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

To evaluate the clinical utility of in vitro calcium oxalate monohydrate (COM) crystallization kinetics measurements and to determine the effect of quantitative removal of urinary Tamm-Horsfall glycoprotein on such measurements, we examined 24-hour, room temperature urine collections of patients from our Stone Clinic and of normal subjects from our research laboratories at Ochsner Medical Institutions in New Orleans, LA, and compared their COM kinetic parameters in vitro before and after urine ultrafiltration (30 kd). Data from 53 calcium oxalate stone-forming patients (26% women; mean age, 47 years) who demonstrated radiographic or other evidence of forming at least one stone were compared with data from 22 healthy volunteers (25% women; mean age, 40 years). Hypercalciuria (> 7.5 mm/24 hr), hyperoxaluria (> 0.5 mm/24 hr), and hypocitraturia (< 2.0 mm/24 hr) were present in 38%, 26%, and 26% of the patient population, respectively. Urinary creatinine, urate, calcium, citrate, phosphate, oxalate, pH, volume, total immunoreactive-disaggregated Tamm-Horsfall glycoprotein, and the urine's effects on COM solubility, percent crystal growth inhibition, and crystal agglomeration inhibition [tm] were determined. Calcium oxalate monohydrate agglomeration inhibition, [tm], was reduced in stone-forming patients. It decreased with increasing stone frequency, making [tm] a useful tool for measuring the risk of stone recurrence. Urinary Tamm-Horsfall glycoprotein and citrate concentrations were linearly related to COM agglomeration inhibition. Their effects were synergistic. Tamm-Horsfall glycoprotein removal from urine reduced COM agglomeration inhibition dramatically. Alkali therapy increased urinary citrate concentration and increased [tm].(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium oxalate stone agglomeration reflects stone-forming activity: citrate inhibition depends on macromolecules larger than 30 kilodalton. 798 66

The serum and 24 hour urinary excretion levels of various lithogenic and inhibitory substances were assessed in 24 male patients with calcium stone and no previous history of urolithiasis and in 19 age-matched controls. Two groups did not differ significantly (P < 0.01) except in the excretions of sodium, citric acid (being higher in normals) and inorganic phosphate (being higher in patients). Fifty percent patients had hyperphosphaturia, 29.2% hypocitraturia, 20.8% hyperoxaluria and 16.7% hypercalciuria. The present data suggests that hypocitraturia in association with phosphaturia might be one of the main risk factors responsible for calcium urolithiasis in this area.
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PMID:Is hypocitraturia associated with phosphaturia--a potential cause of calcium urolithiasis in first-time stone formers. 799 62

Observed loss in body weight gain, increased lipid peroxidation reaction, decreased concentrations of antioxidants, ascorbic acid, alpha-tocopherol and reduced glutathione and antioxidant enzymes, glutathione peroxidase and catalase and increased concentration of hydroperoxides and hydroxyl radicals in vitamin B6 deficient rat liver [J Nutri Biochem, 2 (1991) 245] and kidney [Biochem International, 21 (1991) 599] were nearly normalized on feeding with vitamin E or methionine. Accumulation of oxalate and calcium during vitamin B6 deficiency was abolished by feeding vitamin E or methionine. Calcium oxalate deposition observed in vitamin B6 deficient kidney was completely prevented when fed along with vitamin E or methionine. However the hyperoxaluria and hypercalciuria persisted even after feeding with vitamin E or methionine.
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PMID:Restoration of tissue antioxidants and prevention of renal stone deposition in vitamin B6 deficient rats fed with vitamin E or methionine. 811 61

Although a low concentration of urinary citrate is cited as one of the risk factors promoting stone formation or recurrence among patients with urinary stones, its clinical significance remains obscure. We studied 62 kidney stone patients with a low urinary citrate excretion (hypocitraturia) of less than 320 mg/day, without any apparent cause. The incidence of hypocitraturia in 722 kidney stone patients followed up at our stone clinic was 14.6%. Among the 62 patients, 37 had an uncomplicated hypocitraturia as the sole abnormality, while 25 had other associated stone risk factors, including hypercalciuria in 11% (7/62), hyperuricosuria in 24% (15/62), hyperoxaluria in 5% (3/62) and hypomagnesuria in 24% (15/62). The rate of urinary stone recurrence was 38% (14/37) in uncomplicated hypocitraturia, and 52% (13/25) in complicated hypocitraturia, but no statistical difference was observed. Regarding the outcome of stones, more stones were managed with lithotripsy and more passed spontaneously in the hypocitraturic patients than in the control patients with normal urinary citrate excretion. The diagnosis of hypocitraturia complicated with additional stone risks urged us to treat patients more vigorously with lithotripsy and medication, resulting in a prompt cure.
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PMID:Clinical significance of hypocitraturia in kidney stone patients. 813 38

In order to better understand the role of diet in etiology of urolithiasis, 84 oxalo-phospho-calcic-lithiasic patients (52 men, 32 women) have been studied by a nutritional week-interview and by urinary and blood testing. Diet data were compared to an ideal standard. Total caloric intake was 2428 +/- 651 calories/d; this intake is high in 7% women and 40% men. 79% out of patients are fat. Protidic intake is 87 +/- 21 g/d higher than 1 g/kg/d in 84.5% of patients. Lipids are high in 38.9 +/- 7%, glucid are low in 45.3 +/- 7%. Calcium intake is 934 +/- 406 mg/d, sodium intake is 12.9 + 3 g/d. Water intake is 2305 +/- 759 ml/d. Different groups of patients are studied: a) 21 patients with mean age of 43 +/- 12 years have recurrent lithiasis (R). This group is compared to 48 patients with 37 +/- 44 years who have a single lithiasis. Half of (R) patients have hypercalciuria, hyperphosphaturia and hyperoxaluria. Diet study is no different between these two groups. b) Other groups are studied: 21 have hyperophosphaturia (HPU) without hypophosphoremia and they have hypercalciuria, hyperuraturia and high urinary urea; diet shows higher glucicid and potassium intake than group with normal phosphaturia; 23 have hypercalciuria (HCU) and high uraturia and phosphaturia: diet study shows no difference with a group with normal calciuria. 21 have hyperoxaluria (HOU): diet study of a normal oxaluric group shows higher lipid intake, lower glucidic and calcium intake; 22 have hyperuraturia (HAU) and higher urinary urea, sodium and potassium than normouraturia group: in this group potassium intake is higher.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Results of dietary evaluation during calcium oxalate and calcium phosphate lithiasis]. 814 88

In this paper a thorough study on the composition and structure of calcium oxalate monohydrate (COM) papillary calculi is presented. In 86.4% of these calculi, small amounts of phosphates were detected and generally located at the calculi core. This demonstrates the importance of phosphates as the heterogeneous nucleus of 'pure' COM calculi. Study of the main biochemical parameters of these patients showed that the most frequent biochemical alteration was associated with hypocitraturia (25%), whereas hypercalciuria and/or hyperoxaluria were detected in very few cases. With respect to the urinary pH values, 70% of the patients presented values lower than 6 and 30% higher than 6. These facts indicate that in a number of cases the formation of phosphates is not the result of persistent high urinary pH values, and the presence of occasional papillary microinfections must be suspected. It is clear that, by avoiding the formation of heterogeneous phosphate nuclei, 'pure' COM calculi would not develop, and consequently therapies for these individuals under these conditions must take this into account.
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PMID:New aspects on the composition, structure and origin of calcium oxalate monohydrate calculi. 826 7

The hypothesis that mild hyperoxaluria is more important than hypercalciuria in the pathogenesis of urolithiasis is re-examined in the light of new evidence. Small increments in urinary oxalate in the normal to high-normal range are much more critical than similar rises in urinary calcium for increasing the relative supersaturation of urine with respect to calcium oxalate, the oxalate/calcium ratio in urine, the total volume of calcium oxalate crystals excreted, the proportion of abnormally large crystals and aggregates of calcium oxalate and the severity of the disorder as defined by the recurrence rate of stone-formation. Data from the Arabian Peninsula, where the prevalence of calcium-containing stones is considerably higher than in the West, have shown that this occurs in spite of the almost complete absence of hypercalciuria. On the other hand, there is a strong association between stone-formation and the occurrence of mild hyperoxaluria. The life-time expectancy of stone-formation in men from various countries is strongly correlated with the average daily excretion of oxalate in the urine of the normal men in these countries. This relationship extends to include patients with enteric and hereditary hyperoxaluria. There is no such relationship, however, between the life-time expectancy of stones and urinary calcium excretion in the same populations. Studies on the regulation of urinary oxalate indicate that it is largely controlled by the quantity of "free" dietary oxalate available for absorption in the lower intestine. This can be calculated from the intakes of calcium and oxalate and the urinary excretion of calcium.
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PMID:Importance of mild hyperoxaluria in the pathogenesis of urolithiasis--new evidence from studies in the Arabian peninsula. 831 8

1. Vitamin D seems to play an essential role in the pathogenesis of idiopathic hypercalciuria at least in part via intestinal hyperabsorption of calcium. Hyperabsorption of calcium, in turn, might enhance the intestinal uptake of free oxalate, thus leading to hyperoxaluria. To verify this hypothesis we studied 75 calcium-stone-formers subdivided as follows: group 1 (15 patients) with isolated hyperoxaluria; group 2 (25 patients) with hyperoxaluria and hypercalciuria; group 3 (22 patients) with isolated hypercalciuria; group 4 (12 patients) with no metabolic abnormalities. 2. As expected, urinary calcium excretion differed in the various groups (P < 0.001), being highest in groups 2 and 3; urinary oxalate excretion, by definition highest in groups 1 and 2, was even more pronounced in group 2 than in group 1 (P < 0.05). Although in the normal range, the serum 1,25-dihydroxyvitamin D concentration was higher (P < 0.001) in the two hypercalciuric groups (2 and 3), showing peak levels in group 2. 3. When the data from the 75 stone-formers were pooled, there was a positive correlation between the serum concentration of 1,25-dihydroxyvitamin D and urinary calcium excretion (P < 0.001) and urinary oxalate excretion (P < 0.003), the latter relationship also being present when only the two hypercalciuric groups (groups 2 and 3) were considered together (P < 0.05). 4. Our data seem to confirm a relevant role for the vitamin D system in the pathogenesis of calcium nephrolithiasis due to increased intestinal calcium absorption, but also because this in turn induces a greater intestinal absorption of oxalate, thus leading to the occurrence or exacerbation of hyperoxaluria.
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PMID:Possible link between vitamin D and hyperoxaluria in patients with renal stone disease. 838 34

The treatment of X-linked hypophosphatemia (XLH) consists of phosphate and vitamin D3 derivatives. Transient hypercalciuria and hypercalcemia are well-known signs of vitamin D intoxication. Despite urinary calcium excretion control, the danger of nephrocalcinosis in treated patients has been emphasized. It has recently been suggested that hyperoxaluria might be a causative factor of nephrocalcinosis other than calcium in phosphate-treated XLH patients. We measured urinary oxalate and phosphate excretion in 12 patients with the syndrome of hereditary hypophosphatemic rickets with hypercalciuria (HHRH) receiving only oral phosphates and in 5 XLH patients receiving both oral phosphates and vitamin D. No correlation was found between the dosage of phosphate supplements or urinary phosphate excretion and urinary oxalate excretion, in either group of patients. Nephrocalcinosis, presenting as hyperechogenicity of the medullary pyramids, was found in 2 of the 5 XLH patients and only in 2 HHRH patients who had been treated with excessive doses of vitamin D2 and calcium, prior to the true diagnosis being established. We conclude: (1) hyperoxaluria is not a cause of nephrocalcinosis in phosphate-treated patients with hereditary hypophosphatemic rickets; (2) prolonged phosphate treatment alone does not induce nephrocalcinosis in HHRH patients, and (3) we believe that in XLH patients, nephrocalcinosis is essentially due to vitamin D overdosage at some stage, or noncompliance in phosphate intake, leading to repeated undetected hypercalciuric periods.
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PMID:Hyperoxaluria is not a cause of nephrocalcinosis in phosphate-treated patients with hereditary hypophosphatemic rickets. 839 9

To elucidate the frequency and clinical picture of renal tubular acidosis-1 (RTA-1) in nephrolithiasis, the acid-loading test was performed in 474 patients with calcium-containing stones. RTA-1 was detected in a total of 11 patients (6 men and 5 women, 2.3%). The incidence of RTA-1 in female patients tended to be higher than in male patients (3.2 vs. 1.9%). One male patient had the complete form, the others had incomplete form. There was a tendency that RTA-1 patients were younger than non-RTA-1 patients in men, and the former were older than the latter in women. The percentages of positive family history and positive past history were 27 and 45%, respectively. Stones were single in 7 cases and multiple in 4 cases. They were unilateral in 10 cases, and bilateral in 1 case. Hypercalciuria was detected in 2 of the 11 cases, hyperuricosuria was present in none of the 11 cases, and hyperoxaluria in 2 of 8 cases examined. Stones were composed of calcium oxalate in 2 cases, calcium phosphate in 2, and calcium oxalate mixed with calcium phosphate in 3.
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PMID:Incidence and clinical features of renal tubular acidosis-1 in urolithiasis. 846 Apr 53


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