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

Urinary excretion of gamma-glutamyl transpeptidase, angiotensin I converting enzyme, beta-galactosidase and N-acetyl-beta-glucosaminidase was evaluated in 30 patients with idiopathic calcium oxalate urolithiasis. Higher than normal values were observed and the excretory enzyme pattern suggested tubular damage in patients with stones. A parallel study in the rat showed that an oxalate surcharge can promote increased urinary excretion of these enzymes. It is known that urothelium injury may enhance crystal adhesion. If the damage is primary it may be viewed as a promoting factor. If it is secondary it may be considered a factor capable of increasing salt precipitation.
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PMID:Increased urinary excretion of renal enzymes in idiopathic calcium oxalate nephrolithiasis. 613 62

This paper represents a review on the role played by promoters and inhibitors in the formation of urinary stones. It appears that both mechanisms are, together with the degree of supersaturation, important in the development of urolithiasis. For the promoting activity emphasis has shifted towards the role of crystals of one salt inducing epitactically the precipitation of another salt. For the inhibitors it is important to distinguish the effect on crystal growth and aggregation. While citrate, pyrophosphate and magnesium are probably the most relevant for crystal formation, glycosaminoglycans play the primary role for aggregation. This field is still at its beginnings, and it might be rewarding to focus future investigations both in the laboratory and clinically along these directions.
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PMID:Mechanisms of stone formation: role of promoters and inhibitors. 701 May 71

In a 4x4-wk cross-over study, eight adult cats were given four moist diets containing identical amounts of calcium (13.9 mmol/MJ) but with different ratios of calcium carbonate to calcium chloride, the calcium salts providing half of the total dietary calcium. Increasing amounts of calcium chloride were substituted for equimolar amounts of calcium carbonate. Higher intakes of calcium chloride caused significantly lower pH values in postprandial and 24-h urine samples. The urinary excretion of ammonium and titratable acid rose with increasing calcium chloride intake. The urinary concentrations of calcium and magnesium were not affected by the type of calcium salt, but the urinary excretion and concentration of phosphorus were significantly depressed when the amount of calcium chloride in the diet was increased. The results are discussed in the context of dietary prevention of and therapy for struvite urolithiasis in cats.
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PMID:Substitution of dietary calcium chloride for calcium carbonate reduces urinary ph and urinary phosphorus excretion in adult cats. 787

An extensively updated version of the EQUIL software is described. The former version, designated EQUIL2, is widely used to study urolithiasis and related areas of biomineralization. In this report, we discuss recent enhancements which give EQUIL93 an expanded scope of application. This program has been frequently used in studies of the physicochemical processes underlying stone salt crystallization, especially crystal growth and nucleation, but it has also been employed as an aid for in vivo research and as an evaluator of therapeutic measures. We illustrate several new applications, including some outside the urologic realm, and we discuss how the enhanced software can be helpful in stone risk assessments.
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PMID:EQUIL93: a tool for experimental and clinical urolithiasis. 797 15

Can urolithiasis start as an intratubular event? Under severe hyperoxaluric conditions in animal models at least crystal formation can. Recently models have been presented that assess the chances of crystal formation under more normal conditions. These models describe changes in fluid composition as this passes through the nephron, these conditions being simulated in in vitro experiments. It appears that under naturally occurring intratubular conditions calcium-salt crystallization takes place within the time tubular fluid normally spends in the nephron. Precipitation starts with a calcium-phosphate phase under conditions found in the thin lambs. This crystalline phase then (partly) dissolves when collecting duct conditions are used, thereby inducing formation of calcium oxalates. Under these conditions the latter increase in size by way of crystal growth and agglomeration. Large particle formation and cell adhesion can eventually result in particle retention and subsequent stone formation. Viewing urolithiasis as originally an intratubular event has consequences for in vitro experiments and treatments, which are discussed in this paper.
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PMID:Intratubular crystallization events. 928 50

The calcium (Ca)-restricted diet of urolithiasis patients with absorptive hypercalciuria type II may decrease Ca excretion but increase biochemical markers of risk for osteopenia. We randomly allocated 25 patients from six hospitals into an experimental group (Ca restriction to 500 mg/day, oxalate-rich products discouraged and normalization of animal protein and sodium) and a control group (no restrictions) for one month. The urinary Ca excretion did not decrease significantly, but the oxalate excretion decreased, although not significantly. The hydroxyproline:creatinine ratio in fasting urine seemed to increase and the calcium:creatinine ratio to decrease. The deoxypyridinoline:creatinine ratio in fasting urine did not change. We conclude that our Ca-restricted diet, which is lower in Ca, animal protein and table salt due to the omission of dairy products, may be of benefit for absorptive hypercalciuria type II patients without enhancing the risk for osteopenia. However, a long-term clinical trial is required.
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PMID:The effects of the calcium-restricted diet of urolithiasis patients with absorptive hypercalciuria type II on risk factors for kidney stones and osteopenia. 953 99

A ten-year experience with diagnosis and therapy of metabolic abnormalities and crystallization risks in patients with recurrent urolithiasis is presented. Since 1985, more than 900 persons with recurrent urolithiasis have been examined at the Metabolic Centre of the Hospital in Sternberk. The patients were examined routinely at ambulance or during hospitalization; the examination consisted of repeated urine and blood collections after the diet with various content of calcium and salt. All initial data (case history, physical finding, biochemistry, radiodiagnostics) were processed by a semi-expert computing program SOFT which was also used for monitoring of the therapy. Then the patients were divided into individual risk groups (Pak). Of all probands, the group of 130 patients (satisfying the strict criteria of the study) was selected and the data obtained was processed statistically. The group of 130 patients with recurrent urolithiasis (all of them were drug-treated) was compared to the group of 50 individuals with urolithiasis treated by diet and regimen measures. The patients given drugs showed a significantly increased crystallization inhibitors concentration in urine and reduced crystallization promotors, or relative saturation of some lithiatic substances. The paper analyzes the effect of the mostly administered drugs on crystallization risks and some less known "metabolic" indications of application of some drugs are recommended. It is concluded that the dietary, drinking and regime measures are basic for a good therapy of patients with urolithiasis, but patients with recurrent urolithiasis should be applied a selective metaphylaxis of drugs after routine metabolic examination. This finding is supported by a low number of recurrent urolithiasis.
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PMID:[Personal experience in the diagnosis and monitoring of therapy in metabolic disorders with risk of crystallization in patients with recurrent urolithiasis]. 960 89

In up to one-third of patients with calcium oxalate stones, a hyperoxaluria can be detected. Hyperoxaluria can result from increased endogenous production, from excessive oxalate content of the food, or from intestinal hyperabsorption. For a causal therapy, it is important to discriminate between metabolic and hyperabsorptive hyperoxaluria. Our new 13C-oxalate test allows this differentiation. Under standardized conditions, 50 mg of disodium salt of [13C2]oxalic acid was applied. From the amount of labeled oxalate excreted in urine as measured by a gas chromatographic-mass spectrometric assay, the intestinal absorption was calculated. Seventy patients with recurrent calcium oxalate urolithiasis who had no signs of inflammatory bowel disease were tested. Their mean intestinal oxalate absorption was 9.2+/-5.1%. This was significantly higher than the mean absorption of 50 healthy volunteers (6.7+/-3.9%). There was no difference in oxalate absorption between male (n = 25) and female volunteers. Oxalate absorption correlated with the oxalate excretion in the 24-h urine (volunteers: r = 0.46, P < 0.01; patients: r = 0.62, P < 0.001). Oxalate hyperabsorption was defined as an absorption exceeding 10%. According to this definition, 34% of the patients had oxalate hyperabsorption; 20% of the volunteers showed a hyperabsorption, too. The 13C-oxalate absorption test allows reliable determination of intestinal oxalate absorption. Because of the use of a stable isotope, this test may be repeated as often as required. It will allow the control of therapeutic regimens and also help to unravel genetic influences in stone formation.
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PMID:Intestinal hyperabsorption of oxalate in calcium oxalate stone formers: application of a new test with [13C2]oxalate. 1054 Dec 57

Two cases of urinary retention in male dromedaries due to silica uroliths are presented. The animals were urethrostomized and one dromedary was euthanized 7 months later due to urethrostomy obstruction. The estimated daily intake of silica was 84.44 g. Silica, calcium, phosphorus and pH in urine were determined in healthy animals from the same farms, and the following values were obtained: 174.78 +/- 3.46 mg/l (silica), 41.48 +/- 4.82 mg/l (calcium), 20.4 +/- 3.6 mg/l (phosphorus) and pH 8.2, respectively. Possible causes of urolithiasis were the early castration of the animals and the fact that salt was not added to the diet. To our knowledge, this is the first description of silica urolithiasis in the dromedary camel.
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PMID:Urinary retention in two male dromedaries due to silica uroliths. 1060 61

Treatment of urolithiasis depends on the stone and secretion renal tubular transport disturbances. Conservative treatment of urolithiasis and prevention of stone formation in children should consist of: adequate fluid intake, low salt and animal protein diet in all stone formers; calcium-oxalate stones: diet containing a proper amount of dairy product, low oxalate diet, if indicated: thiazide diuretics, magnesium salts, citrate; uric acid stones: low purine diet, alkalization of urine up to pH 6.5-7.0, if indicated: allopurinol; infection stones: treatment of the urinary tract infection, low phosphate diet; cystinuria: low animal protein diet, alkalization of urine up to pH 7.0, if indicated: captopril, d-penicillamine.
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PMID:[Conservative treatment of urolithiasis in children]. 1089 7


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