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

The effects of some putative inhibitors of oxalate production or urinary oxalate excretion have been investigated in the Cynamolgus monkey and in patients with Type I primary hyperoxaluria (hyperoxaluria with glycollic aciduria). Sodium-1-hydroxybutan-sulphonate, D,L-phenyllactate, succinimide and isocarboxazide did not reduce the urinary oxalate excretion in the monkeys. Pyridoxine reduced the excretion of oxalate and glycollate in some patients, and its therapeutic use has been documented over a five-year period. Succinimide, which has been used by other workers for the treatment of non-hyperoxaluric stone formers, did not decrease the excretion of either oxalate or glycollate in three patients in whom it was tried. It did not change the inhibitory activity of the urine with respect to the growth and aggregation of calcium oxalate crystals in any of the three patients, and it did not have any consistent effect on the excretion of calcium oxalate crystals in the one patient who had detectable crystaluria before treatment. We have identified several metabolites of succinimide in the urine of patients taking the drug. These include 2,3-dehydrosuccinamic, 2-hydroxysuccinamic and 3-hydroxysuccinamic acids. Isocarboxazide, cholestyramine and thiamine did not affect the urinary oxalate excretion in the patients. The significance of these observations from the viewpoint of the treatment of primary hyperoxaluria is discussed.
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PMID:Studies on some possible biochemical treatments of primary hyperoxaluria. 11 1

A 61 year old man had chronic renal failure because of oxaluria and renal calculi. Two years before death, while on hemodialysis, he developed severe progressive peripheral neuropathy. At autopsy calcium oxalate crystals were found in the peripheral nerves and other tissues. Nerve lesions included segmental demyelination, axonal degeneration and crystalline deposits within the myelin sheath. Ultrastructurally there were foci of osmiophilic granular material within myelin lamellae and endoneurium, and pleomorphic lamellar bodies in the perinuclear Schwann cell cytoplasm. It is probable that chronic hemodialysis favors the deposition of oxalate in the Schwann cells and the development of neuropathy in patients with primary hyperoxaluria and renal failure.
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PMID:Peripheral neuropathy in oxalosis. A case report with electron microscopic observations. 17 8

Eighty patients with proved calcium urolithiasis participated in an outpatient study designed to define the most likely metabolic problem related to the cause of the stone disease. Diagnostic categories included absorptive hypercalciuria (33 patients), renal leak hypercalciuria (20 patients), hypomagnesiumuria (27 patients), hyperuricemia and hyperuricuria (16 patients), hyperoxaluria (15 patients), normal stone-former (4 patients), renal tubular acidosis (2 patients) and suspicion of hyperparathyroidism (7 patients). Of the 80 patients 40 had more than 1 defect. Patients with a high suspicion of hyperparathyroidism were excluded from the study. Based on these criteria treatment plans incorporating medications, diet or both were instituted. Of 21 patients observed for greater than 2 years 90 per cent have shown no new stone disease.
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PMID:Outpatient evaluation of patients with calcium urolithiasis. 43 49

The incidence of urolithiasis was registered in 87 patients with chronic inflammatory bowel disease and compared with that of renal oxalate excretion. All patients were studied while on a standardized diet with fixed amounts of fat, calcium, and oxalate. Pyelography had been performed in all. Nine, or 35%, of 26 hyperoxaluric patients had urolithiasis, compared with 14, or 23%, of 61 patients were normal renal oxalate excretion, the difference being statistically insignificant. No significant difference in urinary oxalate or urinary calcium in stone-formers as compared with non-stone-formers could be demonstrated. Oxalate was a more frequent component of calculi in patients with normal renal oxalate excretion than in patients with hyperoxalura. Thus, we were unable to demonstrate an increased incidence of urolithiasis in patients with hyperoxaluria compared with a control group with normal renal oxalate excretion. Our results cast doubt on the concept that enteric hyperoxaluria per se is the cause of stone diathesis in chronic inflammatory bowel disease.
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PMID:Urolithiasis and hyperoxaluria in chronic inflammatory bowel disease. 48 60

The renal handling of oxalate was studied by the injection of 14C-oxalate together with inulin as a glomerular marker into the renal artery in 6 patients. From the recovered amounts of the injected substances in the urine, time-concentration curves were constructed. Oxalate was excreted into urine 2.31 +/- 0.05 (SE) fold when compared to inulin. The maximal concentration of oxalate occurred at the same time as inulin, and there was no urinary precession of oxalate in comparison to inulin. From this part of the study we conclude that oxalate in addition to its filtered amount can probably enter the early part of nephron. In a second type of study, plasma levels of oxalate and inulin were observed over a period of 180 min, following intravenous injections in 7 volunteers. The decline of oxalate plasma concentrations followed first-order kinetics. Calculation of the rate constants of elimination assuming the 'one compartment open' model resulted in an oxalate to inulin ratio of 1.21 +/- 0.05. The oxalate half-life of elimination was 92 +/- 8 min, whereas that of inulin amounted to 112 +/- 9 min. The higher value of the calculated volume of distribution of oxalate compared to that of inulin indicates that oxalate enters a larger space than the extracellular fluid volume. The urinary recovery of intravenously injected oxalate was 97.2 +/- 1.4%, indicating that oxalate is excreted exclusively by the kidney. The observed differences of oxalate excretion, obtained with these two methods, could be attributed to the higher amount of ionized oxalate in the disequilibrium technique (rapid injections), entering the urine in a higher rate. Such a mechanism could explain the hyperoxaluria in calcium oxalate stone-forming patients.
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PMID:Renal elimination kinetics and plasma half-life of oxalate in man. 49 45

To investigate the possibility of measuring urinary oxalate output instead of faecal fat excretion as an outpatient screening test for steatorrhoea, we determined 24 hour urinary oxalate and five day faecal fat excretion before and during an oral load of sodium oxalate 600 mg daily (oxalate 4.44 mmol), in 32 patients with suspected malabsorption on a diet containing oxalate 30 mg (0.33 mmol), fat 50 g (180 mmol), and calcium 1 g (25 mmol). Nineteen patients proved to have steatorrhoea (mean faecal fat 62 mmol/24 h, range 19--186 mmol) of varying aetiologies. On the diet alone, urinary oxalate was raised in only nine of these patients (mean 0.25 mmol/24 h, range 0.08--0.59 mmol) (normal less than 0.20). By contrast, when the diet was supplemented with oral sodium oxalate, all 19 patients with steatorrhoea had hyperoxaluria (mean 0.91 mmol/24 h, range 0.46--1.44 mmol) (normal less than 0.44). There was a significant positive linear relationship between urinary oxalate and faecal fat when the 32 patients were on the high oxalate intake (r = 0.73, P less than 0.001), but not when they were on the low oxalate intake. Mean percentage absorption of orally administered oxalate was 5.8 +/- 0.99% (+/- 1 SD) in normal subjects and 14.7 +/- 6.0% (P less than 0.002) in patients with steatorrhoea. Measurement of urinary oxalate output during oral sodium oxalate loading appears to be a reliable and convenient screening test for steatorrhoea.
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PMID:Oxalate loading test: a screening test for steatorrhoea. 52 84

This work was designed to investigate the site of oxalate hyperabsorption in malabsorption syndromes. 1) Urinary oxalate excretion was measured in 27 patients with ileal resection (IR) and steatorrhea. Mean urinary oxalate excretion was high in 13 patients with IR and intact colon and in 9 subjects with IR and right hemicolectomy (90.2 +/- 11.9 and 108 +/- 18.6 mg per 24 hours; mean +/- S.E.M.), whereas it was normal in 5 patients with IR and ileostomy (21.9 +/- 4.4 mg per 24 hours). Steatorrhea was similar in the three groups. 2) On one patient of the last group in whom the colon had not been removed initially but excluded closure of the ileostomy resulted in the development of frank hyperoxaluria. 3) Intracolonic perfusion of calcium (1.93 g per day) abolished or greatly reduced the hyperoxaluria in 3 patients. These results indicate that the colon is the major site of oxalate hyperabsorption, and the right colon is not necessary for the development of hyperoxaluria in malabsorption syndromes.
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PMID:Evidence for excessive absorption of oxalate by the colon in enteric hyperoxaluria. 63 58

Intestinal absorption of oxalate was assessed indirectly from the increase in renal oxalate excretion following the oral administration of 5 mmol of stable oxalate. When sodium oxalate alone was given without divalent cations to patients in the fasting state, the urinary oxalate increased promptly (within 2 hours). The increase was more prominent and sustained in those with ileal disease (ileal resection or jujunoileal bypass); thus, 35 per cent of the orally administered oxalate eventually appeared in the urine in the group with ileal disease, 8 per cent in the group with stones (renal and absorptive hypercalciurias) and 9 per cent in the control group. This hyperexcretion of oxalate could be largely, but not totally, ameliorated by the concurrent oral administration of divalent cations. Although urinary oxalate decreased significantly following the oral administration of calcium or magnesium, hyperoxaluria persisted in most patients. The results suggested that the hyperabsorption of oxalate in ileal disease cannot be accounted for solely by an increased absorbable oxalate pool associated with calcium-fatty acid complexation. Moreover, although urinary oxalate decreased, urinary calcium increased concurrently when either calcium or magnesium was given. Thus, there was no significant change or increase in the urinary state of saturation with respect to calcium oxalate.
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PMID:Renal oxalate excretion following oral oxalate loads in patients with ileal disease and with renal and absorptive hypercalciurias. Effect of calcium and magnesium. 64 24

143 patients (70 patients with Crohn's disease, 11 with ulcerative colitis, 40 with an intestinal by-pass operation, 9 with non-tropical sprue, 10 with short bowel syndrome, and 3 with other gastrointestinal disease) were studied during a metabolic regime including a fixed oral supply of 70 g fat, 800 mg calcium, and 200 mg oxalate. Faecal fat, 47Ca-absorption, 14C-oxalate absorption, and renal oxalate excretion were measured, and in the majority of patients a 14C-glyco-cholic acid breath test was also performed. 14Ca-absorption was practically identical (r = 0.92), whether determined by whole-body counting or from the accumulation of absorbed 47Ca in the skeleton of the underarm. 14C-oxalate absorption and renal oxalate excretion agreed well (r = 0.85). Steatorrhoea correlated weakly with renal oxalate excretion (r = 0.63, p less than 0.001), whereas no correlation was present between faecal fat and calcium absorption or between oxalate and calcium absorption under the constant conditions prevailing during the study. It is recommended that a "trifixed" regime with absorption studies of fat, calcium, and oxalate be undertaken previous to therapy that aims at a reduction of steatorrhoea or hyperoxaluria or an improvement of calcium absorption in chronic malabsorption syndromes, not least because therapy of these categories of patients most often continues for years.
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PMID:Standardized ("trifixed") diet in the study of chronic malabsorption syndromes. 67 51

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


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