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

The role of the kidney in states of hyperoxaluria and hypercalciuria was investigated in seven patients with hyperoxaluria after jejunoileal bypass (JIB) and six patients with idiopathic hypercalciuria (IHC). Eight apparently healthy persons formed a control group. Besides hyperoxaluria, the patients with JIB displayed an elevated plasma concentration of oxalate and the oxalate clearance was increased and higher than creatinine clearance, indicating a net tubular secretion of oxalate. The JIB patients had lower 24-h urinary excretions of calcium, phosphate, magnesium and citrate and higher serum parathyroid hormone (PTH) than controls, indicating increased secretion of PTH to compensate for calcium malabsorption. IHC patients exhibited increased fasting urinary calcium even though their serum values were similar to those in the controls. These results indicate a reduced tubular calcium reabsorption, which was most pronounced in patients with highest PTH values. We conclude that hyperoxaluria in JIB patients is associated both with intestinal hyperabsorption and with enhanced tubular secretion of oxalate, and that in some patients with IHC hypercalciuria is due to reduced tubular reabsorption of calcium.
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PMID:Hyperoxaluria or hypercalciuria in nephrolithiasis: the importance of renal tubular functions. 212 87

Seventeen hypercalciuria patients (8 control, 9 treatment) with a history of urolithiasis were randomly selected to receive low-calcium, low-oxalate diets with or without the addition of 30 g of dietary fiber as unprocessed wheat bran. Diet alone resulted in a 5.6 percent decrease in calciuria compared with a 23.5 percent decrease with the addition of the fiber. The addition of hydrochlorothiazide and potassium citrate further reduced calciuria by 40.4 percent and 34.5 percent, respectively. Oxaluria was decreased 21.4 percent by diet alone compared with 3.9 percent in the diet and fiber treatment group. Patient compliance to diets was good, and no complications resulted from fiber intake.
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PMID:Effect of unprocessed wheat bran on calciuria and oxaluria in patients with urolithiasis. 215 68

Different mathematical expressions have been proposed in the literature with the aim to reflect the risk of calcium oxalate urolithiasis. Such expressions, as well as a number of new relationships proposed by us, have been evaluated in 76 patients and 34 normal subjects. Stone-formers were divided into two groups: patients with normal calcium and oxalate excretion and patients with hypercalciuria and/or hyperoxaluria. The results obtained were comparatively evaluated. Several formulae gave some acceptable results, but none of them were excellent. This can be explained by the fact that these discrimination indexes more or less reflect supersaturation and/or inhibition deficit, but none of them reflect promoting factors such as heterogeneous nucleation and/or aggregation capacity.
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PMID:Can a relationship reflect the risk of calcium oxalate urolithiasis? 221 Sep 74

A case of primary hyperoxaluria is presented. In a product of consanguinous marriage recurrent stone formation, nephrocalcinosis and increased urinary oxalate excretion revealed the diagnosis of hyperoxaluria. Diagnosis and treatment of primary hyperoxaluria are briefly reviewed and the importance of elevated urinary oxalate level in diagnosis is emphasized.
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PMID:Early onset of stone diseases and primary hyperoxaluria. 221 Sep 75

Enteric hyperoxaluria due to malabsorption syndromes has been well documented to cause renal calculi and chronic tubulointerstitial renal damage. Rarely, in the setting of intestinal bypass operations for morbid obesity, enteric hyperoxaluria has produced acute renal failure. We report two patients who suffered acute deterioration of renal function associated with increased intestinal absorption and renal excretion of oxalate associated with steatorrhea. One patient had a large portion of his small bowel resected many years prior to the onset of the renal failure and the second patient had chronic pancreatitis causing steatorrhea. Both patients had renal biopsy documentation of the acute nature of the tubular damage produced by oxalate deposition. The mechanisms of their deterioration of renal function may relate to sudden increases in steatorrhea in association with episodes of volume depletion. Enteric hyperoxaluria may be an easily overlooked and potentially preventable etiology of acute renal dysfunction.
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PMID:Acute deterioration of renal function associated with enteric hyperoxaluria. 222 62

The part played by hyperoxaluria in the formation of calcium oxalate urinary calculi was studied in 153 patients who had each been diagnosed as having calcium oxalate urinary calculi on one or more occasions. Seventy-seven of the patients excreted normal amounts of calcium (less than 6.2 mmol/d), and 76 had hypercalciuria (excretion greater than or equal to 6.2 mmol/d); each group was divided into a further two groups depending on whether the oxalate concentration was above or below 0.16 mmol/l. Pure calcium oxalate stones were more common in patients whose calcium excretion was normal, and mixed calcium oxalate and phosphate stones were more common among hypercalciuric patients. Urinary concentrations/day of magnesium, citrate, and phosphorus were significantly lower in the two groups in which the oxalate concentrations were below 0.16 mmol/l than in a normal control group, and magnesium and phosphorus were significantly lower in the two groups in which oxalate concentrations were less than 0.16 mmol/l than in the two in which they were above that value. The concentration of citrate was also lower, but not significantly so. In addition, the pH of the urine in patients with mixed stones was significantly higher in all groups than when the stones were composed of pure calcium oxalate.
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PMID:The role of hyperoxaluria in the formation of calcium oxalate urinary calculi, and its association with other biochemical measurements. 223 98

A case of primary hyperoxaluria is presented. In a product of consanguinous marriage, recurrent stone formation, nephrocalsinosis and increased urinary oxalate excretion revealed the diagnosis of hyperoxaluria. Diagnosis and treatment of primary hyperoxaluria briefly reviewed and the importance of elevated urinary oxalate level in diagnosis is emphasized.
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PMID:Early onset of stone diseases and primary hyperoxaluria. 228 20

A 27-year-old woman with multiple bilobal liver metastases of a carcinoid tumour and carcinoid syndrome was treated with the somatostatin analogue Octreotide, 450-600 micrograms daily subcutaneously. This improved previous attacks of marked epigastric pain, while endocrine activity and tumour mass remained unchanged. Shortly after treatment had begun, soft fatty stools and oxaluria were noted. After six months severe renal colics were found to be due to non-opaque caliceal calculi, and a contracted non-functioning gallbladder was discovered. The calculi consisted of oxalate. The enteric hyperoxalosis, oxaluria and urolithiasis were presumably side effects of the Octreotide treatment.
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PMID:[Enteral hyperoxalosis due to therapy with a somatostatin analog]. 229 34

After 1 year of allopurinol treatment in 36 patients with a history of uric acid and/or calcium oxalate lithiasis and hyperuricosuria, we observed that in addition to the desired decreases in uric acid there were apparently significant decreases in urinary oxalate levels: 37 +/- 3 mg. per day (mean +/- standard error) before therapy and 31 +/- 4 mg. per day after a mean decrease of 16% (p less than 0.05) with an equivalent decrease in the supersaturation (calcium oxalate) of the urine. However, the decrease in oxalate could have been related to changes in dietary habits rather than to any specific effects of allopurinol on oxalate metabolism. Therefore, we recruited 26 of the patients for a study in which dietary factors were controlled. Each participant was assigned to 1 of 3 diet groups: low or high protein, or a customary diet. Each patient collected a urine specimen while on allopurinol and again after the medication was discontinued. With analytical procedures that we ascertained to be free of any significant methodological bias, we observed no significant changes in urinary oxalate excretion that could be attributed to allopurinol. There were significant differences in oxalate excretion on versus off allopurinol between the low and high protein groups, with higher oxalate levels found for the latter group. Our results indicate that allopurinol does not have a specific effect on oxalate metabolism or oxaluria.
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PMID:Absence of effect of allopurinol on oxalate excretion by stone patients on random and controlled diets. 235 87

The study was conducted to investigate the effect of vitamin A, B1 and B6 deficiency on oxalate metabolism in rats. A significant hyperoxaluria was the common observation in all the three vitamin deficiencies (vitamin B6 greater than vitamin A greater than vitamin B1). The activities of hepatic glycolate oxidase and glycolate dehydrogenase were markedly enhanced in vitamin-A- and vitamin-B6-deficient rats. However, lactate dehydrogenase levels remained unaltered in these deficiencies as compared to their respective pair-fed controls. Vitamin B1 deficiency of 4 weeks' duration could augment the activity of glycolate oxidase only, with no alterations in the glycolate dehydrogenase and lactate dehydrogenase levels. Intestinal oxalate uptake studies revealed increased bio-availability of oxalate from the gut in vitamin-A- and vitamin-B6-deficient rats. Thus, the results suggest the relative contribution of both exogenous as well as endogenous oxalate in the process of calculogenesis under various nutritional stress conditions in rat.
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PMID:Comparative studies on the effect of vitamin A, B1 and B6 deficiency on oxalate metabolism in male rats. 236 74


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