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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both urate and oxalate are organic acids of considerable clinical interest, owing to their limited solubility. Calcium oxalate is the most frequent constituent of renal calculi and occasionally precipitates in body fluids. Urate precipitations are common in the kidney and in various other tissues. In this paper, a short outline of the present knowledge of renal handling of these substances will be followed by some conclusions as to the possible relevance of this knowledge for the understanding of urolithiasis and intrarenal precipitation. Direct (micropuncture) data are available for urate in the rat (1, 6, 7, 10, 21, 23, 28, 36, 42), rabbit (35), dog (34) and cebus monkey (33) and in the rat only for oxalate (11, 15, 20).
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PMID:Renal handling of urate and oxalate: possible implications for urolithiasis. 11 10

Urolithiasis is seen in our region throughout the year as a periodic appearing disease with peaks not only in summer, but also--somewhat lower--in January, April and October. This appearance is especially caused by the calcium oxalate stones. Uric acid calculi show a rise between May and October. The magnesium ammonium phosphate stones appear almost completely irregular.
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PMID:[Typical annual course of urolithiasis in relation to the chemical structure of the concrements (author's transl)]. 54 53

Urinary concentrations of certain biochemical constituents that play an active role in stone formation were determined in 2 h urine collections in healthy men and women (at four phases of the estrous cycle) to elucidate the sex difference in the incidence of urolithiasis. The excretion of the lithogenic substance, calcium, was higher in men than in women during phase I (p less than 0.01) and phase II (p less than 0.05) of the estrous cycle. Oxalate excretion was marginally elevated in men compared to women during each phase. Urinary citrate was lower in men compared to women during each phase (p less than 0.05). Uric acid excretion was lower (p less than 0.05) in men compared with phase I and phase III in women. Estrous phase-related alterations were also observed in the excretion of calcium and citrate in women. The data suggest that low concentrations of calcium and oxalate with an elevated citrate excretion might be responsible for the reduced risk of stone disease in women compared to men.
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PMID:Urinary composition in men and women and the risk of urolithiasis. 177 89

Serum uric acid and 24-hour urine uric acid levels were determined in 47 patients with urolithiasis and in 177 healthy volunteers. The normal volunteers had serum and urinary uric acid levels of 6.0-6.4 mg/dl, 619.4-683.7 mg/day for males and 4.6-4.8 mg/dl, 531.5-589.6 mg/day for females. Uric acid levels in both serum and urine were higher in male volunteers than in female volunteers (p less than 0.05), whereas, among patients the ranges of serum and urinary uric acid levels were not significantly different between males and females (p greater than 0.05). However, the normal distribution of the determined small experimental data, was statistically different and is obviously reliable. Patients with urolithiasis showed significantly higher levels of serum uric acid (8.0 +/- 0.3 mg/dl) than healthy volunteers (5.5 +/- 0.1 mg/dl) (p less than 0.05), but showed no difference in urinary uric acid levels compared with healthy volunteers (p greater than 0.05). The highest number of urolithiasis in both male and female patients fell within the same age range of 41-50 years. The 24-hour urine pH of healthy volunteers showed a range of 5.1-7.0 while the patients with urolithiasis had a pH range of 4.6-7.0. It was also found that 33 per cent of patients had urine pH less than 5.0.
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PMID:Serum and urinary uric acid levels in healthy subjects and in patients with urolithiasis. 179 85

Attachment of microcrystals to cellular membranes may be an important component in the pathophysiology of urolithiasis. This study characterizes the concentration-dependent binding of uric acid crystals to rat renal inner medullary collecting duct cells in primary culture. Collecting duct cell cultures grew as monolayers with interspersed aggregates of rounded cells. Cultures were incubated with 14C-uric acid crystals, and the crystals that bound were quantitated by adherent radioactivity. Uric acid crystal adherence demonstrated concentration dependent saturation with a 1/alpha value (maximum micrograms of crystals adhering to 1 cm2 of binding area) of 645 micrograms/cm2. The beta values (fraction of cross-sectional area which bound crystals) of uric acid (mean = 0.15) and calcium oxalate monohydrate (mean = 0.13) crystals did not differ significantly. Uric acid crystal binding was inhibited by pre-bound calcium oxalate monohydrate crystals in a concentration dependent manner. These data suggest that uric acid and calcium oxalate crystals exhibit similar binding patterns to rat renal inner medullary collecting duct cells in primary culture.
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PMID:Uric acid crystal binding to renal inner medullary collecting duct cells in primary culture. 210 62

Urinary uric acid excretion was assessed in 38 children to determine whether hyperuricuria was a risk factor in children with urolithiasis. Uric acid excretion (measured per deciliter glomerular filtration rate), and fractional excretion of uric acid were similar in 27 children with hypercalciuria and calcium oxalate urinary stones, in six children with idiopathic calcium oxalate urolithiasis, and in five with uric acid urolithiasis, of whom four were white boys and one was an Asian girl. One boy with a urate stone had cystinosis. Serum uric acid concentrations exceeded 6.0 mg/dl (360 mumol/L) in two children with hypercalciuria and in two patients with idiopathic calcium oxalate urolithiasis. None of the children with calcium urolithiasis had excessive urinary excretion of uric acid. In children with hypercalciuria, uric acid excretion did not change significantly when dietary sodium was increased from 1.0 to 5.0 gm/1.73 m2. We conclude that excessive urinary uric acid excretion is seldom an additional risk factor in children with calcium urolithiasis and that dietary sodium chloride does not have a strong influence on urinary excretion of uric acid in children with hypercalciuria.
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PMID:Uric acid excretion in children with urolithiasis. 258 28

In 13 patients suffering from recurrent calcium-oxalate urolithiasis the circadian course in the excretion of urinary components was investigated before and during treatment with a combination of allopurinol and benzbromarone. The patients were given a diet standardized in food and liquid intake. Urine was collected for 3 days every 3 h from the 7th day of standard diet. On days 8 and 9 each patient received one tablet of the combination. On all 3 days of urine collection a constant circadian course of urine volume was observed; pH values also showed a nearly identical course on all 3 days with increased daytime and low night values. Maximum excretion of uric acid under dietary conditions was discovered between 11 a.m. and 5 p.m. (day 7). After the first application of the compound (day 8, 8 a.m.) a transient increase in uric acid excretion was observed in the third collection period (2-5 p.m.), followed by a sharp decrease. Following the second application (day 9) the transient increase of the uric acid excretion was clearly diminished. Uric acid excretion in the 24-h urine also decreased steadily from 3.46 mmol/day (control) to 3.25 and 3.06 mmol/day (treatment). Serum uric acid decreased significantly from 324.5 to 275.6 mumol/l. After the first application of the compound (day 8) moderate changes of the urinary components - oxalic acid, Na, K, and chloride - significant changes of Ca were observed, whereas after the second application of the compound (day 9) the values no longer differed from control values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of an allopurinol/benzbromaron preparation on the composition of urine in a circadian course]. 357 81

APRT deficiency may be totally benign or life threatening. The importance of early recognition/diagnosis is thus stressed. Urolithiasis (2,8-DHA stones: the precipitating factor in all cases) is treatable. With early recognition and treatment allopurinol without alkali and a diet low in purine homozygotes have remained clinically and biochemically normal to date. 'Uric acid' stones in children must always be suspect and subjected to sophisticated analysis. Diagnosis from red cell APRT activity may also have its pitfalls.
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PMID:Spectrum of 2,8-dihydroxyadenine urolithiasis in complete APRT deficiency. 742 54

Uric acid is formed by catabolism of purine nucleotides. Approximately 25% is excreted through the intestines and the rest through the kidneys. A little less than 5% of the population in western industrialised countries have hyperuricaemia, primarily men and postmenopausal women. Hyperuricaemia is in most cases caused by reduced renal excretion, which may be idiopathic with otherwise normal renal function. But the condition is often associated with hypertension, nephropathy and treatment with diuretics and certain other drugs. Hyperuricaemia due to increased purine metabolism is seen in malignant haematological diseases, other conditions with increased cellular turnover and during initiation of chemotherapy in malignant diseases. Moreover hyperuricaemia is associated with some metabolic disturbances and risk factors of atherosclerotic cardiovascular disease including hypertension, overweight, insulin resistance and hyperlipidaemia. Hyperuricaemia is rarely caused by constitutional enzymatic abnormalities influencing purine metabolism. In most cases hyperuricaemia is asymptomatic. It may though be complicated by gout, urolithiasis and possibly gouty nephropathy. The risk of complications is correlated to the degree and duration of hyperuricemia. Consequently, measures to affect predisposing and associated conditions should be taken including weight reduction, physical exercise and diet guidance, treatment of hypertension and possibly changes in medication. Urate lowering drug treatment is normally not indicated in asymptomatic hyperuricaemic individuals.
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PMID:[Hyperuricemia]. 800 1

Effect of uric acid on sodium oxalate-induced biochemical and histological changes were studied in rats. Rats injected with sodium oxalate (0.7 mg/100 g body wt, ip) show calcium deposits in the lumen of kidney tubules. Uric acid administration was found to potentiate calcium oxalate calculi formation. Lipid peroxide formation was increased up to 100% in kidney and 28% in liver by sodium, oxalate treatment. Uric acid administration was found to reduce lipid peroxide level up to 12% in liver and 20% in kidney. From this study it is concluded that lipid peroxidation may not be the cause of sodium oxalate-induced urolithiasis and the results are discussed with reference to the epitaxic nature of uric acid on kidney stone formation.
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PMID:Effect of uric acid on sodium oxalate-induced urolithiasis in rats--biochemical and histological evidences. 804


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