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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxalic acid seems to play a far greater role in the formation of calcium oxalate stone than calcium. Three grams of calcium lactate and 3 g of sodium potassium citrate were administered to 46 urolithiasis patients, whose stones were mainly composed of calcium oxalate. Urinary oxalate level was reduced significantly without raising urinary calcium level by the administration of the two drugs for two weeks. The reduction of urinary oxalic acid was particularly remarkable in patients without hypercalciuria. The mechanism of action of these drugs was discussed.
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PMID:Reduction of urinary oxalate by combined calcium and citrate administration without increase in urinary calcium oxalate stone formers. 154 Oct 59

The synergistic interaction of fructose and magnesium (Mg) deficiency on kidney calcification was compared in male and female rats. Male and female weanling rats were divided into four dietary groups: fructose or starch, with or without Mg. Rats were fed their respective diets for 9 weeks, and 24 h urine was collected to measure urinary output, pH, Mg, calcium (Ca), and oxalic acid. Rats were fasted overnight. After decapitation, blood was collected immediately, and kidneys were removed to determine their Mg and Ca content. Dietary fructose significantly increased kidney Ca in female rats fed deficient or adequate Mg diet and in male rats fed Mg-deficient diet only; the greatest kidney calcification occurred in female rats fed Mg-deficient diet (P less than 0.0001). Even in starch groups female rats fed the Mg-deficient diet showed some kidney Ca accumulation. The synergistic interaction of fructose and magnesium deficiency on nephrocalcinosis was significantly greater in female than in male rats. Low urinary output, optimal pH 6.8 for calcium phosphate precipitation, hypercalcaemia, hypercalciuria, hypomagnesuria, and low ratio of urinary Mg to Ca may independently or multifactorially contribute to nephrocalcinosis. The possible mechanism of this interaction is discussed.
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PMID:Dietary fructose produces greater nephrocalcinosis in female than in male magnesium-deficient rats. 191 Oct 97

With the development of extracorporeal shock wave lithotripsy treatment, the duration of hospitalization for stone patients fortunately has become shorter. However, a detailed analysis of lithogenesis is not possible during such patients' short hospital stays. We prepared a standard diet to be eaten at home for investigation of lithogenesis at the out-patient clinic. This diet was nutritionally well-balanced and contained the following: energy: 2000 Kcal, total protein: 70-75 g, animal protein: 30-35 g, carbohydrate: 510 g, fat and oil: 50-60 g, calcium: 600-630 mg and magnesium: 320 mg. The urine of 24 male patients with stones on a free diet and the same patients after 3 days on the standard diet was analyzed for urea-nitrogen, uric acid, sodium, calcium, phosphorus, magnesium, citric acid and oxalic acid. The results were compared with those in 17 healthy male subjects who were eating the standard diet (controls). It was found that 66% of hypercalciuria (greater than = 300 mg/day) on a free diet became normocalciuria on the standard diet. The hypercalciuria was therefore thought to be of dietary origin. Moreover, urinary excretion of urea nitrogen, uric acid, sodium and phosphorus by patients remarkably decreased after 3 days on the standard diet, which was not different from that of controls. These results suggest that the standard diet at home is useful in the screening of hypercalciuria and also quite adequate for patients with stones.
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PMID:[Preparation of a standard diet for out-patients in the study of lithogenesis]. 207 1

Oxalic acid seems to be more important for the formation of calcium oxalate stone than calcium. Three grams of calcium lactate and 3 g of uraly U were administered to 35 urolithiasis patients, whose stones were mainly composed of calcium oxalate. Urinary oxalate level was reduced significantly without raising urinary calcium level by the administration of the two drugs for two weeks. The reduction of oxalic acid was particularly remarkable in patients without hypercalciuria. The mechanism of action of these drugs and the relation to dietary management were discussed.
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PMID:[Reduction of urinary oxalate excretion by administration of calcium and citrate]. 260 Dec 15

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

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

Twenty-four-hour urinary excretion of calcium, oxalic acid, inorganic phosphorus, magnesium and citric acid was examined in fifty-nine stone formers with bladder stones. Hypercalciuria and hyperoxaluria were present in 18.6% and 44.1%, respectively, while 11.9% of patients had both abnormalities. Hypomagnesuria and hypocitraturia were present in 67.8% and 69.5%, respectively, while 45.7% had both of these abnormalities. Normal urine chemistry in respect of parameters studied was observed only in 1.7% of cases. In 15.2% one risk factor was present, while 83.1% had two or more risk factors. "Path" analysis of the urinary parameters directly related to calcium lithiasis showed that magnesium and oxalic acid have substantial influence on calcium excretion, whereas citric acid had none. The influence of phosphorus did not provide any consistent trend.
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PMID:Interdependence of urinary factors in calcareous bladder stone patients. 274 86

Oxalate was measured by ion chromatography in the ultrafiltrate of heparinized plasma from peripheral venous blood, using a membrane with a cut-off molecular weight (Mr). The following criteria were established: sensitivity 0.7 mumol.l-1; intra- and inter-assay coefficients of variation 4% and 12%, respectively; precision of duplicate determinations (expressed as standard deviation) 0.08 mumol.l-1; overall recovery (oxalate added and diluted, respectively) 100.7%. These qualified the method for assessment of plasma oxalate in healthy human controls (males: n = 12) as well as patients with idiopathic renal calcium urolithiasis (males: n = 22; females: n = 16). Renal calcium urolithiasis patients were subclassified into those with normocalciuria and idiopathic hypercalciuria. In male and female controls the mean values (and range) of plasma oxalate were 1.98 (1.4-2.5) and 1.78 (0.7-2.9) mumol.l-1, respectively. In male controls ultrafiltration (membrane cut off Mr 10,000) revealed that 11-16% plasma oxalate was bound to constituents having an apparent Mr above 10,000, and that with use of membranes with smaller pore size, the ultrafilterability of oxalate decreases further. In renal calcium urolithiasis the following values were elicited (mumol.l-1): male normocalciuria 1.78 (0.8-4.0), idiopathic hypercalciuria 1.58 (1.2-2.2); female normocalciuria 1.69 (0.8-3.6), idiopathic hypercalciuria 1.21 (0.8-2.1). The difference from controls is significant in idiopathic hypercalciuria (males and females). In contrast, in fasting urine of renal calcium urolithiasis the oxalate excretion rate (5-45 mumol per 120 min) and oxalate clearance (21-328 ml per min) resemble those in controls, whereas in renal calcium urolithiasis the fractional oxalate clearance (30-357% of creatinine clearance) tended to higher values (p less than 0.01, in male idiopathic hypercalciuria versus controls). It is suggested that 1) ion chromatography allows the reliable assessment of ultrafiltrable plasma oxalate in health and disease states, 2) in renal calcium urolithiasis this technique may help to elucidate oxalate pathophysiology, especially the mode of renal handling of oxalate.
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PMID:Oxalate measurement in the picomol range by ion chromatography: values in fasting plasma and urine of controls and patients with idiopathic calcium urolithiasis. 274 68

In the present study Farnolith (a granular powder consisting of different dietary fibres) was given to normals (n = 6), patients suffering from absorptive hypercalciuria type I (n = 6) and to one patient suffering from renal hypercalciuria. Farnolith binds calcium and reduces the calcium absorption from the intestine. In normals the urine- and serum parameters of calcium metabolism (total- and ionised calcium, parathyroid hormone and vitamin-D-metabolites) remained unchanged. In patients suffering from absorptive hypercalciuria type I a significant reduction of hypercalciuria was found; oxalic acid excretion had decreased as well. Lowered parathyroid hormone values returned to normal, vitamin-D-metabolites remained unaffected. In one patient suffering from renal hypercalciuria parathyroid hormone and 1,25-dihydroxy-vitamin D values increased, calcium excretion had not decreased, though. Our investigation shows that Farnolith is suitable for the treatment of absorptive hypercalciuria. Calcium homoeostasis is returned to normal by Farnolith, at the same time it does not produce secondary hyperoxaluria (as e.g. sodium cellulose phosphate). Patients with primary renal calcium loss should not be treated by Farnolith.
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PMID:Calcium metabolism in normal and in hypercalciuric patients on Farnolith, a dietary fibre preparation. 285 67

An assay system for the measurement of the rate of Calcium Oxalate Monohydrate (COM) seed crystal growth in a metastable solution of calcium chloride and sodium oxalate containing traces of 14C-oxalic acid was used to assess the inhibitory activity of pyrophosphate (10(-5) M-10(-4) M), citrate (10(-4) M-10(-3) M) and urines of normal and pyridoxine deficient rats. Both pyrophosphate and citrate were strong inhibitors of COM crystal growth and caused a 50% decrease in crystal growth rate at 1.50 X 10(-5) M and 2.85 X 10(-4) M respectively. Normal rat urine strongly inhibited the COM crystal growth, while pyridoxine deficient animals showed a significant (p less than 0.01) decrease in mean inhibitory activity as compared to pair-fed controls. A lowered urinary inhibitory potential accompanied with hyperoxaluria and hypercalciuria, which is known to be associated with pyridoxine deficiency, may be a contributory risk of calcium oxalate crystallization and stone formation.
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PMID:Inhibition of calcium oxalate monohydrate (COM) crystal growth by pyrophosphate, citrate and rat urine. 302 39


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