acid were important urinary risk factors in the local population. These observations strongly suggest the multifactorial etiology of stone disease in this region. Imbalanced nutrition and urinary tract infection were the principal risk factors for urolithiasis in this study.
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PMID:The etiology of urolithiasis in Udaipur (western part of India). 372 15

Nine cases of the distal type of renal tubular acidosis (RTA) following intestinal bypass were found. Diagnosis was based on inability to acidify the urine to pH values below 5.40 despite systemic acidosis. Acidosis, if not present, was induced by giving ammonium chloride 0.1 g/kg body weight. Patients were examined for diseases known to cause RTA but no already known etiological factor was found. Hyperoxaluria was found in eight of the nine cases with RTA, while not present in patients without RTA or in obese control patients. A causal relationship between hyperoxaluria and RTA is suggested though not proved. Cases reported in the literature of renal damage following bypass are summarized and discussed in relation to presence of hyperoxaluria and RTA.
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PMID:Renal tubular acidosis following intestinal bypass: an etiological study. 672 97

The aetiology of nephrolithiasis was investigated in 32 north Indian children (25 boys, 7 girls, mean age 7.9 +/- 3.3 years). An underlying disorder was detected in 16 (50%) patients and included idiopathic hypercalciuria (8 patients), hyperoxaluria (3 patients) and renal tubular acidosis, primary hyperparathyroidism and hyperuricosuria (1 patient each). Magnesium ammonium phosphate calculi were found in 2 patients with recurrent urinary tract infections, 1 of whom had a duplex pelvic collecting system. In 16 patients (50%) a cause for renal calculi was not identified. Our findings suggest that an underlying disorder is present in a large proportion of children with nephrolithiasis where appropriate treatment may be beneficial.
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PMID:Aetiology of nephrolithiasis in north Indian children. 757 12

Fifty-five Tunisian children with urinary stones, between the ages of 8 months and 15 years, underwent morphological and infrared spectrophotometric analysis of their stones. This study provides an approach to the aetiological profile of urinary stones in Tunisian children. The nucleus of the stones was composed of acidic ammonium urate in 48% of cases with a morphology suggestive of phosphorus deficiency associated with a history of diarrhoea. In 24% of cases, the nucleus contained struvite indicating the presence of urinary tract infection by urease-positive bacteria. The main growth factors of urinary stones were hyperoxaluria and urinary tract infection. In 5 cases, the stones were due to a hereditary lithogenic metabolic disease : cystinuria in 1 case and primary hyperoxaluria in 4 cases.
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PMID:[Etiologic factors of urinary lithiasis in Tunisian children]. 877 1

The in vivo effect of cyclosporin A (CsA) on renal calcium oxalate (CaOx) crystal retention in experimental hyperoxaluric rats was investigated. Further, the effect of pretreatment of vitamin E on the above conditions was also studied. Male Wistar rats were divided into two major groups each containing 40 rats. One of the groups was pretreated with vitamin E. Both major groups were then subgrouped into four groups: group 1 received the vehicle (olive oil); group 2 received CsA in olive oil (50 mg/kg); group 3 received 3% ammonium oxalate (AmOx), and group 4 received CsA + AmOx. Nephrotoxicity was assessed by the activities of urinary marker enzymes and also by histopathology. Urinary oxalate excretion as well as the activities of lactate dehydrogenase, gamma-glutamyltranspeptidase, alkaline phosphatase and inorganic pyrophosphatase enzymes were elevated either in CsA-alone or AmOx-alone treated groups. On combined administration of both CsA and AmOx, further elevations of these enzymes were observed. Urinary excretion of oxalate concentration positively correlated with urinary excretion of these enzymes. Deposition of CaOx crystals was seen only in the kidneys of rats that received combined treatment. On pretreatment with vitamin E the observed increased urinary activities of the enzymes and oxalate, histopathological changes and the deposition of CaOx crystals by administration of CsA in hyperoxaluria were prevented suggesting that vitamin E could be supplemented to prevent CsA-induced membrane damage.
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PMID:Vitamin E pretreatment prevents cyclosporin A-induced crystal deposition in hyperoxaluric rats. 903 Dec 74


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