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

Of 93 patients with small bowel bypass for massive exogenous obesity, three developed calcium oxalate urinary calculi, four stones in their gallbladder, and one developed both gallstones and urinary calculi during a mean follow-up period of 17.6 plus or minus 9.0 months. The urinary oxalate excretion increased from 21.6 to 67.8 mg/24 hours (P smaller than .001); simultaneously, the urinary output decreased from 1,775 to 1,101 ml/24 hours (P smaller than .001). Postoperatively, there was a significant increase in the rate of bile salt synthesis from 1.6 to 4.9 gm/day (P smaller than .02) and in the bile sale glycine/taurine ratio from 4.6 to 6.8 (P smaller than .05). It is suggested that the postbypass increase in the biliary glycine/taurine ratio, with its consequent decrease in the zeta potential of the micelles in bile, is at least partly responsible for the increased incidence of cholelithlasis. The pathogenic basis for the increased incidence of urinary calculi is hyperoxaluria, which is probably related to an increased bile salt and glycine synthesis.
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PMID:Biliary and urinary calculi: pathogenesis following small bowel bypass for obesity. 115 48

The effect of calcium concentration (0-10 mmol 1(-1)) on oxalate uptake and transport was investigated in vitro using everted gut segments and sacs. Increase in calcium concentration in the incubation medium led to an increase in the amounts of precipitated oxalate on the intestine; however, the net oxalate flux to the serosal side decreased. The ions, i.e. Ca2+, Ox2-, H2PO4-, HPO4(2-), present in the incubation medium favoured formation of hydroxyapatite and calcium oxalate crystals, as evidenced by Equil II analysis and free energy of the system. The nature of precipitates was confirmed by elemental analysis, X-ray diffraction spectrometry and electron microscopy. Oxalate precipitated on the intestine following incubation with calcium could be released into a calcium- and oxalate-free medium. Animals fed oxalate in the absence and presence of calcium revealed that, during 1 h in the absence of calcium, oxalate moved down the intestinal tract as a distinct peak of greater than 50% (70-90 cm in the intestine), leaving less than 10% in the stomach and first 50 cm of the intestine. In the case of animals fed calcium along with oxalate, 35% of the oxalate was still present in the stomach, and the amounts of oxalate in the intestinal segments gradually increased from 4.5% to 21.7% (0-90 cm) and dropped to 2.1% in the next 20 cm. Since oxalaemia and oxaluria appear to be influenced by intestinal oxalate absorption, the present observations may help to improve understanding of the pathophysiology of disorders exhibiting altered oxalate metabolism.
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PMID:Effect of calcium on oxalate uptake and transport by the rat intestine. 133 82

Abnormal dietary habits that lead to hypercalciuria, hyperoxaluria, hypereruricosuria, and hypocitraturia do not always result in nephrolithiasis. A concept is emerging according to which, to account for renal stone formation in the face of the aforementioned biochemical disorders, one must search for underlying conditions in patients with the disease. Work carried out over the past few years and reviewed herein definitely supports this idea and includes the following processes: 1) interleukin-1 production by monocytes to augment the impact of dietary hypercalciuria; 2) disturbed activation of pyridoxine to pyridoxal 5'-phosphate to aggravate dietary hyperoxaluria; 3) abnormal intestinal transport of citrate to aggravate dietary hypocitraturia; 4) molecular abnormalities of glycoprotein inhibitors to aggravate the promotive effect of the diet on urinary crystallization; and 5) renal tubular lesions to favor particle retention and stone formation. This article reviews the most recent literature and discusses the author's "powder keg and tinderbox" theory of idiopathic calcium stone disease.
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PMID:Renal stone disease in the 1990s: the powder keg and tinderbox theory. 136 43

We report the case of a 31-year-old patient who underwent combined liver and kidney transplantation for primary hyperoxaluria type I. Intensive hemodialysis was performed before the intervention and post-operatively in order to maintain plasma oxalate levels near the normal range. In spite of the correction of the liver enzyme deficiency, oxalate removal from the tissular stores led to prolonged hyperoxaluria, more longer than one year after the transplantation, as already reported. This increased urinary oxalate excretion exposes the renal graft to the risk of recurrence of calcium oxalate deposits and stone formation during a prolonged period. Hemodialysis in the postoperative period and fluid intake allowing a large urine volume might be able to decrease the concentration of urinary oxalate under the critical value of 300 mumol/l, at which supersaturation of urine in respect of calcium oxalate occurs.
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PMID:Combined liver kidney transplantation in primary hyperoxaluria type I. Prevention of the recidive of calcium oxalate deposits in the renal graft. 139 63

In idiopathic recurrent calcium urolithiasis (RCU) in men (n = 37) the metabolic effects of oral tripotassium citrate (PC) were investigated in a longitudinal field study. The patients were either normo- (n = 22) or hypocitraturic (n = 15). Laboratory examinations were performed before, and after 3, 6, and more than 12 months of medication. Acceptance of PC was poor, mainly because of the salty taste of the tablet preparation chosen, and a number of participants dropped out of the study. In the remaining participants, compliance was acceptable when evaluated on the basis of urinary potassium and undesired side effects did not occur. In the short term (up to 3 months), PC evoked compensated metabolic alkalosis (pH and citrate in urine increased; blood gases remained normal), a drop in urinary calcium, together with increasing oxaluria, hydroxyapatite supersaturation, and calcium phosphate crystalluria. In the long term (greater than 12 months) PC urinary pH and citrate "dissociated", in that pH returned to pretreatment baseline values, whereas citrate stayed at high levels. In normocitraturics but not in hypocitraturics, urinary urea and sodium increased with PC. Hypocitraturics appeared to be less sensitive to the effects of PC, as reflected by the relatively small rise in urinary pH and citrate, and they maintained higher mean levels of indicators of bone metabolism (osteocalcin, alkaline phosphatase, hydroxyproline) despite continuous administration of PC. It was concluded that although the PC tablet preparation was effective it may not be an ideal anti-stone drug treatment in the long term and that, especially in hypocitraturics, the intrinsic metabolic defect of RCU may not be sufficiently well controlled.
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PMID:Citrate and recurrent idiopathic calcium urolithiasis. A longitudinal pilot study on the metabolic effects of oral potassium citrate administered over the short-, medium- and long-term medication of male stone patients. 155 90

Population based data on 24-h urinary excretion of calcium, oxalate, magnesium, phosphate, uric acid and creatinine were collected from 220 children (aged 3-16 years) living in Cimitile, Campania, southern Italy. Mean excretion rates for 7 days were correlated with age, body weight, body mass index and height. The prevalence of hypercalciuria (greater than 4 mg/kg body weight) and of hyperoxaluria (greater than 60 mg/day) were 9.1% and 1.8%, respectively. The same 20 children were also identified as hypercalciuric when a calcium/creatinine ratio of greater than 0.15 was considered. No significant differences between boys and girls were found in the urinary excretion of the five constituents implicated in urolithiasis. The study data provide additional childhood reference values for urinary excretion of compounds related to stone formation.
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PMID:Population based data on urinary excretion of calcium, magnesium, oxalate, phosphate and uric acid in children from Cimitile (southern Italy). 157 Dec 11

A small group of patients with nephrolithiasis who forms mixed (calcium oxalate and uric acid) calculi presents particular problems in their clinical management. In 3,158 stones analyzed in our laboratory, we found 158 mixed calculi in 86 of the patients. In this work, the clinical and biochemical results obtained from 27 patients with mixed stones were compared with those from 27 control patients with calcium oxalate renal lithiasis. A significant difference was found in oxalate and citrate urinary elimination (mean +/- SD) in mixed stone formers versus pure calcium oxalate stone formers: oxaluria (mg/24 h: 38 +/- 15 vs. 28 +/- 12; p less than 0.01) and citraturia (mg/24 h: 214 +/- 139 vs. 437 +/- 303; p less than 0.01). Citraturia was decreased in a high proportion (77%) in mixed stone formers, and only a reduced percentage of them (23%) presented normal values, although in the low limit of normality. As treatment and prophylactic measure, we proposed oral administration of citrates in mixed stone patients because citrate inhibits spontaneous nucleation of calcium salts and crystal growth, and it also increases the urinary pH with a consequent increase in uric acid solubility.
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PMID:Hypocitraturia as a pathogenic risk factor in the mixed (calcium oxalate/uric acid) renal stones. 158 30

A 58-year-old female patient admitted to hospital for advanced renal failure had a 40 years' history of Crohn's disease and had undergone ileocecal resection. Nevertheless, chronic diarrhea persisted. Subsequently calcium oxalate stones in the urine were repeatedly observed. Progressive renal failure developed. The investigation of the patient showed severe steatorrhea and pronounced hyperoxaluria, and renal biopsy showed severe chronic interstitial nephritis with calcium oxalate crystals. The skin biopsy revealed severe calcium oxalate vasculitis. The pathophysiology and therapy of secondary hyperoxaluria due to small bowel resection are discussed.
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PMID:[Secondary oxalosis following small bowel resection with kidney insufficiency and oxalate vasculopathy]. 160 91

Recently a technique to measure intact parathyroid hormone (PTH), i.e. the biologically active hormone, has been available. The aim of the present study was to apply this method to evaluate the parathyroid function in a material of recurrent renal stone formers (n = 324). Intact PTH was found to be inversely related to both urinary calcium (r = -0.15; p less than 0.01) and serum calcium (p less than 0.02) indicating that in the majority of the patients with hypercalciuria this was accounted for by intestinal hyperabsorption and not by high serum PTH. Hyperabsorption was also the likely explanation for the finding of a positive relationship between the urinary calcium and oxalate excretions (r = 0.22; p less than 0.001) in medication-free patients without intestinal disorders, i.e. without enteric hyperoxaluria. Altogether 25 patients (7%) had elevated serum PTH concentrations. They were followed up with fasting serum and urinary electrolytes and an oral calcium loading test (1 g of calcium) in order to evaluate the importance of renal and intestinal factors responsible for the elevated serum PTH concentrations. The investigation was carried out on a free diet and on low and high calcium intakes, respectively. The incidence of intestinal malfunction, which was sometimes present without clinical symptoms, was found to be approximately the same as that of impaired renal conservation of calcium. The findings in the patients with intestinal malfunction were a reduced intestinal absorption of calcium and an enhanced tubular reabsorption of calcium (TRCa), with greater reabsorption of calcium for higher PTH values. In patients with impaired renal conservation of calcium despite the raised PTH there was no correlation between PTH and TRCa. When PTH was suppressed during the oral calcium load the TRCa was found to be inappropriately low and the renal defect obvious. The intestinal calcium absorption was secondarily increased to compensate for the renal losses.
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PMID:Parathyroid function in relation to intestinal function and renal calcium reabsorption in patients with nephrolithiasis. 163 8

Administration of ascorbic acid, at 150 mg/100 ml of water intake, for one month, induced hyperoxaluria in the rats (P less than 0.001) and decreased citraturia (P less than 0.001) magnesuria (P less than 0.001) and pyrophosphaturia (P less than 0.01). The same disorders were observed when the dose administered was 300 mg/100 ml, excepted that oxaluria was considerably enhanced in this group. Despite these variations, renal deposits were not observed, even in the animals receiving 300 mg of ascorbate/100 ml of water intake. This protection was due to decreased calcium excretion (P less than 0.01 in two groups) and probably to acidification of the urine.
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PMID:[The effects of high-dose ascorbic acid administration on the factors of lithogenesis in the rat]. 166 24


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