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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

Clinical studies suggest that steatorrhoea can be associated with excessive absorption of dietary oxalate. We examined the influence of bile salts, Ca++, and long-chain fatty acid on the absorption of oxalate and water by rat intestine in vivo. Absorption was measured under steady-state conditions during single-pass infusions. Each intestinal segment served as its own control. In jejunum, 10 mM taurocholate, the principal salt in rat bile, depressed absorption of oxalate and water. Absorption was not depressed further by Ca++ or linoleic acid. In ileum, 10 mM taurocholate did not inhibit absorption. Linoleic acid, 2 mM, depressed absorption of both oxalate and water. In colon 10 mM taurocholate decreased absorption. Net water transport was depressed further when linoleic acid was added to the infusion, but oxalate absorption was enhanced. Ca++ negated these effects of linoleic acid. It is concluded that long-chain fatty acids may enhance the absorption of oxalate from the rat colon. This observation may be relevant to understanding hyperoxaluria in patients with steatorrhoea.
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PMID:Regional differences in oxalate absorption by rat intestine: evidence for excessive absorption by the colon in steatorrhoea. 115 92

These studies were designed to evaluate the effect of bile salts and fatty acids on colonic oxalate absorption. Five millimolar deoxycholate significantly increased oxalate absorption from 34.2 +/- 9.4 nmoles per min per g dry weight to 330.4 +/- 47.3 (P less than 0.001) and changed water absorption to water secretion. Deoxycholate also increased the absorption of urea, decreased the electrical potential difference, and increased colonic clearance of oxalate, observations which are consistent with an increase in colonic mucosal permeability. In contrast, taurocholate did not increase oxalate absorption. Ricinoleic acid also significantly increased the absorption. These results suggest that bile salts and fatty acids increase colonic absorption of oxalate. Oleic acid had similar effects on oxalate absorption but was less effective than ricinoleic acid. Octanoic acid, a medium chain fatty acid, did not alter oxalate absorption of oxalate by a nonspecific alteration of mucosal permeability. These observations may further explain many of the clinical phenomena associated with enteric hyperoxaluria.
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PMID:Effect of bile salts and fatty acids on the colonic absorption of oxalate. 126 69

A case of massive ingestion of ethylene glycol is described. The clinical characteristics of this disorder such as persistent metabolic acidosis and oxaluria as well as changes in serum osmolality that may accompany ingestion of certain toxins are emphasized. The rapid clearance of ethylene glycol from the blood during hemodialysis is noted and the use of ethyl alcohol to block metabolic conversion of ethylene glycol to oxalic acid, which is also a toxin, is described. The importance of early diagnosis and therapy is stressed.
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PMID:"Bicarbonate resistant" metabolic acidosis in association with ethylene glycol intoxication. 127 68

A case is presented in which primary hyperoxaluria and oxalosis in a 14-year-old Caucasian female were diagnosed. Generalized root resorption resulted in a remarkable mobility of her maxillary central and lateral incisors, although no bone loss was noted. The management of the patient's dental concerns in this rare heritable metabolic disorder consisted of removing the maxillary incisor teeth and placing two sequential prostheses, which the patient tolerated well. A history of trauma to the maxillary incisors was ruled out, so this case adds previously unreported information to our knowledge about the effect of oxaluria on teeth and oral tissues.
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PMID:Primary hyperoxaluria in a pediatric dental patient: case report. 130 27

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

Hyperoxaluria is frequently seen in patients with inflammatory bowel disease, or after resection of the ileum. It is assumed to be responsible for the development of nephrolithiasis, nephrocalcinosis (oxalate nephrosis) and progressive renal impairment in these patients. Steatorrhea may aggravate the severity of hyperoxaluria. A 60-year-old male underwent massive resection of the jejunum and ileum 10 years prior to admission, due to strangulation of the small bowel, with occlusion of the superior mesenteric artery. He remained well except for steatorrhea which developed two-and-a-half years prior to admission, when microhematuria, proteinuria and oxaluria developed progressively. Since that time, the nephrolithiasis, nephrocalcinosis and renal failure have continued to worsen despite therapy with oxalate restriction and oxalate-binding agents. A renal biopsy, performed late in the clinical course, showed severe changes in the renal parenchyma. The decline in renal function proved irreversible. The unusual metabolic consequences of massive resection of the small intestine and their mechanisms are discussed.
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PMID:Hyperoxaluria, nephrolithiasis, nephrocalcinosis and renal failure after massive resection of the small intestine: report of a case. 136 95

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

The characteristics of nonspecific immunity were studied on an outpatient material of 80 non-smoking women aged 38-60 years, with manifestations of hereditary primary enzymopathy (hyperoxaluria syndrome). Hyperoxaluria was shown to be related to immunologic imbalance of some components of nonspecific resistance by the cellular and humoral type. In addition to biochemical differences, the group of patients with prognostically favourable chronic asthmatic bronchitis have got immunologic differences with the alternative group.
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PMID:[Asthmatic bronchitis as the first manifestation of secondary immunodeficiency in hereditary enzymopathy in women]. 144 Feb 77


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