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

The prevalence of arterial hypertension (HT) was investigated in 258 patients (171 m, 87 f, 22-68 years) with a history of primary stone disease. HT was detected in 64 patients (24.8%), with no difference between males (25.7%) and females (23.0%). The prevalence of HT by age was very similar to that of a general population, especially in the calcium stone group. The discriminant analysis demonstrated that the composition of stones, other than the age and body weight of the patients, were the main factors associated with HT. As far as the different kind of stone is concerned, the prevalence of HT was higher in patients with uric acid (17/37, 45.9%) and struvite stones (11/27, 40.7%) than in calcium stone formers (35/188, 18.6%) (chi 2 16.31, p < 0.001). The prevalence of hypercalciuria was higher in the calcium stone group than in uric acid or struvite stone patients (36.4 vs. 9.7 vs. 13.7%; chi 2 10.35, p < 0.01). Furthermore, the hypercalciuria showed a trend to be more prevalent in the untreated (47.0%) than in the treated (31.2%) hypertensives, or normotensives (35.1%). Uric acid stone formers were older, heavier and with higher triglycerides and uric acid plasma levels than calcium or struvite patients. Also the struvite stone formers were older than the calcium stone ones. Our data suggest that the prevalence of HT in kidney stone patients and particularly in calcium stone formers is similar to that of a general population. The role of hypercalciuria as the link for HT-urolithiasis association seems quite uncertain. Struvite and uric acid stone formers have higher risk for HT than calcium stone formers, probably due to the old age or to the associated metabolic abnormalities.
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PMID:Hypertension in kidney stone patients. 885 53

Hyperuricosuria with or without hypercalciuria amounted to about 23% of the possible cause of urolithiasis in my clinical experience. Approximately three forth of urolithiasis caused by hyperuricosuria was calcium oxalate stones and the rest was uric acid stones. Uric acid is one of the composition of urinary stones itself, but it has an activity of calcium oxalate stone formation. The hypotheses why the uric acid induced calcium oxalate stones were introduced. The preventive effect of allopurinol on the recurrent calcium oxalate stone formers was proved in our previous study which may revealed the urinary uric acid promoted calcium oxalate stone formation or masked the inhibitory activity of urinary macromolecular inhibitors. On the basis of above statement, I emphasize the importance of the treatment of hyperuricosuria in preventing urinary stones.
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PMID:[Hyperuricosuria and urolithiasis]. 897 4

Urolithiasis is a very frequent finding in the Sudan, but stone analysis is not routinely performed in this country. It would, however, give important evidence for the metabolic basis of stone formation. We therefore set out to analyze urinary stones in 80 Sudanese patients (45 male, 35 female), 12 of whom where children. Fourier-transformed infrared spectroscopy was used for stone analysis. As is known from other countries, calcium oxalate (CaOx) stones were the most frequent, with 68.7% of all stones in adults and 43.7% of childhood stones. Uric acid and uric acid dihydrate stones were more often seen in adults (13.2%) than in children (4. 1%). Ammonium urate stones are common in the Sudan, especially in children (32.9%), which is typical for underdeveloped countries. Infectious stones (struvite and carbonate apatite) were more often found in women (7.0%) and in children (5.3%) than in men (1.4%). Brushite stones were seldom seen and cystine stones did not occur.
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PMID:Mineral composition of renal stones from the Sudan. 993 35

Uric acid (UA), a waste product of purine metabolism, may be involved in calcium phosphate crystallization and deposition. Rats, which develop nephrocalcinosis on high-fat or magnesium-deficient diets, and patients with idiopathic calcium urolithiasis have hyperproteinuria, especially of nonalbumin protein, and a shift toward elevated serum UA. In rats, an increase in UA precursors and renal UA suggests hypoxemia, which stimulates xanthine oxidase. In patients, a primary increase in renal xanthine oxidase would explain the low urine UA in the presence of an elevated serum concentration. For calcium phosphate deposition (rats) or incorporation into stones (humans) to occur, a crucial factor may be xanthine oxidase-mediated overproduction of free radical species and subsequent tissue damage. Another factor may be whether sufficient UA is synthesized to neutralize these free radicals. Allopurinol use, which inhibits xanthine oxidase and has long been favored for the treatment of idiopathic calcium urolithiasis, may not prevent stones, because it also diminishes the availability of UA. An investigation of the factors that control serum UA homeostasis may be rewarding in research into the etiology of idiopathic calcium urolithiasis.
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PMID:Is there a role for uric acid in an animal model of calcium phosphate nephrocalcinosis and calcium phosphate crystallization in urine of patients with idiopathic calcium urolithiasis? An orientational study. 1060 15

Kidney stones have been associated with use of the ketogenic diet in children with refractory seizure disorders. We performed a case-control study examining risk factors for the development of stones on the ketogenic diet, and prospectively followed children initiating the ketogenic diet to evaluate the incidence of urolithiasis. Clinical characteristics of 18 children presenting with stones (8 uric acid stones, 6 mixed calcium/uric acid stones, 1 calcium oxalate/phosphate stone, 3 stones not evaluated) were compared with characteristics of non-stone-forming children initiating the ketogenic diet at Johns Hopkins since July 1996. Since July 1996, 112 children initiating the ketogenic diet have been followed for development of stones. Follow-up times on the diet range from 2 months to 2.5 years. Of 112 children, 6 have developed stones (3 uric acid, 3 mixed calcium/uric acid stones) (0.8 children developing stones/ 100 patient-months at risk). Comparisons of children presenting with stones on the ketogenic diet with characteristics of the entire cohort initiating the ketogenic diet suggest younger age at diet initiation and hypercalciuria are risk factors for the development of stones. Prospective evaluation of children initiating the ketogenic diet revealed that almost 40% of patients had elevated fasting urine calcium: creatinine ratios at baseline; this increased to 75% after 6 months on the diet. Median urine pH was 5.5 at diet initiation, and remained at 6.0 thereafter. In a subset of patients tested, urinary citrate excretion fell from a mean of 252 mg/24 h pre diet initiation to 52 mg/24 h while on the diet. Uric acid excretion remained normal. Patients maintained on the ketogenic diet often have evidence of hypercalciuria, acid urine, and low urinary citrate excretion. In conjunction with low fluid intake, these patients are at high risk for both uric acid and calcium stone formation.
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PMID:Risk factors for urolithiasis in children on the ketogenic diet. 1109 28

The objective of this study was to develop a practical method for the analysis of purine derivatives in urinary calculi using high-performance liquid chromatography (HPLC). The method presented herein includes extraction of purine derivatives from urinary stones, followed by chromatography on a reversed-phase column with UV detection. A simpler isocratic method was applied to quantitate 6 purines known to be components of urinary stones, namely uric acid, xanthine, hypoxanthine, 2,8-dihydroxyadenine, oxypurinol and allopurinol. Gradient method separated 10 additional peaks representing methyl derivatives of uric acid or xanthine (1-, 3-, 7-, and 9-methyluric acid, 1,3-,1,7-, and 3,7-dimethyluric acid, and 1-, 3-, and 7-methylxanthine) (Fig. 1). Detection limits for individual compounds ranged from 25 to 140 micrograms purine per g stone weight and precision (RSD%) was 0.5-2.4%. Both methods were next used to analyze purine derivatives in urinary calculi from 48 residents of Western Pomerania. Uric acid was the main component of 9 stones. All of the uric acid stones showed admixtures of 9 other purine derivatives: natural metabolites (hypoxanthine, xanthine, 2,8-dihydroxyadenine) and methyl derivatives of uric acid (1-,3-, and 7-methyluric acid, 1,3-dimethyluric acid, 3-, and 7-methylxanthine) originating from the metabolism of exogenous methylxanthines (caffeine, theophylline and theobromine) (Tab. 1,2). Methyl derivatives of uric acid and xanthine, with a maximal content in stones of 1.7%, have hitherto not been considered constituents of urinary calculi. Statistical analysis of the results revealed strong positive correlations between the level of uric acid and of other purine derivatives in stones (Fig. 2). Correlations were also found between levels of some purines and inorganic compounds (Tab. 3). The sensitivity and specificity of HPLC with UV detection satisfy the requirements of a reference method for the analysis of purines in urinary stones. Isocratic separation is simpler in terms of technique and equipment, and therefore more suitable for hospital laboratories. Examination of purine derivatives in stones may be very helpful for the diagnosis of abnormal purine metabolism and urolithiasis, particularly in dihydroxyadeninuria, xanthinuria and during treatment with allopurinol. Gradient separation requiring more sophisticated instrument seems useful for research purposes when the content of methyl derivatives of purines must be known. The present results indicate that urinary purines at concentrations lower than saturation point may nevertheless coprecipitate with oversaturated uric acid and appear as admixtures in urinary stones. The content of a purine derivative in stone depends on its average urinary excretion in the general population, similarity to the chemical structure of uric acid, and content of the latter in stone. These findings suggest that purines in stones represent a solid solution with uric acid as solvent. It is also plausible that methylxanthines, ubiquitous components of the diet and drugs, are involved in the pathogenesis of urolithiasis. Interpretation of results and practical significance of the determination of purine derivatives in stones is discussed, and future studies to assess the clinical importance of endo- and exogenous purine derivatives in urinary calculi are suggested.
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PMID:[Identification and quantitation of purine derivatives in urinary calculi as markers of abnormal purine metabolism by using high-performance liquid chromatography (HPLC)]. 1171 16

Urolithiasis is a common urologic disease. Stones may occur in the kidney, ureter, or urinary bladder. We collected 1,000 stone samples in the subtropical area of southern Taiwan. Stone components were analyzed by Fourier transform infrared spectroscopy. Mixed components of calcium oxalate and calcium phosphate were the most common form of stones (52.3%), followed by calcium oxalate (27.8%) and calcium phosphate (9.3%). Uric acid stones accounted for 7.6%. Magnesium ammonium phosphate stones accounted for 3.0%. Only one cystine stone was found. In the study of urinary stone formation mechanism and prevention of recurrent urolithiasis, knowing the stone composition is important.
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PMID:Urinary stone analysis of 1,000 patients in southern Taiwan. 1733 67

The prevalence of urolithiasis has been increasing for the past few decades in industrialized nations. Uric acid calculi account for a significant percentage of urinary stones. Certain risk factors may be involved in the pathogenesis of uric acid nephrolithiasis, including hyperuricosuria, low urinary volume, and persistently low urinary pH. Patients with medical conditions that promote profound hyperuricosuria are at high risk of developing uric acid calculi. These conditions include chronic diarrheal states; myeloproliferative disorders; insulin resistance, including diabetes mellitus; and monogenic metabolic disorders, such as Lesch-Nyhan syndrome. Computed tomography can provide a definitive diagnosis. Except in cases in which there is severe obstruction, progressive azotemia, serious infection, or unremitting pain, the initial treatment of patients with uric acid nephrolithiasis should be medical dissolution therapy because this approach is successful in the majority of cases. A thorough review of the epidemiology and pathophysiology of uric acid nephrolithiasis is crucial for the diagnosis, treatment, and prevention of stones in patients with this condition.
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PMID:Uric Acid nephrolithiasis: recent progress and future directions. 1739 68

Uric acid is the end-product of purine catabolism. Hyperuricaemia is implicated in disorders such as gout and urolithiasis and recent epidemiological evidence suggests an association between increasing uric acid levels and increased cardiovascular morbidity and mortality. A direct causal role remains to be established but recent studies of losartan, atorvastatin and fenofibrate suggest that uric acid reduction contributes to attenuation of cardiovascular risk. Furthermore, several small studies of xanthine oxidase inhibition (the most common method of uric acid reduction) have shown improvements in measures of cardiovascular and endothelial function of a similar magnitude to those of other proven preventative strategies. This review introduces the epidemiological data, discusses strategies to lower uric acid and outlines the available clinical trial data supporting uric acid reduction as a potential and novel method of reducing the burden of cardiovascular disease.
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PMID:Uric acid reduction: a new paradigm in the management of cardiovascular risk? 1762 23

Urate lowering treatment is indicated in patients with recurrent acute attacks, tophi, gouty arthropathy, radiographic changes of gout, multiple joint involvement, or associated uric acid nephrolithiasis. Uricosuric agents like benzbromarone and probenecid are very useful to treat hyperuricemia as well as allopurinol (xanthine oxidase inhibitor). Uricosuric agents act the urate lowering effect through blocking the URAT1, an urate transporter, in brush border of renal proximal tubular cells. In order to avoid the nephrotoxicity and urolithiasis due to increasing of urinary urate excretion by using uricosuric agents, the proper urinary tract management (enough urine volume and correction of aciduria) should be performed.
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PMID:[Uricosuric agent]. 1840 25


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