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

100 g of spinach a day was added to the hospital diet of fifty-four patients with suspected malabsorption. Hyperoxaluria was found in thirty-eight patients; all of them had steatorrhoea. No patient with steatorrhoea had a urinary oxalate excretion of less than 40 mg a day. Ten other patients had hyperoxaluria, but the faecal fat determinations were regarded as unreliable in almost all and malabsorption could not be confirmed. It is suggested that in clinical practice determination of urinary oxalate after an oral load of oxalate could replace faecal fat determination in most patients with suspected malabsorption.
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PMID:Urinary oxalate on a high-oxalate diet as a clinical test of malabsorption. 7 94

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

A patient with chronic renal disease due to primary hyperoxaluria developed a rapidly progressing motor neuropathy with marked impairment of nerve conduction. Pathological studies demonstrated the presence of both axonal degeneration and segmental demyelination, together with the presence of oxalate crystals within axons. It is suggested that the development of peripheral neuropathy complicating hyperoxaluria is a consequence of the increased life-span mad possible by haemodialysis.
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PMID:Peripheral neuropathy complicating primary hyperoxaluria. 18 38

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

Hydroxypyruvate and glycolate inhibited the oxidation of [U-14C]glyoxylate to [14C]oxalate in isolated perfused rat liver, but stimulated total oxalate and glycolate synthesis. [14C]Oxalate synthesis from [14C]glycine was similarly inhibited by hydroxypyruvate, but conversion of [14C1]glycolate to [14C]oxalate was increased three-fold. Pyruvate had no effect on the synthesis of [14C]-oxalate or total oxalate. The inhibition studies suggest that hydroxypyruvate is a precursor of glycolate and oxalate and that the conversion of glycolate to oxalate does not involve free glyoxylate as an intermediate. [14C35Hydroxypyruvate, but not [14C1]hydroxypyruvate, was oxidized to [14C]oxalate in isolated perfused rat liver. Isotope dilution studies indicate the major pathway involves the decarboxylation of hydroxypyruvate forming glycolaldehyde which is subsequently oxidized to oxalate via glycolate. The oxidation of serine which is subsequently oxidized to oxalate via glycolate. The oxidation of serine to oxalate appears to proceed predominantly via hydroxypyruvate rather than glycine or ethanolamine. The hyperoxaluria of L-glyceric aciduria, primary hyperoxaluria type II, is induced by the oxidation of the hydroxypyruvate, which accumulates because of the deficiency of D-glyceric dehydrogenase, to oxalate.
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PMID:The synthesis of oxylate from hydroxypyruvate by isolated perfused rat liver. The mechanism of hyperoxaluria in L-glyceric aciduria. 62 64

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

A 26-year-old woman, who had undergone jejunoileal bypass surgery six years previously for obesity, had symptoms of intermittent fever, myalgia, polyarthralgia, and aseptic joint swelling. These symptoms commenced one year after her surgery and gradually grew in intensity and frequency of occurrence. The patient, observed to have moderately decreased renal function, hyperoxaluria, and circulating cryoglobulins, underwent liver and renal biopsies. Both organ specimens demonstrated granulomatous involvement, but the kidneys exhibited no evidence of oxalate deposition. The findings of circulating cryoglobulins and suppression of symptoms with doxycycline, taken collectively with the circumstances surrounding this case, suggest that the observed granulomatous disease may be due to systematically adsorbed bacterial antigen(s).
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PMID:Jejunoileal bypass surgery and granulomatous disease of the kidney and liver. 63 46


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