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

The excretion of urinary acidic metabolites by 10 patients undergoing gastric or biliary tract surgery has been studied. Five patients were infused with xylitol and 5 with glucose. Four of the xylitol-infused patients had hyperglycollic aciduria and 3 of the glucose-infused patients had hyperlactic aciduria. There was no hyperoxaluria. Four of the xylitol-infused patients excreted more tetronic acids than any of the glucose-infused patients. Threonic acid was the predominant tetronic acid excreted by most (4/5) of the xylitol-infused subjects. Erythronic acid predominated in the glucose-infused as in control ambulant non-hospitalised subjects. It is suggested that these changes point to overloading of the transketolase pathway during xylitol infusion.
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PMID:Metabolic investigations during xylitol infusion. 82 85

Renal calcifications have been described in very low birth weight (VLBW) infants, and diuretic drug-associated hypercalciuria is believed to play a role in the pathogenesis of this lesion. Hyperoxaluria is an important cause of renal stone formation in children and adults. Because parenteral nutrition solutions contain the oxalate precursors ascorbate and glycine, the relationship between total parenteral nutrition administration and oxalate excretion in VLBW infants was examined. Administration of approximately 0.5 g of total parenteral nutrition protein per kilogram per day to VLBW infants was associated with an increased urinary oxalate concentration and an increased urinary oxalate to creatinine ratio, when compared with VLBW infants receiving a glucose and electrolyte solution. A further increase in urinary oxalate concentration and oxalate to creatinine ratio was noted when total parenteral nutrition protein was increased to approximately 1.5 g of protein per kilogram per day. In VLBW infants who receive total parenteral nutrition, elevated urinary oxalate concentrations may develop and may be a factor in the pathogenesis of nephrocalcinosis in these infants.
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PMID:Urinary oxalate excretion by very low birth weight infants receiving parenteral nutrition. 250 54

We studied urinary calcium and oxalate excretion in response to oral fructose load and to oral glucose load each on two different randomized mornings in twelve healthy subjects. Oral fructose load provoked an increase in calciuria and a decrease in oxaluria while oral glucose load induced an increase in both calciuria and oxaluria. These results suggested that in healthy subject, the decrease in oxaluria observed during fructose load reduced the product urinary [calcium] x [oxalate] which was the main factor in the genesis of urinary calcium oxalate stones while glucose load increased the risks of urolithiasis by means of the rise in both calciuria and oxaluria.
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PMID:Urinary calcium and oxalate excretion during oral fructose or glucose load in man. 272 35

Massive (70%) resection of the small bowel was performed in seven newborn infants. Follow-up study was undertaken in four of these patients and the growth and endocrinological status were evaluated. Body weight and height of three patients were below 50th percentile. On glucose tolerance test, peak IRI was low and insulinogenic indices were below normal range. These findings suggest that there are some mechanisms which suppress the secretion of insulin. Pituitary and thyroid function were within normal limits but secondary sexual manifestation was not seen in a fifteen year old boy. Hyperoxaluria was seen in three children, and one had kidney stone with some impairment of renal function.
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PMID:[Endocrinological and metabolic disorders in the patients with massive bowel resection in the newborn period]. 306 77

In children, tubulo-interstitial nephritis (TIN) is often associated with obstructive uropathy, metabolic disorders or hereditary diseases. The author reviewed congenital metabolic disorders (Fanconi syndrome, cystinosis, Lowe's syndrome, and hyperoxaluria) as causes of TIN. The Fanconi syndrome is caused by numerous disorders including cystinosis and Lowe's syndrome, and refers to a dysfunction of the proximal tubule leading to excessive urinary excretion of amino acids, glucose, phosphate, bicarbonate, etc. Prognosis of idiopathic Fanconi syndrome is not so bad if electrofluid balance is well maintained. On the other hand, prognosis of the infantile type of cystinosis, Lowe's syndrome, or hyperoxaluria "type 1" is poor. The pathophysiology of each disease should be fully understood for early diagnosis and treatment.
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PMID:[Congenital metabolic disorder]. 756 41

We have previously shown that an oral glucose load increased both calciuria and oxaluria while the ingestion of fructose induced a rise in calciuria and a decrease in oxaluria. This latter effect remains unclear and might be linked to the reduced intestinal oxalate absorption subsequent to digestive intolerance in some subjects. Such a hypothesis could be enlightened by the study of a parenteral fructose load. Therefore in 7 healthy subjects, we compared the effects of fructose infusion (F) (15 min iv infusion at 0.185 mmol/kg BW/min) to a control glucose infusion (G) on urinary calcium and oxalate. In this study, glycemia and insulinemia increased less after (F) than after (G) (respectively + 21% vs + 216%, p < 0.001 and + 230% vs + 402%, p < 0.05) and phosphatemia decreased less after (F) than after (G) (-7% vs -14%, p < 0.05). Urinary calcium and oxalate increased only after (F) (respectively + 64%, p < 0.01 and + 60%, p < 0.05). Urinary uric acid, another urolithiasis factor, increased after both (F) and (G) (respectively + 45%; p < 0.01 and + 42%; p < 0.01) but uricemia increased only after (F) (+ 25%; p < 0.01). Our results suggest an additional reason to avoid the use of fructose in parenteral nutrition, particularly in individuals with a known history of either calcium oxalate or urate urolithiasis.
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PMID:Increase in urinary calcium and oxalate after fructose infusion. 760 7

A shortened small intestine may end at a stoma or be anastomosed to the colon. Patients with a jejunostomy, but not those with a colon, lose large amounts of sodium. The intake and absorption of sodium can be increased by sipping a sodium-glucose solution; stomal loss can be reduced by restricting water or low-sodium drinks. If a stoma is situated less than 100 cm along the jejunum, a constant negative sodium balance may necessitate parenteral saline supplements. Gastric anti-secretory drugs or a somatostatin analogue reduce jejunostomy losses in such patients but do not restore a positive sodium balance. Loperamide or codeine phosphate benefit some patients. Magnesium deficiency can usually be corrected by oral magnesium oxide supplements. An elemental or hydrolysed diet is not beneficial. Patients with a jejunostomy can maintain a normal diet without fat reduction. When the colon is present, unabsorbed carbohydrate is fermented to absorbable short chain fatty acids. Unabsorbed long chain fatty acids and bile salts cause watery diarrhoea and increased colonic oxalate absorption with hyperoxaluria. Such patients benefit from a high carbohydrate, low-fat and low-oxalate diet. Parenteral nutrition is needed only by the few patients unable to maintain health or avoid socially disabling diarrhoea despite these measures.
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PMID:Review article: practical management of the short bowel. 769 44

Chocolate, a foodstuff rich in sucrose, fat and oxalate, is considered unsuitable in cases of obesity, diabetes mellitus, urolithiasis and postprandial hypoglycemia. However the pathophysiological effects of chocolate are poorly documented. Therefore we investigated the effects of ingestion of 100 g dark chocolate bar (45 g cocoa and 55 g sucrose) on carbohydrate, calcium and oxalate metabolisms in 10 healthy subjects. Results were compared to those of 55 g sucrose intake (control group) performed on another day. Chocolate caused i) a lesser but longer increase in plasma glucose, insulin, and C-peptide than sucrose (respectively +23% of baseline vs +60%, p < 0.001; +436% of baseline vs +755%, p < 0.01 and +200% of baseline vs +331%, p < 0.01), ii) a striking increase in triglyceridemia, calciuria and oxaluria (respectively +96%, p < 0.01; +147%, p < 0.01 and +213%, p < 0.001). Thus, chocolate (cocoa+sucrose) causes a lesser pancreatic stimulation than sucrose. However, the increases in both calciuria and oxaluria (induced respectively by sucrose and cocoa) following chocolate ingestion might contribute to urinary conditions favoring the development of calcium oxalate calculi.
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PMID:Increase in calciuria and oxaluria after a single chocolate bar load. 780 35

Polyols are widely used instead of glucose and sucrose in sweets and dietary products because they are barely cariogenic, and their energy value is lower. In addition, it has been shown that calciuria and oxaluria increase after an oral glucose (Glu) load. We, therefore, investigated the effects of a single polyol ingestion on carbohydrate, calcium, phosphate, and oxalate metabolism in 10 healthy subjects. On 5 experimental days, subjects ingested 20 g Glu, Lycasin (Lyc), Maltisorb (Mal), sorbitol (Sor), or xylitol (Xyl). Glu, Lyc, and Mal intake caused an increase in glycemia [respectively, +34% (P < 0.001), +15% (P < 0.001), and +15% (P < 0.001)], insulinemia [respectively, +358% (P < 0.001), +88% (P < 0.05), and +94% (P < 0.01)], and C-peptide level [respectively, +170% (P < 0.001), +15% (P < 0.01), and +15% (P < 0.001)]. Conversely, no change occurred in glycemia, insulinemia, or C-peptide levels after ingestion of Sor or Xyl. Urinary calcium increased after Glu (+64%; P < 0.01) and Xyl (+74%; P < 0.01) intake, and urinary phosphate increased after Xyl (+27%; P < 0.05), but decreased after a Glu load (-68%; P < 0.01). Only Xyl increased urinary excretion of oxalate (+53%; P < 0.05). Our results suggest that ingestion of polyols causes a much lesser pancreatic stimulation than Glu intake. Also, Lyc, Mal, and Sor sweeteners have no effect on urinary excretion of calcium and oxalate, whereas calciuria and oxaluria increase after Xyl ingestion.
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PMID:Carbohydrate metabolism and urinary excretion of calcium and oxalate after ingestion of polyol sweeteners. 834 42

Aspartame is the artificial sweetener most extensively used as a substitute for glucose or sucrose in the food industry, particularly in soft drinks. As glucose ingestion increases calciuria and oxaluria, the two main determinants of urinary calcium-oxalate saturation, we considered it worthwhile to determine whether aspartame ingestion also affects calcium-oxalate metabolism. Our study compares the effects of the ingestion of similarly sweet doses of aspartame (250 mg) and glucose (75 g) on calcium and oxalate metabolisms of seven healthy subjects. Urinary calcium excretion increased after the intake of both aspartame (+86%; P < 0.01) and glucose (+124%; P < 0.01). This may be due to the rise in calcemia observed after both aspartame (+2.2%; P < 0.05) and glucose ingestion (+1.8%; P < 0.05). The increased calcemia may be linked to the decrease in phosphatemia that occurred after both aspartame (P < 0.01) and glucose (P < 0.01) load. Aspartame did not alter glycemia or insulinemia, whereas glucose intake caused striking increases in both glycemia (+59%; P < 0.001) and insulinemia (+869%; P < 0.01). Although insulin was considered the main calciuria-induced factor after glucose load, it is unlikely that this mechanism played a role with aspartame. Urinary oxalate excretion did not change after aspartame, whereas it increased (+27%; P < 0.05) after glucose load. Thus, as aspartame induced a similar increase in calciuria as did glucose but, conversely, no change in oxaluria, substituting glucose by aspartame in soft drinks may appear to be of some potential benefit.
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PMID:Aspartame ingestion increases urinary calcium, but not oxalate excretion, in healthy subjects. 992 Jan 15


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