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

An organic marine hydrocolloid (OMH) charged with calcium ('Ox-Absorb') was studied in vitro for oxalate binding and in patients with enteric hyperoxaluria to investigate oxalate excretion and the inhibitory activity on crystal formation of the urine. In-vitro experiments showed complete binding of oxalate to OMH. In clinical studies in nineteen patients with intestinal disorders and stone formation, urinary oxalate excretion was significantly lower during OMH treatment than off treatment. The activity product index of calcium oxalate was reduced on treatment. A pronounced rise in the inhibitory activity of urine was seen in two patients with very low pretreatment values. Most patients experienced virtual normalisation of bowel function, and in those with severe stone formation there was substantial clinical improvement. It is concluded that OMH has the capacity to bind oxalate in vitro and to reduce urinary oxalate excretion. These observations suggest a new promising treatment for enteric hyperoxaluria.
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PMID:Treatment of enteric hyperoxaluria with calcium-containing organic marine hydrocolloid. 257 Sep 57

Jejunoileal bypass (JIB) has been widely performed for treatment of excessive obesity. Formation of calcium oxalate stones is a common side effect. Since, under physiological conditions, the intestinal absorption of calcium and that of oxalate are interrelated, intestinal oxalate and calcium absorption were measured in the present study by isotope techniques in 19 JIB patients and 20 healthy controls. The JIB patients showed pronounced hyperoxaluria and markedly increased absorption of oxalate, with a urinary excretion of 14C-oxalate of 29 +/- 19% (controls 6.2 +/- 3.7%; p less than 0.001). There was a strong correlation between the intestinal absorption and urinary excretion of oxalate in the JIB patients (r = 0.72; p less than 0.001). Furthermore, their oxalate kinetics was altered, with continued urinary excretion of 14C-oxalate for up to 48 hours. The JIB patients also had reduced calcium absorption (36 +/- 9.1% vs. 47 +/- 9.0%; p less than 0.001) and patients with malabsorption of calcium and low urinary calcium had the highest intestinal absorption and urinary excretion of oxalate. It is concluded that hyperoxaluria in JIB patients is due to a significant extent to hyperabsorption of oxalate.
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PMID:Intestinal absorption of oxalate and calcium in patients with jejunoileal bypass. 259 24

This article reviews the mechanisms involved in the synthesis, absorption, excretion and transport of oxalic acid, and the factors controlling these processes in man. The clinical syndromes associated with hyperoxaluria and recurrent calcium oxalate stone disease are reviewed, including new studies that raise the possibility of a generalized oxalate transport abnormality in some patients with renal stone disease. The important role of oxalate in the determination of calcium oxalate solubility in patients with calcium oxalate stone disease is emphasized and future directions for research in the prevention of recurrent calcium oxalate stone disease are discussed.
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PMID:Oxalate synthesis, transport and the hyperoxaluric syndromes. 264 33

The morphological and infrared spectrophotometric analysis of the urinary stones of 300 patients have been reported in this article. Calculi are classified into six morphological types with their corresponding mineralogical natures. The type I (whewellite or C1) is pure in 18 p. cent of lithiasis, more often present in the center than on the surface, with hyperoxaluria in 81 p. cent. Calculi linked to piridoxilate intake (3 p. cent) have this composition. The type II (weddellite or C2) rarely pure, often associated with calcium phosphate are present in 47 p. cent of lithiasis, more often on the surface than in the center, and linked to hypercalciuria in 70 p. cent. The oxalates (C1 plus C2) are the most frequent components of calculi (75 p. cent). The type IIIa and IIIb (anhydrous and dehydrated uric acid) are pure in 8 p. cent, mixed in 6 p. cent; due to hyperuraturia in 55 p. cent, due to urinary acid pH in 60 p. cent. The type IVa (carbapatite) is pure in 5 p. cent, mixed in 26 p. cent, linked to hypercalciuria in 40 p. cent. The types IVb and IVc (struvite plus carbapatite) are present in 12 p. cent, due to urinary infection (90 p. cent), linked to proteus (70 p. cent). The type V (cystine) is rare, linked to hypercystinuria. The type VIa (1 p. cent) is made of proteins. The type VIb (2 p. cent) is composed of medications (triamterene, glafenine, antrafenine).
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PMID:[Correlation of the cause and composition of renal calculi. Value of morphologic and infrared analysis]. 264 1

The incidence and prevalence of urolithiasis in the Czechoslovak Socialist Republic is as high as in other countries of Central and Western Europe, and lower than in the Scandinavian countries. Apart from its high incidence, urolithiasis is characterized by its high tendency to recurrence. New knowledge of its pathogenesis helps to diagnose metabolic disorders responsible for increased excretion of concretion-producing substances and/or for deficiency in protective factors. In case of calcium oxalate lithiasis, with the highest incidence, attention is to be paid to its various forms of hypercalciuria, and, more recently, to moderate hyperoxaluria, and as regards protective factors, to magnesium, citrates, pyrophosphates and mucopolysaccharides. The determination of the type of metabolical disorder in patients with lithiasis enables to modify the diet and/or medication leading to causal prophylaxis against recurrence, i.e. metaphylaxis. At our Prague urological clinic, a consultation centre for lithiatic patients has been in operation since 1977. Long-term experience has shown that it has been successful especially in preventing recurrence or a in a substantial reduction in recurrence in 94% of the followed-up patients. Although the centre's activity is demanding both on the personnel and laboratory, even first sufferers from ilthiatic attacks should take advantage of it. At this early stage, such patients were found to have a metabolic disorders in 60%. In the past 7 years of treating nephrolithiasis and ureterolithiasis, new methods have been introduced which substantially improve the results and are less invasive than a classical operation. Among others, they comprise percutaneous endoscopic methods of disintegration and concrement extraction from the kidney and ureter, uteroscopy and extracorporeal shock-wave lithotripsy. It is to be expected that these methods will replace classical operations at a rate of 90%.
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PMID:[Urolithiasis. Review of present knowledge of epidemiology, pathogenesis, metaphylaxis and treatment]. 266 71

Hyperoxaluria and hypercalciuria are common features of renal calcium stone disease. The purpose of the present investigation was to examine the relationships between the intestinal absorption and the renal handling of oxalate and calcium in patients with idiopathic renal stone disease and in patients with enteric hyperoxaluria following jejunoileal bypass (JIB), in comparison with healthy controls. Hyperoxaluria was associated with a higher frequency of both stone episodes and stone operations than a lower urinary oxalate concentration. Patients with idiopathic stone disease showed increased intestinal uptake of both oxalate and calcium, which was probably of importance for their propensity to form calcium oxalate-containing stones. Hyperoxaluria in patients with JIB was found to be a result of hyperabsorption of oxalate, and these patients displayed altered oxalate kinetics with continued urinary excretion of orally administered 14C-oxalate for more than 48 hours. The prolonged excretion is assumed to be due to a prolonged absorption and/or an increased oxalate pool. Malabsorption of calcium and low fasting urinary calcium excretion in the JIB patients were associated with high tubular reabsorption of calcium, the latter presumably attributable to a compensatory increase in circulating parathyroid hormone (PTH). In most recurrent renal stone formers the urinary calcium concentration was increased, with an inverse relationship to serum PTH, indicating intestinal hyperabsorption of calcium. A subgroup of hypercalciuric patients showed increased urinary calcium due to reduced tubular reabsorption of calcium. It is suggested that this is a renal defect resulting in a compensatory rise in PTH. Two different mechanisms of similar prevalence might explain enhanced secretion of PTH in normocalcaemic stone disease, namely reduced calcium absorption and a renal defect in the form of reduced tubular reabsorption of calcium. Glycosaminoglycans efficiently inhibit calcium oxalate crystal growth by binding to the surface of calcium oxalate crystals. In this study the binding was dependent on ionic strength. Higher affinity to the crystals may be the reason why highly charged glycosaminoglycans were more efficient inhibitors of calcium oxalate crystal growth. A calcium-containing organic marine hydrocolloid with the capacity to bind oxalate in vitro was shown to reduce enteric hyperoxaluria. In addition to biochemical effects considerable improvements in diarrhoeal symptoms were reported.
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PMID:Oxalate metabolism in renal stone disease with special reference to calcium metabolism and intestinal absorption. 266 21

The mechanism of stone formation in the urinary tract is reviewed. Diet, urinary tract infection and metabolic disorders account for the different epidemiological patterns of stone formation. The diagnosis and management of renal tract calculi are discussed. Calcium stones are associated with hypercalciuria, urine acidification defects, the use of furosemide in premature babies, hypercalcaemia, hyperoxaluria, hyperuricosuria, an alkaline urine and hypocitraturia. Uric acid stones occur in acid urine, from increased purine synthesis with lympho- or myeloproliferative disorders or from several inborn errors of purine metabolism which can also cause xanthine or dihydroxyadenine stones. Cystinuria, inherited as an autosomal recessive disorder is best treated with a low sodium diet, a fluid intake exceeding 40 ml/kg per day maintaining urine pH between 7.5 and 8 and, if necessary, with oral penicillamine. Oxalate stones occur in relation to diet, bowel disease and primary inherited defects in oxalate metabolism. Urinary tract infection causing struvite and carbonate apatite formation is the commonest cause of stones in Europe.
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PMID:Urolithiasis in children: current medical management. 270 15

Primary hyperoxaluria type I (PH I) is characterized by an excessive endogenous production and excretion of oxalic and glycolic acid. Prognosis of this "inborn error of metabolism" is not favorable due to calcium-oxalate depositions in kidney and other organs. Vitamin B6 administration and/or renal transplantation can greatly improve the prognosis, as reported in literature. In this article our experience with 5 patients with vitamin B6 resistant hyperoxaluria is reported. Symptomatology and progression of the primary disease are described. The results of treatment interfering with oxalate production and calcium-oxalate crystallization are given. Three patients underwent renal replacement therapy. In these, oxalosis developed during hemodialysis and progressed following transplantation; a disabling bone disease was the most severe complication. Outcome of transplantation was disappointing. In two out of three patients, there was recurrence of the primary disease in the graft. In only one of them long-term graft function was satisfying. However, even this good function could not prevent disabling symptoms of oxalosis. Therefore, evaluation of the results of transplantation should not only include data related to graft function and survival, but also the complications due to calcium-oxalate depositions in various organs. To prevent oxalosis, kidney transplantation should be performed before end stage renal disease is achieved in patients with vitamin B6 resistant PH I.
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PMID:Vitamin B6 resistant primary hyperoxaluria type I. Report of 5 cases. 270 72

Oxalate excretion was measured in healthy subjects and idiopathic calcium stone-formers on dietary regimens which differed in the type and amount of protein allowed; 24-h urine collections were obtained from 41 practising vegetarians and 40 normal persons on a free, mixed, "mediterranean" diet. Twenty idiopathic calcium stone-formers were also studied while on two low calcium, low oxalate diets which differed in that animal protein was high in one and restricted in the other. Vegetarians had higher urinary oxalate levels than controls and although the calcium levels were markedly lower, urinary saturation with calcium/oxalate was significantly higher. This mild hypercalciuria was interpreted as being secondary to both a higher intake and increased fractional intestinal absorption of oxalate. Changing calcium stone-formers from a high to a low animal protein intake produced a significant decrease in calcium excretion but there was no variation in urinary oxalate. As a result, the decrease in calcium oxalate saturation was only marginal and not significant. It was concluded that dietary animal protein has a minimal effect on oxalate excretion. Mild hyperoxaluria of idiopathic calcium stone disease is likely to be intestinal in origin. Calcium stone-formers should be advised to avoid an excess of animal protein but the risks of a vegetable-rich diet should also be borne in mind.
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PMID:Effect of animal and vegetable protein intake on oxalate excretion in idiopathic calcium stone disease. 271 14

Metabolic disorders are the most frequent risk factor for the development of urolithiasis. They are manigenic substances or deficiency of inhibitors of crystalgenic substances or deficiency of inhibitors of crystallization and aggregation. The authors use for their diagnosis a modification of Pak's procedure. It involves examination of 24-hour urine with the patient on a low-calcium diet, supplemented by urine examination on fasting and after a 1000 mg calcium load. The procedure includes also examination of serum and bacteriological examination of urine. A total of 93% of patients with calcium lithiasis had a metabolic disorder, 42% suffered from idiopathic hypercalciuria, 32% from hyperuricosuria, 19% from hyperoxaluria, 15% from magnesium deficiency and 38% from hypocitraturia. On the other hand, patients with uric acid lithiasis had a detectable metabolic disorder only in 62%. Active detection of metabolic disorders is essential for the introduction of effective, specific metaphylaxis of urolithiasis.
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PMID:[Detection of metabolic disorders as a cause of urolithiasis in clinical practice]. 272 Jul 28


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