Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We prospectively studied 15 infants who, before 3 months of age, underwent resection of the small intestine-proximal in 3 infants, mid in 6, and distal in 6. Two died before one year of age. Many required prolonged parenteral nutrition, but by one year, 12 of the 13 survivors were on oral feedings only, and seven were above the third percentile for height and weight. Developmental delay occurred in the early postoperative period but diminished with time. There was compensatory adaptation of the remaining gut, shown by improving fat and B12 absorption and duodenal bile-salt concentrations. Bacterial contamination complicating end-to-side anastomoses occurred in two cases (P), gastric hyperacidity in four of 12 (1P, 3M), and hyperoxaluria in eight of 14 (1P, 5M, 2D). Studies of immune competence revealed normal cellular immune function (11/11), transient hypogammaglobulinemia (3/14), hypocomplementemia (1/12), and serum autoantibodies (3/10). Thus, massive resection of the small intestine did not preclude spontaneous improvement in absorptive function, growth, and development.
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PMID:A clinical study of young infants after small intestinal resection. 10 3

Urinary oxalate excretion was studied in healthy subjects and before and after surgery in patients with Crohn's disease. Urinary oxalate excretion in relation to the length of diseased or resected ileal segment in patients subjected to restorative and colectomy procedures, as well as in relation to faecal excretion of fat and bile salts and to urinary excretion of vitamin B12 and calcium, was also studied. The studies were performed in patients on a free diet or standard hospital diet and on a high-oxalate and/or high-fat diet. When patients subjected to ileal resection in conjunction with minor colonic resection were studied on a high-oxalate diet, urinary oxalate excretion increased with length of ileum resected and correlated with faecal fat excretion and urinary excretion of vitamin B12 but not with faecal excretion of bile salts. Increasing the dietary fat intake in these patients further increased urinary oxalate excretion. Although urinary oxalate excretion increased somewhat in colectomized patients on a high-oxalate diet, indicating an increased absorption of dietary oxalate, this increase showed no correlation either to faecal fat or bile salt excretion, or to urinary excretion of vitamin B12. The result are consistent with the "solubility theory". A diet low in fat and oxalate and high in calcium is recommended in patients with hyperoxaluria.
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PMID:Urinary oxalate excretion related to ileocolic surgery in patients with Crohn's disease. 67 58

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

Previous studies have provided evidence that an anaerobic bacterium, which degrades dietary oxalate to CO2 and formate, is present in colonic contents of a number of herbivorous species, laboratory rodents and humans. The present study examines the possibility that these bacteria degrade significant amounts of oxalate and can influence colonic oxalate absorption. Guinea pigs adapted to a diet containing 2% sodium oxalate or fed a normal diet were challenged with 67, 135, 170 or 200 mg of sodium oxalate containing 0.5 microCi of [14C]oxalate, which was injected into the cecum. Adapted animals excreted approximately 2% of the 14C in the urine, regardless of the dose, whereas unadapted animals excreted significantly higher amounts in the urine at the two lower doses and died at the two higher doses. Conversely, antibiotic treatment of adapted guinea pigs reduced the ability of their cecal flora to degrade oxalate, and a correspondingly greater percentage of an injected oxalate load was excreted in the urine. Oxalate degradation rates in cecal fluid were depressed by the secondary bile salt deoxycholate, and in vitro studies with pure isolates of guinea pig and human strains of oxalate degraders confirmed that these bacteria were highly sensitive to low concentrations of deoxycholate. Results indicate that these bacteria may be important in preventing excess absorption of oxalate and raise the possibility that the hyperoxaluria associated with bile salt malabsorption of ileal disease in part may be due to suppression of these bacteria by the bile salts.
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PMID:Intestinal oxalate-degrading bacteria reduce oxalate absorption and toxicity in guinea pigs. 337 43

Pyridoxilate is a salt formed from glyoxylic acid and pyridoxine. It has been used therapeutically as an antianoxic drug in the treatment of various arterial complaints. Its use is based theoretically on its ability to block the conversion of glyoxylic acid into oxalic acid. The following cases suggest, however, that pyridoxilate can cause stones. Intraperitoneal injection of glyoxylate in doses of 130 mg/kg will cause oxalate stones in rats. The same effect results from injection of 427 mg/kg pyridoxilate (i.e. an equivalent dose of glyoxylate). In human subjects, intravenous injection of 200 mg of pyridoxilate results in a fourfold increase in the urinary oxalic acid content in the two hours following the injection. Thirteen cases of chronic progressive oxalate stone disease have recently been reported in patients receiving a prolonged course of pyridoxilate at 450 to 600 mg daily. Eight of these patients had no previous history of lithiasis. Oxaluria levels of 80 to 100 mg daily are observed in all cases of lithiasis in patients receiving pyridoxilate. The levels fell after cessation of the pyridoxilate treatment, and reverted to normal (30 mg/24 hours) in all but three patients. These three patients maintained levels of close to 50 mg and all three had a previous history of urolithiasis.
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PMID:[Calcium oxalate stones and hyperoxaluria secondary to treatment with pyridoxilate]. 408 39

The effects of clofibrate feeding (5 g/kg diet) on oxalate metabolism were investigated in male and female rats. Following clofibrate feeding, 24-hour urinary excretion of oxalate increased until 4 days and then reached a plateau. Whereas the contribution of dietary oxalate (1.4 g/kg diet, as potassium salt) to urinary oxalate was less than 5% in both control and clofibrate-treated male rats, the contribution of dietary glycolate (1.0 g/kg diet, as sodium salt) to urinary oxalate was six times higher in clofibrate-treated male rats compared with controls, indicating that the clofibrate-induced hyperoxaluria is due to increased endogenous biosynthesis of oxalate. This was supported by the increased lactate dehydrogenase (LDH) activity observed in liver supernatants of clofibrate-treated rats compared with controls, and the increased rate of conversion of glycolate and glyoxylate to oxalate by clofibrate-treated male rat liver supernatants. Female rats had lower excretion of urinary oxalate and lower levels of liver glycolic acid oxidase (GAO) as compared with males. Clofibrate-treated female rat liver supernatants had higher LDH levels and produced more oxalate from glyoxylate. Thus, it can be concluded that the increase in LDH activity may be the cause of the increased endogenous biosynthesis of oxalate leading to increased urinary excretion of oxalate in male and female rats treated with clofibrate.
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PMID:Clofibrate feeding to Sprague-Dawley rats increases endogenous biosynthesis of oxalate and causes hyperoxaluria. 903 Aug 17

Nephrolithiasis is uncommon after kidney transplantation. However, calcium (Ca) supplementation, which has been proposed as a treatment of post-transplant osteopenia, might increase calciuria and bolster Ca stone formation. Therefore, in 24-hour urine of 82 normocalcemic long-term renal transplant recipients (RT) and in 82 healthy subjects (HS), we assessed some Ca nephrolithiasis risk factors and the Ca-salt saturation estimated by the ion-activity product index (AP) and relative supersaturation (RS). In RT, calciuria was lower (mean +/- SD, 3.20 +/- 2.25 vs. 4.61 +/- 1.71 mmol/day; P < 0.001), urinary volume higher (2.41 +/- 0.83 vs. 1.39 +/- 0.53 liter/day; P < 0.001), oxaluria higher (419 +/- 191 vs. 311 +/- 79 mumol/day; P < 0.001) and citraturia lower (1.40 +/- 1.36 vs. 3.77 +/- 1.36 mmol/day; P < 0.001) than in HS. As a result, Ca-oxalate supersaturation was lower in RT than HS (AP, 1.07 +/- 0.69 vs. 2.07 +/- 1.13, P < 0.001; and RS, 0.62 +/- 0.26 vs. 0.94 +/- 0.21, P < 0.001), and was similar in subgroups of RT (N = 37) and HS (N = 37) matched for urinary volume, demonstrating that even without any larger urinary volume, Ca-oxalate saturation was not higher in RT than HS, and suggesting that opposite changes in Ca and oxalate in RT likely canceled their effects on lithogenic risk. In RT which had similar urinary pH and phosphate (P) than HS, Ca-P supersaturation was lower than in HS for brushite (AP, 3.25 +/- 6.67 vs. 6.01 +/- 4.85, P < 0.001; RS, -0.33 +/- 0.76 vs. 0.48 +/- 0.53, P < 0.001) and octacalcium phosphate (RS, -0.95 +/- 0.72 vs. 0.21 +/- 0.85, P < 0.001), and similar for apatite. Finally, fasting calciuria and calciuric response to a single oral Ca load were similar in RT (N = 19) and HS (N = 8). Together, these results argue strongly against a higher risk of Ca stone formation in RT than HS, even in case of Ca supplementation.
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PMID:Lack of increased urinary calcium-oxalate supersaturation in long-term kidney transplant recipients. 906 14

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

The primary care physician has a responsibility not only to recognize and treat acute stone passage but to ensure that the patient with recurrent stones has metabolic evaluation and appropriate preventive care. Renal colic is typically severe, radiates to the groin, is associated with hematuria, and may cause ileus. About 90% of stones that cause renal colic pass spontaneously. The patient with acute renal colic should be treated with fluids and analgesics and should strain the urine to recover stone for analysis. Highgrade obstruction or failure of oral analgesics to relieve pain may require hospitalization; a urinary tract infection in the setting of an obstruction is a urologic emergency requiring immediate drainage, usually with a ureteral stent. Several approaches are available when stones do not pass spontaneously, including extracorporeal shock wave lithotripsy, percutaneous lithotripsy, and ureteroscopic laser lithotripsy. Calcium stone disease has a lifetime prevalence of 10% in men and causes significant morbidity. Renal failure is unusual. Stone types include calcium oxalate, uric acid, struvite, and cystine. Stone analysis is particularly important when a noncalcareous constituent is identified. The majority of patients with nephrolithiasis will have recurrence, so prevention is a high priority. High fluid intake is a mainstay of prevention. Metabolic evaluation will indicate other appropriate preventive measures, which may include dietary salt and protein restriction, and use of thiazide diuretics, neutral phosphate, potassium citrate, allopurinol, and magnesium salts. Dietary calcium restriction may worsen oxaluria and negative calcium balance (osteoporosis).
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PMID:Nephrolithiasis: acute management and prevention. 965 69


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