Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increasing the concentration of urate promotes the crystallization of calcium oxalate in human urine. In this study the possibility that this effect might be attributable to the attenuation of the inhibitory activity of urinary glycosaminoglycans (GAGs) was explored. Urine sample were collected from 20 men with no history of urolithiasis and the intact GAGs removed by 10 kDa ultrafiltration. Ten of these specimens, designated type A, spontaneously precipitated calcium oxalate crystals when the median urate concentration was increased from 3.13 to 7.33 mmol/liter by the addition of a saturated solution of sodium urate. In the remaining more dilute urines, which were designated type B, spontaneous calcium oxalate crystallization did not occur when the median urate concentration was raised from 2.20 to 6.40 mmol/liter. In these samples crystallization was induced by a standard load of oxalate above the empirically determined metastable limit. Addition of urate significantly reduced the median metastable limit from the control value of 125 to 46 mumol oxalate, and the volume of calcium oxalate deposited was increased fourfold from 25,000 to 104,000 microns 3/microliters. The median size of the precipitated particles was also increased in the presence of urate from 12.06 microns to 14.3 microns; this was confirmed by scanning electron microscopy, which demonstrated that the crystals precipitated in the presence of added urate, though individually smaller, were markedly more numerous and more highly aggregated than those deposited in the control. Re-ultrafiltration of the urines to which urate had been added did not alter the urate concentration, and SEM examination of the ultrafiltration membranes did not reveal the presence of any particulate material.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium oxalate crystallization in urine: role of urate and glycosaminoglycans. 159 51

Calcium phosphate urolithiasis and bilateral renal dysplasia was diagnosed in an 8-week-old Border Terrier with a history of urine dribbling, which had been observed from the time of birth. Most reported cases of calcium phosphate urolithiasis are secondary to hypercalcemic disorders, but this was not detected. In addition, despite renal dysplasia, there was no evidence of renal failure. After cystotomy and calculus removal, the dog has remained clinically normal.
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PMID:Calcium phosphate urolithiasis and renal dysplasia in a young dog. 161 88

Formation of agglomerates of calcium oxalate monohydrate (COM) crystals on semi-batch precipitation performed at conditions relevant to urolithiasis (37 degrees C, pH = 6, initial ratio [Ca]/[Ox] = 10), but without any specific admixture, was followed by both optical and electron microscopy. COM crystals formed on precipitation developed into large agglomerates consisting of intergrown crystals by a mechanism of primary agglomeration. Primary agglomeration of COM crystals represents an important mechanism of COM renal calculi growth.
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PMID:Role of agglomeration in calcium oxalate monohydrate urolith development. 163 May 37

In a randomised trial based on a parallel design to determine the prophylactic effect of thiazide on stone formation, 210 calcium urolithiasis patients with idiopathic hypercalciuria were allocated either to treatment with trichlormethiazide (4 mg/day) or no treatment with only close follow-up; 35 patients were excluded for various reasons, including voluntary withdrawal. The background of the remaining 175 patients (82 in the thiazide group and 93 in the control group), including age and sex, was similar for both groups. In patients treated with thiazide there was a statistically significant fall in urinary calcium output. Statistical analyses also demonstrated that the stone formation rate in the thiazide group was significantly less than that in the control group. Adverse clinical reactions probably due to the drug were observed in 9 patients. These findings indicate that trichlormethiazide has a prophylactic effect on calcium urolithiasis in patients with idiopathic hypercalciuria.
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PMID:Thiazide treatment for calcium urolithiasis in patients with idiopathic hypercalciuria. 163 40

The effect of chondroitin sulfate upon the growth of calcium oxalate crystals was measured in vivo by using an experimental model in rats. Adult male Wistar rats were treated by chronic i.p. injections of chondroitin sulfate solutions (1, 5 or 10 mg in 0.3 ml of saline, every 2 days). This treatment led to a dose-dependent increase in the urinary chondroitin sulfate concentration. Urolithiasis was induced by the introduction of a calcium oxalate seed into the bladder of the animals. Urine samples were collected and the calculi formed were removed after 42 days. The chondroitin sulfate concentration have decreased in the lithiasic urines, as compared to controls and higher chondroitin sulfate doses correlated with larger calculi. The presence of chondroitin sulfate in the matrices of stones obtained from chondroitin sulfate-treated animals suggested that there was some adsorption of chondroitin sulfate on to the growth sites of the calcium oxalate crystals. In contrast to the chondroitin sulfate effect observed in vitro, which inhibits the growth of calcium oxalate crystals, our results suggest that in vivo chondroitin sulfate promotes the growth of stones in the urinary tract.
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PMID:Possible role for chondroitin sulfate in urolithiasis: in vivo studies in an experimental model. 163 45

The study aimed at presenting own experience in prevention of new urinary calculi in 18 patients with metabolically active calcium urolithiasis treated with hydrochlorothiazide in daily doses of 100 mg (group I) for 2 years, and in 6 patients with the same disease treated with magnesium oxide in daily doses 300 mg twice a day (group II) for average period of 10 months. In 9 patients a new calculus was formed during the treatment with hydrochlorothiazide, in 7 patients no recurrence was noted, and in 2 remaining patients the results were controversial (coral calculus). Therefore, patients were subdivided into group Ia (failure of hydrochlorothiazide therapy), and group Ib (no recurrence noted). Hydrochlorothiazide did not lead to the stable decrease in the saturation of the urine with calcium oxalate in group Ia whereas in group Ib (without recurrence of urolithiasis) the content of calcium oxalate in the urine was significantly lower than that in group Ia after a 2-year treatment with hydrochlorothiazide (p < 0.01) Recurrence of the disease was seen only in one patient of group II, i.e. treated with magnesium oxide. The treatment of the recurrent calcium urolithiasis is justified and efficient in those patients in whom therapy decreases the content of calcium oxalate in the urine.
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PMID:[Hydrochlorothiazide, allopurinol and magnesium oxide in the treatment of recurrent calcium urolithiasis]. 166 48

The interaction between calcium and glycosaminoglycans (GAGs) was studied using a calcium ion-selective electrode. The Ca-binding capacity of GAGs involved 16% of total calcium in the presence of chondroitin sulphate and 28% in the presence of pentosan polysulphate. The action of GAGs on the nucleation of uric acid and sodium urate was examined and inhibitory effects were observed. The action of uric acid as a heterogeneous nucleant of calcium oxalate was studied, and considerable promotion of the heterogeneous nucleation of calcium oxalate by uric acid was found, which could be inhibited by the action of GAGs. From these summarised in vitro results, we conclude that uric can constitute an important risk factor for calcium oxalate urolithiasis through heterogeneous nucleation and the GAGs can play an important role as preventive agents.
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PMID:Glycosaminoglycans, uric acid and calcium oxalate urolithiasis. 175 32

To evaluate underlying causes of calcium oxalate urolithiasis, 24-hour excretion of urine metabolites was measured in 6 Miniature Schnauzers that formed calcium oxalate (CaOx) uroliths during periods when they were fed a standard diet and during periods when food was withheld. Serum concentrations of parathyroid hormone and 1,25-dihydroxyvitamin D also were evaluated. Serum calcium concentrations were normal in all 6 affected Miniature Schnauzers; however, during diet consumption, mean 24-hour urinary excretion of calcium was significantly (P = 0.025) higher than calcium excretion when food was withheld. In 1 dog, urinary calcium excretion was lower during the period of food consumption, compared with the period when food was withheld. Compared with clinically normal Beagles, Miniature Schnauzers that formed CaOx uroliths excreted significantly greater quantities of calcium when food was consumed (P = 0.0004) and when food was withheld (P = 0.001). Miniature Schnauzers that formed CaOx uroliths excreted significantly less oxalate than clinically normal Beagles during fed (P = 0.028) and nonfed (P = 0.004) conditions. Affected Miniature Schnauzers also excreted abnormally high quantities of uric acid. Excretion of citrate was not different between Miniature Schnauzers with CaOx urolithiasis and clinically normal Beagles. In 5 of 6 Miniature Schnauzers with CaOx urolithiasis, concentrations of serum parathyroid hormone were similar to values from age- and gender-matched Miniature Schnauzers without uroliths. The concentration of serum parathyroid hormone in 1 dog was greater than 4 times the mean concentration of clinically normal Miniature Schnauzers. Mean serum concentrations of 1,25-dihydroxyvitamin D in Miniature Schnauzers with calcium oxalate urolithiasis were similar to concentrations of clinically normal Miniature Schnauzers.
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PMID:Evaluation of urine and serum metabolites in miniature schnauzers with calcium oxalate urolithiasis. 176 76

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

The main risk factors for calcium urolithiasis that are clinically detectable are low diuresis, hypercalciuria, hyperruricuria, alkaline urinary pH, hyperoxaluria, hypomagnesuria, hypocitraturia. They should be evaluated, all the more precisely that the disease is active, under both the urological and metabolic points of view, using 24 hour urine collection made at home on a free diet with a dietary record. In the majority of the cases the calcic urolithiasis is idiopathic, i.e. not related to a cause of secondary hypercalciuria like primary hyperparathyroidism, or to a hyperroxaluria either primary or of digestive or toxic origin. Its treatment if mainly dietary with high fluid intake (diuresis greater than 2 1/24 h), normoclacic diet (800-1000h mh/24 h) with meat but not dairy product restriction, oxalate salts, carbohydrate and alcohol restriction. These dietary recommendations should be controlled by measuring the above cited parameters in the 24 hour urine samples and by measuring urea excretion which should not exceed 0.33 g/kg of body weight. When diet fails, drugs may be added mainly allopurinol, thiazides and potassium citrate.
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PMID:[Physiopathology, exploration and treatment of calcium lithiasis]. 178 95


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