allopurinol and Urinary-Calculi

Hypouricemia is defined when a serum urate concentration is less than or equal 2.0mg/dl. Differential diagnosis is made by fractional uric acid excretion with the identification of urate transporters and intracellular proteins involved in the tubular transport of uric acid. This review examines current knowledge on uric acid tubular transport and the various clinical situations of hypouricemia.

Topics: Absorption; Biological Transport; Diabetes Complications; Diagnosis, Differential; Fluid Therapy; Glucose Transport Proteins, Facilitative; Humans; Kidney Tubules, Proximal; Models, Biological; Organic Anion Transporters; Organic Cation Transport Proteins; Prevalence; Renal Tubular Transport, Inborn Errors; Uric Acid; Urinary Calculi; Xanthine; Xanthine Oxidase

Drug-induced urinary calculi, although they account for only 1-2% of urinary calculi, deserve consideration because most of them are preventable. In the drug-containing calculi resulting from the crystallization of a certain drug and its metabolites in the urine, stone analysis can identify the responsible drug. While, in the drug-induced metabolic calculi caused by interference with calcium, oxalate and purine metabolism, careful clinical inquiry is necessary to reveal involvement of a certain drug in stone formation. Better awareness of the possible drugs with lithogenic potential and close surveillance of patients on long-term treatment with these drugs are necessary. Especially, in patients with a history of urolithiaisis, prescription of lithogenic drugs deserve careful consideration.

Topics: Allopurinol; Anti-Bacterial Agents; Ascorbic Acid; Benzbromarone; Calcium; Calcium Compounds; Carbonic Anhydrase Inhibitors; Crystallization; Diuretics; Drug Combinations; Furosemide; Glucocorticoids; Humans; Magnesium Silicates; Oxalates; Protease Inhibitors; Purines; Time Factors; Triamterene; Urinary Calculi; Vitamin D

Many urinary tract stones consist of calcium, and has high relapse rate. Accordingly, it is very important to prevent calcium-containing stone formation. This paper describes about effects and mechanisms for Xanthine oxidase inhibitor, citrate formulation, magnesium formulation, thiazides, vitamin B(6), extract of Quercus salicina Blume and chorei-to (medical herb) . Recent new drugs and the elucidation of new metabolic pathways may lead to the development of prevention of urolithiasis.

Topics: Allopurinol; Animals; Calcium; Citrates; Drugs, Chinese Herbal; Humans; Magnesium Compounds; Phytotherapy; Plant Extracts; Secondary Prevention; Sodium Chloride Symporter Inhibitors; Urinary Calculi; Vitamin B 6; Xanthine Oxidase

In recent years stone disease has become more widespread in developed countries. At present the prevalence is 5.2 and 15% of men and 6% of women are affected. The increase is linked to changes in lifestyle, eating patterns and obesity which has become very common. The 'metabolic syndrome' includes all the diseases, e.g. hypertension, lipid imbalances, type 2 diabetes mellitus, gout and cardiovascular disease, which are concomitant in the majority of stone formers. Dietary patterns, besides leading to stone formation, also determine stone chemistry. With a diet that is rich in oxalates, calcium oxalate will constitute 75% of stones, struvite 10-20%, uric acid 5-6% and cystine 1%. As approximately 50% of patients with stones suffer recurrences, metabolic and/or pharmacological prophylaxis is recommended.

Topics: Allopurinol; Calcium Oxalate; Cystine; Diet; Dietary Supplements; Drinking; Humans; Life Style; Renal Agents; Secondary Prevention; Sodium Chloride Symporter Inhibitors; Uric Acid; Urinary Calculi; Urolithiasis

Topics: Allopurinol; Arteriosclerosis; Benzbromarone; Enzyme Inhibitors; Gout; Humans; Hyperuricemia; Kidney Diseases; Probenecid; Prognosis; Risk; Uricosuric Agents; Urinary Calculi; Xanthine Oxidase

Topics: Allopurinol; Calcium Oxalate; Diet; Gout; Humans; Hydrogen-Ion Concentration; Hyperuricemia; Tomography, Spiral Computed; Urinary Calculi; Urine

Treatment of asymptomatic hyperuricemia is not necessary in most patients, unless perhaps they have very high levels of uric acid or are otherwise at risk of complications, such as those with a personal or strong family history of gout, urolithiasis, or uric acid nephropathy.

Topics: Age Factors; Allopurinol; Cardiovascular Diseases; Clinical Trials as Topic; Gout; Gout Suppressants; Humans; Hypoxanthine Phosphoribosyltransferase; Reference Values; Uric Acid; Urinary Calculi

Topics: Allopurinol; Antimetabolites; Ascorbic Acid; Calcium Oxalate; Calcium, Dietary; Citric Acid; Dietary Fiber; Dietary Proteins; Drinking; Glycosaminoglycans; Humans; Magnesium; Patient Compliance; Phosphates; Recurrence; Thiazoles; Urinary Calculi

Diagnostic and therapeutic drugs may enhance urolithiasis in one or a combination of ways, including: (1) alteration of urine pH in such fashion as to create an environment that increases the solubility of some lithogenic substances, (2) alteration of glomerular filtration rate, tubular reabsorption, and tubular secretion of drugs of endogenous substances so as to enhance promoters or impair inhibitors of urolithiasis, and (3) precipitation (e.g., drugs or their metabolites) to form a portion or all of a urolith.

Topics: Allopurinol; Animals; Anti-Bacterial Agents; Anti-Infective Agents; Anticonvulsants; Cat Diseases; Cats; Dog Diseases; Dogs; Enzyme Inhibitors; Fluoroquinolones; Primidone; Sulfonamides; Tetracycline; Urinary Calculi; Xanthine Oxidase

Drug-induced urolithiasis are observed in 1.6% of the urinary calculi in France. Drugs crystals are identified in two thirds of these stones. Other drugs are responsible for stones which have an apparent metabolic origin (one third of the cases). Stone analysis using physical methods such as infrared spectroscopy is needed to unambiguously identify stones containing drugs. The inquiry is an important step to identify lithogenetic drugs which do not crystallize in the stones. The main substances which were identified in stones over the past decade were indinavir monohydrate (31.4%), triamterene (11.1%), sulphonamides (10.5%) and amorphous silica (4.5%). The main drugs involved in the nucleation and growth of metabolic stones were calcium and vitamin D supplementation (15%) and long-term treatment with carbonic anhydrase inhibitors (8%). Stone prevention is based on drug withdrawal or change in dosage with additional measures including an increase of diuresis and, if necessary, changes in the urine pH.

Topics: Acetazolamide; Allopurinol; Aluminum Hydroxide; Calcium; Cathartics; Diuretics; HIV Protease Inhibitors; Humans; Indinavir; Pyridoxine; Silicates; Sulfonamides; Triamterene; Urinary Calculi; Vitamin D

Calcium stones arise from imbalances between urinary excretions of insoluble salts and water. Idiopathic hypercalciuria and hyperparathyroidism are the calcium disorders usually associated with elevated levels of calcium in the urine. Renal tubular acidosis is associated with a disordered acid-base status that results in low urine citrate. Hypocitraturia itself is a cause of calcium stones because it leaves urine calcium free to complex with either oxalate or phosphate. Elevated urine oxalate is commonly associated with dietary excesses, bowel disease, and, rarely, primary hyperoxaluria. Hyperuricosuria, usually of dietary origin, when reversed can cause a fall in new calcium stones.

Topics: Allopurinol; Antimetabolites; Benzothiadiazines; Clinical Trials as Topic; Diuretics; Humans; Hypercalcemia; Hyperparathyroidism; Prognosis; Sodium Chloride Symporter Inhibitors; Urinary Calculi

Adenine phosphoribosyltransferase(APRT) deficiency is an autosomal recessive disorder and the homozygotes develop 2,8-dihydroxyadenine(DHA) urolithiasis and, in severe cases, renal failure. The prevalence is higher among the Japanese than other ethnic groups. So far 120 cases have been reported among the Japanese. The disease is classified into 2 types; type I and II are associated with complete and partial deficiencies, respectively. While all non-Japanese cases were of type I, about 78% of the Japanese patients were of type II. Each of the type II patients has at least one APRT*J allele with a ATG(Met) to ACG(Thr) base substitution at codon 136. All APRT*J alleles were derived from a single ancestor. All type I patients and some type II patients possess APRT*QO alleles with various point mutations or large gene abnormality. Type II patients tend to develop first symptoms later than the type I patients. The diagnoses of homozygotes and heterozygotes can be done by the cell culture methods. Both enzyme assay and molecular diagnostic methods are useful but not as reliable as the cell culture methods Excessive water intake, restriction of foods with high adenine contents and administration of allopurinol are useful treatments.

Topics: Adenine; Adenine Phosphoribosyltransferase; Alleles; Allopurinol; Heterozygote; Homozygote; Humans; Kidney Failure, Chronic; Nucleic Acid Hybridization; Point Mutation; Polymerase Chain Reaction; Urinary Calculi

A critical appraisal of the evidence commonly cited to support a link between high urate excretion and calcium oxalate (CaOx) urinary calculi is presented. Two theories have been invoked to provide a scientific explanation for urate's apparent promotory effect. The first proposes that urinary urate crystals promote CaOx precipitation by the phenomenon of epitaxy; the second hypothesis is that colloidal particles of urate reduce the inhibitory activity of urinary glycosaminoglycans (GAGs) which normally prevent the crystallization of CaOx. However, to the present, neither has been verified experimentally. More recent research from our group has revealed that at normal physiological pH values dissolved urate directly promotes CaOx precipitation by the classic 'salting-out' effect by enhancing nucleation, growth and aggregation of CaOx crystals. It is therefore suggested that the beneficial effect of allopurinol in reducing CaOx stone recurrences may be attributed to its lowering the urinary output of urate and thereby reducing the probability that CaOx will be salted out of urine, rather than to epitaxy or inactivation of urinary GAGs.

Topics: Allopurinol; Calcium Oxalate; Glycosaminoglycans; Gout; Humans; Hydrogen-Ion Concentration; Hyperoxaluria; Kidney Calculi; Uric Acid; Urinary Calculi

Uric acid is the end-product of purine nucleotide metabolism in man. The renal handling of urate is a complicated process, resulting in a fractional clearance of 8.2-10.3%. The anhydrous form is thermodynamically the most stable uric acid crystal. Uric acid is a weak acid that ionizes with a Pka at pH 5.75. At the normal acidic region, uric acid solubility is strongly increased by urinary pH. The prevalence of uric acid stones varies between countries, reflecting climatic, dietary, and ethnical differences, ranging from 2.1% (in Texas) to 37.7% (in Iran). The risk for uric acid stone formation correlates with the degree of uric acid supersaturation in the urine, depending on uric acid concentration and urinary pH. Hyperuricosuria is the major risk factor, the most common cause being increased purine intake in the diet. Acquired and hereditary diseases accompanied by hyperuricosuria and stone disease include: gout, in strong correlation with the amount of uric acid excreted, myelo- and lymphoproliferative disorders, multiple myeloma, secondary polycythemia, pernicious anemia and hemolytic disorders, hemoglobinopathies and thalassemia, the complete or partial deficiency of HGPRT, superactivity of PRPP synthetase, and hereditary renal hypouricemia. A common denominator in patients with idiopathic and gouty stone formers is a low urinary pH. Uric acid nephrolithiasis is indicated in the presence of a radiolucent stone, a persistent undue urine acidity and uric acid crystals in fresh urine samples. A radiolucent stone in combination with normal or acidic pH should raise the possibility of urate stones.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Allopurinol; Diet; Humans; Kidney; Kidney Calculi; Models, Biological; Purines; Uric Acid; Urinary Calculi; Water-Electrolyte Balance

APRT deficiency is an enzyme disorder which is inherited as an autosomal recessive trait. The use of adenine in purine metabolism is disturbed and it accumulates in the body, where it is oxidised by xanthine oxidase to poorly insoluble 2, 8-dihydroxyadenine (DHA). The dihydroxyadenine forms stones which cause recurrent urolithiasis, frequent episodes of urinary tract infection or interstitial nephritis, and finally renal insufficiency in some cases. We report a case of APRT deficiency discovered by urine examination. The patient was a 33-year-old man who had never had any episodes of urolithiasis. He was admitted to our hospital because of pseudoarthrosis of his left arm caused by a traffic accident. His urinalysis revealed no proteinuria nor hematuria, but disclosed numerous round brown crystals in the sediment. These crystals had the characteristics of 2, 8-DHA. The enzyme activity of APRT in his blood was completely deficient. He was diagnosed as an APRT* QO homozygote. In addition, diagnostic imaging revealed that his right kidney was poorly hypoplastic and the pelvis of his left kidney was extra-renal. The renal function was slightly disturbed. In Japan 6 cases of 2, 8-DHA urolithiasis associated with hypoplastic kidney had been reported by 1989. Theoretically, the incidence of hypoplastic kidney is around 20% of all 2, 8-DHA urolithiasis cases. We suspect a genetic correlation between hypoplastic kidney and APRT deficiency. This patient was treated with Allopurinol, which inhibits the process of xanthine oxidation, after which crystals were no longer detected in his urine.

Topics: Adenine; Adenine Phosphoribosyltransferase; Adult; Allopurinol; Crystallization; Homozygote; Humans; Kidney Diseases; Male; Urinary Calculi

Topics: Allopurinol; Animal Feed; Animals; Breeding; Dog Diseases; Dogs; Drinking; Hydrogen-Ion Concentration; Uric Acid; Urinary Calculi; Urine

Topics: Adenine Phosphoribosyltransferase; Adolescent; Adult; Allopurinol; Child; Child, Preschool; Diet; Female; Genotype; Humans; Infant; Japan; Male; Middle Aged; Mutation; Phenotype; Purine-Pyrimidine Metabolism, Inborn Errors; Urinary Calculi

Uric acid stones are the consequences of abnormalities in purine metabolism, urate/uric acid renal handling, or excess dietary protein. Treatment is aimed at preventing additional formation by decreasing the degree of urate and uric acid supersaturation in urine, by altering diet, fluid intake, and the urine pH, and by blocking steps in uric acid production.

Topics: Adenine Phosphoribosyltransferase; Humans; Kidney Calculi; Lesch-Nyhan Syndrome; Purines; Risk Factors; Uric Acid; Urinary Calculi; Xanthine Oxidase

This review evaluates the epidemiologic, clinical and experimental evidence for an etiological link between urinary uric acid and the propensity to develop calcium oxalate calculi. While epidemiologic and laboratory studies provide only equivocal support for a synergistic relationship, several clinical trials with allopurinol have demonstrated a reduction in calculus recurrence. These beneficial effects are observed only when allopurinol is given to subjects with calcium oxalate calculi who have isolated hyperuricosuria. The specificity of this effect suggests that there is an important interaction between uric acid and calcium oxalate but the mechanism(s) remain to be elucidated.

Topics: Allopurinol; Calcium Oxalate; Humans; Uric Acid; Urinary Calculi

Topics: Allopurinol; Benzothiadiazines; Diuretics; Humans; Lithotripsy; Sodium Chloride Symporter Inhibitors; Urinary Calculi

Calcium oxalate uroliths are commonly called metabolic uroliths because they are sequelae of a variety of metabolic abnormalities that alter the composition of body fluids and urine. Factors incriminated in the etiopathogenesis of calcium oxalate urolithiasis include hypercalciuria, hyperoxaluria, and hyperuricosuria. The predominant type of calcium oxalate urolith encountered in dogs is the monohydrate form; however, the dihydrate form may also occur. Male dogs have been more frequently affected than female dogs. Medical therapy should be formulated with the goal of reducing urine concentration of calculogenic substances.

Topics: Allopurinol; Animals; Benzothiadiazines; Calcium Oxalate; Cellulose; Citrates; Crystallization; Diuretics; Dog Diseases; Dogs; Hypercalcemia; Magnesium; Methylene Blue; Phosphates; Sodium Chloride Symporter Inhibitors; Uric Acid; Urinary Calculi

Topics: Allopurinol; Benzothiadiazines; Calcium; Cellulose; Citrates; Citric Acid; Diuretics; Humans; Magnesium; Pentosan Sulfuric Polyester; Phosphorus; Phytic Acid; Pyridoxine; Sodium Chloride Symporter Inhibitors; Succinimides; Urinary Calculi

Topics: Allopurinol; Calcium, Dietary; Female; Humans; Kidney Calculi; Male; Oxalates; Recurrence; Ureteral Calculi; Urinary Calculi

Topics: Allopurinol; Calcium; Calcium Oxalate; Female; Humans; Male; Oxalates; Urinary Calculi

Topics: Acute Kidney Injury; Adenine; Adenine Phosphoribosyltransferase; Allopurinol; Diagnosis, Differential; Diet; Heterozygote; Homozygote; Humans; Pentosyltransferases; Purine-Pyrimidine Metabolism, Inborn Errors; Uric Acid; Urinary Calculi

Topics: Allopurinol; Balneology; Benzofurans; Crystallization; Diagnosis, Differential; Exercise Therapy; Glomerular Filtration Rate; Gout; Probenecid; Sulfinpyrazone; Uric Acid; Urinary Calculi

Topics: Acidosis, Renal Tubular; Bacterial Infections; Citrates; Crystallization; Cystinuria; Diphosphates; Female; Gastrointestinal Diseases; Humans; Hypercalcemia; Hyperparathyroidism; Magnesium; Male; Metabolism, Inborn Errors; Mucoproteins; Oxalates; Quaternary Ammonium Compounds; Sarcoidosis; Solubility; Uric Acid; Urinary Calculi; Vitamin D; Xanthine Oxidase

Topics: Acidosis, Renal Tubular; Allopurinol; Anti-Bacterial Agents; Bacterial Infections; Cystinuria; Diet; Female; Humans; Hydrochlorothiazide; Hyperparathyroidism; Kidney Calculi; Magnesium Oxide; Male; Medullary Sponge Kidney; Metabolism, Inborn Errors; Methylene Blue; Penicillamine; Phosphates; Urinary Calculi; Xanthine Oxidase

Topics: Allopurinol; Bile Acids and Salts; Calcium; Diuretics; Humans; Hydrogen-Ion Concentration; Hyperparathyroidism; Kidney; Lesch-Nyhan Syndrome; Purines; Uric Acid; Urinary Calculi

Topics: Acid-Base Equilibrium; Allopurinol; Diet Therapy; Humans; Postoperative Complications; Uric Acid; Urinary Calculi; Urinary Catheterization; Urinary Tract Infections

Topics: Administration, Oral; Age Factors; Allopurinol; Animals; Anti-Bacterial Agents; Bicarbonates; Cystine; Diet Therapy; Dog Diseases; Dogs; Female; Hydrogen-Ion Concentration; Male; Oxalates; Phosphates; Postoperative Complications; Sex Factors; Uric Acid; Urinary Calculi; Urinary Tract Infections

Topics: Adult; Allopurinol; Child; Drug Hypersensitivity; Drug Interactions; Gout; Humans; Iron; Kidney Diseases; Nucleic Acids; Purines; Pyrimidines; Tryptophan; Uric Acid; Urinary Calculi; Xanthines

Topics: Adolescent; Adult; Aged; Alkalies; Allopurinol; Chemistry Techniques, Analytical; Child; Child, Preschool; Citrates; Diet; Female; Humans; Hypoxanthines; Infant; Male; Middle Aged; Purines; Uric Acid; Urinary Calculi; Xanthines

Topics: Humans; Purines; Spectrophotometry; Urinary Calculi; Xanthine Oxidase; Xanthines

Higher urinary uric acid excretion is a suspected risk factor for calcium oxalate stone formation. Febuxostat, a xanthine oxidoreductase inhibitor, is effective in lowering serum urate concentration and urinary uric acid excretion in healthy volunteers and people with gout. This work studied whether febuxostat, compared with allopurinol and placebo, would reduce 24-hour urinary uric acid excretion and prevent stone growth or new stone formation.. In this 6-month, double-blind, multicenter, randomized controlled trial, hyperuricosuric participants with a recent history of calcium stones and one or more radio-opaque calcium stone ≥ 3 mm (as seen by multidetector computed tomography) received daily febuxostat at 80 mg, allopurinol at 300 mg, or placebo. The primary end point was percent change from baseline to month 6 in 24-hour urinary uric acid. Secondary end points included percent change from baseline to month 6 in size of index stone and change from baseline in the mean number of stones and 24-hour creatinine clearance.. Of 99 enrolled participants, 86 participants completed the study. Febuxostat led to significantly greater reduction in 24-hour urinary uric acid (-58.6%) than either allopurinol (-36.4%; P=0.003) or placebo (-12.7%; P<0.001). Percent change from baseline in the size of the largest calcium stone was not different with febuxostat compared with allopurinol or placebo. There was no change in stone size, stone number, or renal function. No new safety concerns were noted for either drug.. Febuxostat (80 mg) lowered 24-hour urinary uric acid significantly more than allopurinol (300 mg) in stone formers with higher urinary uric acid excretion after 6 months of treatment. There was no change in stone size or number over the 6-month period.

Topics: Adult; Allopurinol; Biomarkers; Calcium Oxalate; Double-Blind Method; Enzyme Inhibitors; Febuxostat; Female; Humans; Male; Middle Aged; Multidetector Computed Tomography; Thiazoles; Time Factors; Treatment Outcome; United States; Uric Acid; Urinary Calculi; Xanthine Oxidase

Sixty-six active recurrent stone formers (RSF), i.e., with at least one stone annually over 3 years prior to the first examination at our stone clinic, were retrospectively evaluated. All received specific drug metaphylaxis which was discontinued after 5.5 +/- 2.1 years (period 1). They were reclassified according to the above definition into active and inactive RSF and were then left on a general metaphylactic regimen with regular urological follow-up every 6 months (period 2). 32 patients observed these recommendations for 5.7 +/- 2.6 years (group 1), 34 did not. 20 of these 34 could be reexamined after 6.3 +/- 2.2 years (group 2). Group 1 comprised 10 active and 22 inactive, group 2 comprised 1 active and 19 inactive RSF. While the recurrence rates among the inactive RSF of groups 1 and 2 decreased significantly during period 2, a statistically significant difference between them was not observed. Conversely, there was only a slight reduction of the recurrence rate in the active RSF. Both findings argue against a stone clinic effect. Interviews of the patients showed that stone formation was periodical for a mean of 12 +/- 8 years, after which it gradually faded out. This period is termed 'phase of regular stone formation' and appears to be an autonomous process that cannot usually be influenced by metaphylactic measures. This could explain the wide variability of reported success rates for the various metaphylactic regimens, as they would merely reflect the number of stone formers who are in their phase of regular stone formation.

Topics: Adult; Aged; Allopurinol; Benzothiadiazines; Clinical Protocols; Combined Modality Therapy; Diuretics; Drinking Behavior; Drug Therapy, Combination; Feeding Behavior; Female; Follow-Up Studies; Humans; Male; Middle Aged; Recurrence; Remission Induction; Retrospective Studies; Sodium Chloride Symporter Inhibitors; Time Factors; Urinary Calculi

Between 1978 and 1992 (mean 9.2 years), metaphylaxis was introduced to 110 patients originally hospitalized for recurrent urinary calcium stones (mostly bilateral or multiple). Patients with hyperparathyroidism or with sponge kidney were excluded from the study. Until 1984, the condition had been treated mostly using conventional drug metaphylaxis (thiazides and allopurinol in 75% and 57%, respectively). After that year, there was a gradual decrease in the number of patients treated with thiazides (to 15%) and allopurinol (to 10%). This was associated with a steep rise in the proportion of patients treated with inhibitors (magnesium to 36% and citrates to 30%), or exclusively with non-medicamentous therapy (to 31%). These fundamental changes in approach have not reduced the effectiveness of metaphylaxis, and recurrence rates in individual years have not changed significantly either. Metaphylaxis was successful in 105 patients (95%) and the rate of recurrence has declined from 0.9 to 0.08 stones per year. The restriction of conventional drug metaphylaxis has entailed a marked decrease in the incidence of side effects of therapy and, consequently, a reduced need for follow-up tests and outpatient follow-up.

Topics: Allopurinol; Benzothiadiazines; Calcium; Citrates; Diuretics; Drug Therapy, Combination; Follow-Up Studies; Humans; Magnesium; Recurrence; Remission Induction; Sodium Chloride Symporter Inhibitors; Treatment Outcome; Urinary Calculi

Patients with bilateral urolithiasis diagnosed at their first visit were followed for at least one year after the start of treatment. In this retrospective study of 123 patients, the basic metabolic workup revealed no specific underlying cause of simultaneously occurring bilateral nephrolithiasis, and none of the currently used therapeutic regimes proved to be efficient in attaining clinically acceptable stone-free rates at the 3, 6 and 12-month follow-ups. Of 38 patients treated with extracorporeal shockwave lithotripsy (SWL), 21 underwent treatment of both kidneys and 10 (48%) were free of stones bilaterally after 12 months. All of the 17 patients treated with unilateral SWL failed to achieve a stone-free state on the contralateral side. In another group, treated with medication alone to minimize risks of stone recurrence, only 3 of 26 (11.5%) patients were stone-free on both sides 12 months after the start of medication. Since we achieved a stone-free state of both kidneys in no more than 12% of the non-medicated cases, it seems warranted to treat bilateral urolithiasis with SWL more frequently, particularly when patients cannot return regularly to the stone clinic for a longterm follow-up.

Topics: Adult; Allopurinol; Citrates; Citric Acid; Combined Modality Therapy; Female; Humans; Lithotripsy; Male; Middle Aged; Recurrence; Retrospective Studies; Trichlormethiazide; Urinary Calculi

We treated 87 patients with calcium-containing urinary stones with either allopurinol alone (44 patients) or in combination with thiazide (43 patients) and studied new stone formation before, during, and after the discontinuation of the drug therapy. The number of stones formed were 1.18, 0.24, and 0.13 before, during, and after discontinuation of the drug therapy, respectively, in the patients treated with allopurinol alone and 1.32, 0.20, and 0.09 in those treated in combination with thiazide. No differences were observed in these values and the duration of each observation period between the two groups. Decreases in the incidence of stone formation even after interruption of drug therapy suggested that recurrence-preventive effects observed following administration of these drugs include the effects of medical guidance. However, allopurinol therapy was effective in preventing recurrence in patients with hyperuricosuria.

Topics: Allopurinol; Calcium; Calcium Oxalate; Calcium Phosphates; Citrates; Drug Therapy, Combination; Humans; Incidence; Male; Oxalates; Recurrence; Trichlormethiazide; Uric Acid; Urinary Calculi

Topics: Allopurinol; Clinical Trials as Topic; Humans; Hydrogen-Ion Concentration; Uric Acid; Urinary Calculi

Topics: Allopurinol; Clinical Trials as Topic; Drug Evaluation; Humans; Urinary Calculi

Topics: Allopurinol; Enzyme Therapy; Gout; Humans; Kidney Calculi; Uric Acid; Urinary Calculi; Xanthine Oxidase

Hereditary renal hypouricemia type 1 (RHUC1) is caused by URAT1/SLC22A12 dysfunction, resulting in urolithiasis and exercise-induced AKI (EIAKI). However, because there is no useful experimental RHUC1 animal model, the precise pathophysiologic mechanisms underlying EIAKI have yet to be elucidated. We established a high HPRT activity. The novel

Topics: Acute Kidney Injury; Allopurinol; Animals; Disease Models, Animal; Enzyme Inhibitors; Hypoxanthine Phosphoribosyltransferase; Kidney; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Nitriles; NLR Family, Pyrin Domain-Containing 3 Protein; Organic Anion Transporters; Physical Exertion; Pyridines; Renal Tubular Transport, Inborn Errors; Sodium-Potassium-Exchanging ATPase; Urate Oxidase; Urinary Calculi; Xanthine Dehydrogenase

Topics: Acute Kidney Injury; Allopurinol; Antioxidants; Child; Cystinosis; Diagnosis, Differential; Fanconi Syndrome; Female; Genetic Testing; Glucose Transport Proteins, Facilitative; Humans; Inappropriate ADH Syndrome; Kidney Tubules; Organic Anion Transporters; Organic Cation Transport Proteins; Renal Reabsorption; Renal Tubular Transport, Inborn Errors; Uric Acid; Urinary Calculi

Hereditary xanthinuria (type I) is caused by an inherited deficiency of the xanthine oxidorectase (XDH/XO), and is characterized by very low concentration of uric acid in blood and urine and high concentration of urinary xanthine, leading to urolithiasis. Type II results from a combined deficiency of XDH/XO and aldehyde oxidase. Patients present with hematuria, renal colic, urolithiasis or even acute renal failure. Clinical symptoms are the same for both types. In a third type, clinically distinct, sulfite oxidase activity is missing as well as XDH/XO and aldehyde oxidase. The prevalence is not known, but about 150 cases have been described so far. Hypouricemia is sometimes overlooked, that´s why we have set up the diagnostic flowchart. This consists of a) evaluation of uric acid concentrations in serum and urine with exclusion of primary renal hypouricemia, b) estimation of urinary xanthine, c) allopurinol loading test, which enables to distinguish type I and II; and finally assay of xanthine oxidoreductase activity in plasma with molecular genetic analysis. Following this diagnostic procedure we were able to find first patients with hereditary xanthinuria in our Czech population. We have detected nine cases, which is one of the largest group worldwide. Four patients were asymptomatic. All had profound hypouricemia, which was the first sign and led to referral to our department. Urinary concentrations of xanthine were in the range of 170-598 mmol/mol creatinine (normal < 30 mmol/mol creatinine). Hereditary xanthinuria is still unrecognized disorder and subjects with unexplained hypouricemia need detailed purine metabolic investigation.

Topics: Adult; Aldehyde Oxidase; Allopurinol; Child; Child, Preschool; Czech Republic; Diagnosis, Differential; Humans; Metabolism, Inborn Errors; Purine-Pyrimidine Metabolism, Inborn Errors; Purines; Renal Tubular Transport, Inborn Errors; Uric Acid; Urinary Calculi; Xanthine; Xanthine Dehydrogenase

Renal hypouricemia (RHUC) is a hereditary disease characterized by a low level of plasma urate but with normal urinary urate excretion. RHUC type 1 is caused by mutations of the urate transporter URAT1 gene (SLC22A12). However, the plasma urate levels of URAT1 knockout mice are no different from those of wild-type mice. In the present study, a double knockout mouse, in which the URAT1 and uricase (Uox) genes were deleted (Urat1-Uox-DKO), were used as an experimental animal model of RHUC type 1 to investigate RHUC and excise-induced acute kidney injury (EIAKI). Mice were given a variable content of allopurinol for one week followed by HPLC measurement of urate and creatinine concentrations in spot urine and blood from the tail. The urinary excretion of urate in Urat1-Uox-DKO mice was approximately 25 times higher than those of humans. With allopurinol, the plasma urate levels of Urat1-Uox-DKO mice were lower than those of Uox-KO mice. There were no differences in the urinary urate excretions between Urat1-Uox-DKO and Uox-KO mice administered with 9 mg allopurinol /100 g feed. In the absence of allopurinol, plasma creatinine levels of some Urat1-Uox-DKO mice were higher than those of Uox-KO mice. Consequently, hypouricemia and normouricosuria may indicate that the Urat1-Uox-DKO mouse administered with allopurinol may represent a suitable animal model of RHUC type 1. Urat1-Uox-DKO mice without allopurinol exhibited acute kidney injury, thus providing additional benefit as a potential animal model for EIAKI. Finally, our data indicate that allopurinol appears to provide prophylactic effects for EIAKI.

Topics: Acute Kidney Injury; Allopurinol; Animals; Creatinine; Disease Models, Animal; Gout Suppressants; Male; Mice, Knockout; Organic Anion Transporters; Physical Conditioning, Animal; Renal Tubular Transport, Inborn Errors; Urate Oxidase; Uric Acid; Urinary Calculi

Stone analysis is not always available, and recent studies reveal interlaboratory reporting differences, suggesting inaccurate reports. We sought to determine whether appropriate medical therapy could be made without stone analysis when imaging, history, and laboratory data were available.. One hundred stone formers (SFs) were categorized as calcium oxalate, calcium phosphate, uric acid, or struvite based on a single analysis. Age, gender, body mass index, comorbidities, serum chemistries, 24-hour urine, and imaging information were incorporated into a "Megaprofile." Radiographic details about patients' stones were recorded. Attenuation: Size ratios were calculated to predict stone composition. Stone composition data were then withheld and three urologists (S.L.B., S.S., and S.Y.N.) evaluated each Megaprofile, making nutritional and pharmacologic recommendations. Next, a repeat evaluation ensued with stone analyses. Recommendations were compared with the gold standard being those made using stone composition data.. Without stone analysis, the panel recommended targeted nutrition therapy in 91% of cases, which remained unchanged once composition was revealed. Medication was prescribed in 68% of cases. Overall, therapy based on the Megaprofile without stone composition data was appropriate 93% of the time. In 7% of cases, therapy was changed after stone composition was revealed. In 21% of patients with recurrent urinary tract infections (UTIs), knowledge of stone composition altered therapy.. Medical, laboratory, and radiographic data provide sufficient information to direct both nutritional and pharmacologic therapy in most SFs (93%), but those with recurrent UTIs may derive more benefit from stone analysis prior to directed medical therapy.

Topics: Adult; Aged; Allopurinol; Anti-Bacterial Agents; Body Mass Index; Calcium Oxalate; Calcium Phosphates; Cohort Studies; Diet Therapy; Diuretics; Enzyme Inhibitors; Female; Humans; Magnesium Compounds; Male; Middle Aged; Phosphates; Potassium Citrate; Struvite; Thiazides; Time Factors; Uric Acid; Urinary Calculi; Urology

Topics: Acute Kidney Injury; Adolescent; Allopurinol; Athletic Injuries; Biomarkers; Drug Administration Schedule; Gout Suppressants; Humans; Male; Renal Tubular Transport, Inborn Errors; Secondary Prevention; Treatment Outcome; Urinary Calculi

A 2-year-old, neutered, crossbreed bitch was presented as an emergency with painful abdomen, fever and vomiting. The cause of the acute abdomen was a pyonephrosis of the left kidney, caused by four xanthine stones, which had blocked the ureter. After surgical removal of the heavily altered left kidney, the bitch recovered rapidly. Because of a leishmaniasis the bitch had been treated with allopurinol over an extended period, the xanthine stone formation is likely to have resulted from allopurinol usage. Because there were additionally small concrements in the right kidney, the medication was stopped. Subsequently, the dog has received a low purine diet, and the leishmaniasis titer and renal function have been monitored regularly.

Topics: Allopurinol; Animals; Dog Diseases; Dogs; Female; Leishmaniasis; Pyonephrosis; Urinary Calculi; Xanthines

2,8-dihydroxyadeninuria (DHA) disease (also called 2,8 dihydroxyadeninuria) is a rare autosomal recessive disorder caused by complete adenine phosphoribosyltransferase deficiency and typically manifests as recurrent nephrolithiasis. Only rare cases of DHA nephrolithiasis have been reported from the USA. Herein, we report three American patients who developed DHA crystalline nephropathy leading to end-stage renal disease (ESRD) with recurrence in the allograft.. Three cases of DHA crystalline nephropathy were identified from the Renal Pathology Laboratory of Mayo Clinic. Detailed clinical and pathologic descriptions are provided.. All three patients were Caucasian adults with no history of obstructive nephropathy. Two patients had no history of nephrolithiasis and one had a single episode of stones 36 years prior to presentation. All patients presented with severe renal failure with a mean serum creatinine of 7.5 mg/dl. Renal biopsies revealed numerous tubular and interstitial brown DHA crystals, tubular degenerative changes and moderate to marked tubulointerstitial scarring. Two patients were initially misdiagnosed, one as primary hyperoxaluria and the other as chronic interstitial nephritis. All three patients progressed to ESRD, within 1 month following renal biopsy in two and after 9 months in one. All three patients underwent renal transplantation with early disease recurrence in three allografts in two patients.. DHA disease is an under-recognized condition that can lead to irreversible renal failure and frequently recurs in the transplant. It should be included in the differential diagnosis of crystalline nephropathy, even in the absence of history of nephrolithiasis.

Topics: Adenine; Adenine Phosphoribosyltransferase; Adult; Allopurinol; Crystallization; Diagnosis, Differential; Female; Genes, Recessive; Humans; Hyperoxaluria, Primary; Kidney; Kidney Diseases; Kidney Failure, Chronic; Kidney Transplantation; Male; Middle Aged; Recurrence; United States; Urinary Calculi

In earlier studies, we have confirmed that in most patients with calcium oxalate stone formation, a combination of allopurinol and pyridoxine is best suited for treatment and prevention of the stone forming process. The objective of this study is to identify the most effective directed medical treatment of urinary stones. The drug dose adjustment was based on clinical, radiological, biochemical, and microscopic parameters. 444 patients with proved calcium oxalate stone disease who were getting a combination of allopurinol and pyridoxine for a minimum period of 36 months were enrolled in this prospective study. The dosage schedule of these patients was recorded. Dosage adjustment was made depending upon the various clinical, biochemical, microscopic, and radiological changes during the study period. The dosage schedules were in six categories, namely very high dose chemotherapy (VHDC), i.e. allopurinol 600 mg/day and pyridoxine 240 mg/day, high-dose chemotherapy (HDC), i.e. allopurinol 300 mg/day and pyridoxine 120 mg/day, moderate dose prophylaxis (MDP), i.e. allopurinol 200 mg/day and pyridoxine 80 mg/day, low-dose prophylaxis (LDP), i.e. allopurinol 100 mg/day and pyridoxine 40 mg/day, and very low-dose prophylaxis (VLDP), i.e. allopurinol 50 mg/day and pyridoxine 20 mg/day and intermittent VLDP, wherein the VLDP was given on alternate months and still later at longer intervals. The temporary risk was assessed at each visit and dosage adjustment was made. The effect of the intervention was assessed during the next visit. All the patients involved in the study needed dose adjustment. The following schedules were initiated: VHDC (12) 3.5%, HDC (103) 23.2%, MDP (78) 17.57%, or LDP (251) 56.53%. Patients who defaulted for more than a month were excluded from the study. During each visit for follow up, all patients were advised change over of dose depending upon the clinical situation at the time of review. Patients on VHDC were advised reduction to lower doses systematically. On passage of stones, the dose was immediately reduced to LDP in all situations unless prevented by the presence of significant crystalluria or severe pain. All patients on MDP had reduction of dose to LDP subsequently. Patients started on LDP needed elevation in dose in 63 (16.8%) to HDC and 23 patients (12.87%) to MDP. Dose of 247 patients could be reduced to VLDP (55.63%) and later on to intermittent VLDP 85 (19.14%). 74 (16.7%) patients continued to be on LDP throughout the period

Topics: Allopurinol; Antimetabolites; Calcium Oxalate; Dose-Response Relationship, Drug; Drug Therapy, Combination; Follow-Up Studies; Humans; Prospective Studies; Pyridoxine; Urinary Calculi

Topics: Allopurinol; Antimetabolites; Calcium Oxalate; Humans; Recurrence; Urinary Calculi

Urinary excretion of citrate is dependent on glomerular filtration, tubular reabsorption, and excretion. Acid base status is thought to play a significant role in urinary citrate excretion. It has been assumed that increased urinary citrate will increase urinary pH. The aim of this study was to confirm the association of increased urinary citrate levels with increased urinary pH.. The 24-hour urine collections of all patients with stones referred to our clinic in the past 4 years were reviewed. The samples were collected and analyzed for routine stone risk profiles by a commercial laboratory (Litholink, Chicago, Ill). The Student t test and analysis of variance were used to compare the mean values as applicable. Pearson's correlations were also calculated for each variable.. A total of 572 patients had at least one 24-hour urine sample from the past 4 years. The mean urinary citrate was 305 mg/day. The mean urinary pH of all patients was 6.14. Statistical evaluation of all patients showed no correlation between urinary citrate and pH (r = -0.04, P = 0.36). In a subset of patients with urinary potassium greater than 100 mEq/day (n = 100), urinary citrate and urinary pH were both increased; however, there was still no correlation between the two (r = 0.011, P = 0.806).. Despite the current dogma that increasing urinary citrate increases urinary pH, in a cohort of patients with urinary stone formation who provided 24-hour urine specimens, no correlation was found between urinary citrate and urinary pH levels.

Topics: Aged; Alkalies; Allopurinol; Citrates; Female; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Potassium Citrate; Urinary Calculi; Urine

Hypoxanthine phosphoribosyltransferase (HPRT) deficiency is an inherited disorder. Complete deficiency of HPRT activity is phenotypically expressed as the devastating Lesch-Nyhan syndrome. Partial HPRT deficiency usually causes hyperuricemia, precocious gout, and uric acid nephrolithiasis. We describe an 18-year follow-up of a 5-year old boy with partial HPRT deficiency and report a novel mutation in his HPRT gene. He presented with overproduction of uric acid and passage of uric acid renal stones, and without gout or neurological and behavioral abnormalities. Treatment with allopurinol, adequate hydration, urinary alkalization, and a low-purine diet was started. No subsequent nephrolithiasis has occurred. After 18-year of this therapy his physical and neuropsychological status were normal, merely his glomerular filtration rate (GFR, normal 97-137 mL min(-1)/1.73 m(2)) fell from normal to 65.1 mL min(-1). The most likely cause of initial renal impairment in our patient is uric and/or xanthine crystalluria. A missense and transition mutation 169A>G (57ATG>GTG, 57met>val) in exon 3 of the patient's HPRT gene was identified and the mother was the carrier of the mutation. As far as we are aware, the identified mutation has not previously been reported. We named the mutant HPRT Maribor.

Topics: Allopurinol; Child, Preschool; Enzyme Inhibitors; Follow-Up Studies; Humans; Hyperuricemia; Hypoxanthine Phosphoribosyltransferase; Lesch-Nyhan Syndrome; Male; Point Mutation; Treatment Outcome; Uric Acid; Urinary Calculi

Hyperuricemia and secondary urate nephropathy are uncommon in the paediatric setting outside of tumour lysis syndrome. We describe the case of a 12-year-old boy who presented at 3 years of age with acute renal failure. The cause of this remained unknown until the development of uric acid renal calculi 9 years later. This, and the availability of the previously unknown family history, provided the subsequent diagnosis of partial hypoxanthine-guanine phosphoribosyltransferase (HPRT) deficiency. Detailed family history is important for early detection of this heterogeneous group of disorders. Early treatment may minimise long-term renal morbidity and mortality from renal insufficiency.

Topics: Acute Kidney Injury; Age of Onset; Allopurinol; Buffers; Cells, Cultured; Child; Enzyme Inhibitors; Erythrocytes; Female; Fibroblasts; Follow-Up Studies; Genetic Linkage; Greece; Heterozygote; Humans; Hyperuricemia; Hypoxanthine Phosphoribosyltransferase; Male; Pedigree; Skin; Sodium Bicarbonate; Time Factors; Treatment Outcome; Ultrasonography; Urinary Calculi

We report a patient with complete adenine phosphoribosyltransferase deficiency and urolithiasis, in whom 4 consecutive cadaveric renal transplantations were performed; 2,8-dihydroxyadenine crystal nephropathy recurred within weeks in the first and second graft when the patient was not treated with allopurinol immediately after transplantation. In the third graft, recurrence of disease could be prevented by immediate allopurinol treatment. This graft was lost due to chronic allograft nephropathy without significant crystal deposition. After a fourth transplantation, again without initial allopurinol, the disease recurred following an initial vascular rejection. Addition of allopurinol significantly improved renal function of the 2nd and 4th graft. This case indicates that outcome of renal transplantation in patients with adenine phosphoribosyltransferase deficiency critically depends on immediate postoperative pharmacotherapy with allopurinol, which is able to prevent 2,8-dihydroxyadenine nephropathy in the graft. Furthermore, rapid recurrence of disease without allopurinol seems to be triggered by delayed graft function and acute rejection.

Topics: Adenine Phosphoribosyltransferase; Adult; Allopurinol; Cadaver; Graft Rejection; Humans; Kidney Failure, Chronic; Kidney Transplantation; Male; Postoperative Complications; Recurrence; Renal Dialysis; Urinary Calculi

Renal tubular epithelium is the major target for oxalate induced injury, and sustained hyperoxaluria together with CaOx crystal formation/deposition may induce renal tubular cell damage and/or dysfunction. This may express itself in cell apoptosis. To evaluate the possible protective effects of certain agents (vitamin E, potassium citrate, allopurinol, verapamil and MgOH) on the presence and the severity of apoptotic changes caused by hyperoxaluria on renal tubular epithelium, an experimental study in rabbits was performed. Seventy rabbits were divided into seven different groups (each group n = 10): in group I severe hyperoxaluria was induced by continuous ethylene glycol (0.75%) administration started on day 0 and completed on day 14. Histologic alterations including crystal formation together with apoptotic changes (by using the TUNEL method) were evaluated on days 21 and 42, respectively. In the remaining experimental groups (groups II-VI), animals received some agents in addition to the induction of hyperoxaluria in an attempt to limit apoptotic changes. Group VII) animals constituted the controls. Kidneys were examined histopathologically under light microscopy for the presence and degree of crystal deposition in the tubular lumen. The percentage of apoptotic nuclei in the control group was significantly different from the other group animals (2.9-2.4%) in all study phases (P < 0.05). Apart from potassium citrate and allopurinol, the other medications seemed to prevent or limit the formation of apoptotic changes in renal tubular epithelium during the early period (day 21). The percentage of positively stained nuclei in animals undergoing potassium citrate medication ranged from 24.3% to 28.6%, with an average of 27.1%. This was 18.4% in animals receiving allopurinol. On the other hand, animals receiving magnesium hydroxide (MgOH), verapamil and vitamin E demonstrated limited apoptotic changes (11.2, 9.7, 8.7%, respectively) during this phase(P < 0.05). In the long-term (day 42), the animals receiving allopurinol and vitamin E showed a decrease in the percentage of the positively stained nuclei (13.5% and 8.3%, respectively). Animals in the other groups showed an increase in the number and percentage of apoptotic cells. Although, there was a significant decrease in the mean values of apoptosis in animals receiving vitamin E (8.7%-8.3%) and allopurinol (18.4%-13.5%) (P < 0.05), animals on verapamil, MgOH and potassium citrate medication had an increas

Topics: Allopurinol; Animals; Apoptosis; Cells, Cultured; Disease Models, Animal; Hyperoxaluria; In Situ Nick-End Labeling; Kidney Tubules; Male; Oxalates; Potassium Citrate; Rabbits; Random Allocation; Reference Values; Sensitivity and Specificity; Urinary Calculi; Urothelium; Verapamil; Vitamin E

Renal injury is considered as one of the prerequisites for calcium oxalate retention. In order to determine the role of lipid peroxidation related effects for hyperoxaluria, we evaluated the alterations in lipid peroxidation, antioxidants and oxalate synthesizing enzymes in lithogenic rats with response to vitamin E + selenium treatment. In kidney of lithogenic rats, the level of lipid peroxidation and the activities of oxalate synthesizing enzymes were found to be increased whereas the levels/activities of non-enzymatic and enzymatic antioxidants were found to be decreased. The urinary excretion of both oxalate and calcium were significantly elevated. Supplementation of lithogenic rats with vitamin E + selenium decreased the levels of lipid peroxides and the activities of oxalate synthesizing enzymes like glycolic acid oxidase (GAO), lactate dehydrogenase (LDH), xanthine oxidase (XO) with a concomitant increase in the activities of enzymatic antioxidants like superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glucose-6-phosphate dehydrogenase (G6PDH) and increased levels of non-enzymatic antioxidants like ascorbic acid, alpha-tocopherol and reduced glutathione (GSH). The urinary excretion of oxalate and calcium were normalized. The antioxidants vitamin E + selenium thereby protected from hyperoxaluria.

Topics: Alcohol Oxidoreductases; Animals; Antioxidants; Ascorbic Acid; Calcium Oxalate; Catalase; Dietary Supplements; Glucosephosphate Dehydrogenase; Glutathione; Glutathione Peroxidase; Hyperoxaluria; Kidney; L-Lactate Dehydrogenase; Lipid Peroxidation; Liver; Male; Rats; Rats, Wistar; Selenium; Superoxide Dismutase; Urinary Calculi; Vitamin E; Xanthine Oxidase

Oral chemolysis of uric acid stones was performed retrospectively. Twenty-one patients with upper urinary uric acid stones were given alkaline citrate (Uralyt-U) orally. In the case of hyperuicemia, allopirinol was combined. In 11 out of 15 patients (73.3%) treated with oral chemolysis alone, stones were dissolved. In 4 out of 6 cases (66.7%) combined with extracorporeal shock-wave lithotripsy, administration of alkaline citrate shortened the period to be stone-free. In conclusion, we successfully treated 15 out of 21 cases (71.4%) with the administration of alkaline citrate.

Topics: Administration, Oral; Allopurinol; Citric Acid; Combined Modality Therapy; Drug Therapy, Combination; Humans; Hyperuricemia; Lithotripsy; Retrospective Studies; Treatment Outcome; Uric Acid; Urinary Calculi

Oxalate in urine can cause tubular cellular damage by the production of free radicals. Then, cell death and cellular debris may promote the retention of calcium oxalate crystals and finally the formation of stones. The two most abundant urinary proteins, Tamm-Horsfall protein (THP) and albumin, were tested for the effects of antioxidants.. By using xanthine-xanthine oxidase reaction, purified THP and albumin were tested for the inhibitory effect. OD(295) was used as a spectrophotometric method to measure the production of uric acid during the reaction.. Both proteins can inhibit the reaction of xanthine oxidase on xanthine, although the effect was decreased after enzymatic deglycosylation of sialic acid. Albumin has an IC(50) of 10.7 nM in native condition and 11.9 nM after deglycosylation, whereas THP has 69.6 nM in native condition and 102.0 nM in deglycosylated condition. The data indicates that THP and albumin have an antioxidant effect. Sialic acid in THP has partly an inhibitory effect and is associated with calcium oxalate formation. Studies have indicated that further investigation of the role of free radicals in the formation of urolithiasis and of sialic acid in protein function is needed.

Topics: Adjuvants, Immunologic; Albumins; Calcium Oxalate; Crystallization; Electrophoresis, Polyacrylamide Gel; Free Radicals; Humans; Male; Mucoproteins; Urinary Calculi; Uromodulin; Xanthine; Xanthine Oxidase

Topics: Allopurinol; Enzyme Inhibitors; Humans; Male; Meningitis, Aseptic; Middle Aged; Urinary Calculi; Xanthine Oxidase

Calculi were located in the kidneys, the ureters and the bladder of a two-year-old male dachshund. The yellow-greenish calculi developed as a result of impaired transformation of xanthine to uric acid resulting in an increased concentration of xanthine in the urine. The cause of the impaired catabolism of xanthine was probably a disorder of the xanthine oxidase enzyme, which catalyses the transformation of xanthine to uric acid.

Topics: Animals; Dog Diseases; Dogs; Male; Uric Acid; Urinary Calculi; Xanthine; Xanthine Oxidase

The objective of this study was to evaluate treatment of uric acid urolithiasis and prevention of uric acid stone formation in children. We treated 18 children (11 boys and 7 girls) with uric acid urolithiasis. Complete dissolution of stones was achieved in 16 children (89%). During a two year follow-up period, 14 children (78%) were recurrence free.

Topics: Adolescent; Allopurinol; Child; Child, Preschool; Diet Therapy; Enzyme Inhibitors; Female; Follow-Up Studies; Humans; Infant; Male; Treatment Outcome; Urinary Calculi

Hyperxanthinuria and xanthine uroliths have been recognized with increased frequency in dogs with ammonium urate uroliths that had been given allopurinol. We hypothesized that dietary modification might reduce the magnitude of uric acid and xanthine excretion in urine of dogs given allopurinol. To test this hypothesis, excretion of metabolites, volume, and pH were determined in 24-hour urine samples produced by 6 healthy Beagles during periods of allopurinol administration (15 mg/kg of body weight, PO, q 12 h) and consumption of 2 special purpose diets: a 10.4% protein (dry matter), casein-based diet and a 31.4% protein (dry matter), meat-based diet. Significantly lower values of uric acid (P = 0.004), xanthine (P = 0.003), ammonia (P = 0.0002), net acid (P = 0.0001), titratable acid (P = 0.0002), and creatinine (P = 0.01) excreted during a 24-hour period were detected when dogs consumed the casein-based diet and were given allopurinol, compared with the 24-hour period when the same dogs consumed the meat-based diet and were given allopurinol. For the same 24-hour period, urine pH values, urine volumes, and urine bicarbonate values were significantly (P = 0.0004, P = 0.04, and P = 0.002, respectively) higher during the period when the dogs were fed the casein-based diet and given allopurinol than when they were fed the meat-based diet and given allopurinol. Endogenous creatinine clearance was significantly (P = 0.006) lower when dogs were fed the casein-based diet and given allopurinol than when they were fed the meat-based diet and given allopurinol.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Allopurinol; Ammonia; Animals; Diet, Protein-Restricted; Dietary Proteins; Dogs; Female; Food-Drug Interactions; Uric Acid; Urinary Calculi; Xanthines

Topics: Allopurinol; Arthritis, Gouty; Humans; Uric Acid; Urinary Calculi

Topics: Adenine; Adenine Phosphoribosyltransferase; Adolescent; Adult; Age Factors; Allopurinol; Child; Child, Preschool; Diet; Humans; Male; Purines; Urinary Calculi

Clinical features and laboratory findings were evaluated in 10 dogs that formed xanthine-containing urinary calculi during the period that they were given allopurinol (9 to 38 mg/kg of body weight/d). Duration of allopurinol treatment was 5 weeks to 6 years. Of the 10 dogs, 9 (all Dalmatians) had formed uric acid-containing calculi at least once before allopurinol treatment was initiated. It was not possible to recognize xanthine as a crystalline component of the calculi by use of a chemical colorimetric method or by polarized light microscopy. We concluded that the best diagnostic method for recognition of xanthine-containing calculi was high-pressure liquid chromatography because it is quantitative, sensitive, and accurate, and can be conducted on a small amount (1 to 2 mg) of crystalline material.

Topics: Allopurinol; Animals; Breeding; Dog Diseases; Dogs; Male; Urinary Calculi; X-Ray Diffraction; Xanthine; Xanthines

Urine composition in terms of calcium oxalate (CaOx) supersaturation was studied in 802 patients with calcium stone disease before any intervention and during follow-up. Supersaturation was expressed as the AP(CaOx) index, a simplified estimate of the ion activity product of CaOx, and a similar index calculated for a 24-hour urine volume of 1.5 liters the AP(CaOx) index(s). The AP(CaOx) index was significantly reduced in men with and without medical treatment who remained stone-free during follow-up (p less than 0.001), but not in men who continued to form stones. For the AP(CaOx) index(s), a significant reduction was observed only in patients on medical treatment without new stone formation (p less than 0.01). In women, significantly lower AP(CaOx) index values were recorded in recurrent as well as non-recurrent stone formers on medical treatment, whereas in the group without medical treatment and without recurrences the difference did not reach a statistically significant level. This was similar to the effect on the AP(CaOx) index(s) in non-recurrent women with medical treatment. The small number of women with recurrences might have influenced the result. Significantly reduced levels of the AP(CaOx) index were recorded for patients given thiazide, thiazide + magnesium, magnesium, and alkaline citrate. The AP(CaOx) index(s) was reduced in patients given thiazide + magnesium, magnesium, and alkaline citrate. Comparison between the effects on urine composition and clinical response showed that the reduced CaOx supersaturation observed with thiazide, thiazide + magnesium, and alkaline citrate, corresponded to a low rate of stone formation during follow-up. The inefficiency of allopurinol and orthophosphate in affecting urine supersaturation was reflected in a higher recurrence rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Allopurinol; Bendroflumethiazide; Calcium Oxalate; Citrates; Citric Acid; Female; Follow-Up Studies; Humans; Hydrochlorothiazide; Magnesium Oxide; Male; Outpatient Clinics, Hospital; Phosphates; Recurrence; Urinary Calculi

After 1 year of allopurinol treatment in 36 patients with a history of uric acid and/or calcium oxalate lithiasis and hyperuricosuria, we observed that in addition to the desired decreases in uric acid there were apparently significant decreases in urinary oxalate levels: 37 +/- 3 mg. per day (mean +/- standard error) before therapy and 31 +/- 4 mg. per day after a mean decrease of 16% (p less than 0.05) with an equivalent decrease in the supersaturation (calcium oxalate) of the urine. However, the decrease in oxalate could have been related to changes in dietary habits rather than to any specific effects of allopurinol on oxalate metabolism. Therefore, we recruited 26 of the patients for a study in which dietary factors were controlled. Each participant was assigned to 1 of 3 diet groups: low or high protein, or a customary diet. Each patient collected a urine specimen while on allopurinol and again after the medication was discontinued. With analytical procedures that we ascertained to be free of any significant methodological bias, we observed no significant changes in urinary oxalate excretion that could be attributed to allopurinol. There were significant differences in oxalate excretion on versus off allopurinol between the low and high protein groups, with higher oxalate levels found for the latter group. Our results indicate that allopurinol does not have a specific effect on oxalate metabolism or oxaluria.

Topics: Adult; Allopurinol; Dietary Proteins; Female; Humans; Male; Middle Aged; Oxalates; Urinary Calculi

Factors relating alterations in plasma and urine composition to recurrence of urinary stones during drug therapy were investigated by using a multiple regression analysis technique. These factors were influenced not only by the efficacy of the drugs but also by other factors (plasma or urinary constituents and overall health of the patients, etc.). In order to study the effect of drug therapy or other treatment on the alteration of plasma and urine constituents, multiple regression analysis is more appropriate than Student's paired t-test which has been used by some workers. These two analytical methods yield different results even if used on the same data.

Topics: Adult; Allopurinol; Calcium; Chlorothiazide; Creatinine; Drug Combinations; Electrolytes; Humans; Middle Aged; Recurrence; Uric Acid; Urinary Calculi

The authors examined 133 patients with urolithiasis, treated with hydrochlorothiazide and 81 patients treated with allopurinol. In those treated with hydrochlorothiazide the calciuria and Ca/creat. index declined, and uricaemia rose. After treatment uricosuria increased significantly in 41% patients. The detection of diabetes did not exceed the prevalence in the population. In patients treated with allopurinol the uricaemia and uricosuria declined, a hepatic disorder with supraliminal rise of ALT was recorded in 23% of the patients and led to discontinuation of treatment in 15% of the patients.

Topics: Allopurinol; Humans; Hydrochlorothiazide; Uric Acid; Urinary Calculi

The beneficial effect of allopurinol treatment in metaphylaxis of hyperuricosuric calcium oxalate lithiasis has been analyzed in a retrospective study covering 10 years. 83 patients with hyperuricosuric calcium oxalate lithiasis (48 recurrent stone formers, 35 patients with a single stone episode) were treated with 300 mg allopurinol for 33.1 +/- 11.5 months. Subsequently, each patient was controlled for 43.9 +/- 27 months without therapy. The overall relapse rate was 28.9% but there is no statistically significant difference between treatment with and without allopurinol (Mann-Whitney: p = 0.16). The only striking difference was the fact that, with one exception, stone relapses occurred only in the group of recurrent stone formers, whereas the group with single stone formation seemed to be at a clearly decreased risk for stone recurrence during follow-up. This would suggest that factors other than those investigated in this study are responsible for the phenomenon of recurrent stone formation.

Topics: Allopurinol; Calcium Oxalate; Female; Follow-Up Studies; Humans; Male; Middle Aged; Recurrence; Retrospective Studies; Time Factors; Uric Acid; Urinary Calculi

We report the first patient in Finland and Scandinavia with a deficiency of adenine phosphoribosyltransferase (APRT). About 30 clinically affected patients have been reported in the literature. APRT deficiency is an enzyme disorder which is inherited autosomally in a recessive manner. The use of adenine in purine metabolism is disturbed and it accumulates in the body, where it is oxidised to poorly insoluble 2,8-dihydroxyadenine by xanthine oxidase. The dihydroxyadenine forms stones which can be mistaken for uric acid stones. Our patient had had frequent episodes of urolithiasis and the diagnosis was finally made after pyelolithotomy and stone analysis. The total APRT deficiency was detected in the haemolysate of erythrocytes. Partial deficiency of APRT in the patient's relatives showed heterozygosity of the enzyme defect. The only clinical manifestation of the defect is the formation of urinary stones. This can be prevented by diet and allopurinol.

Topics: Adenine; Adenine Phosphoribosyltransferase; Allopurinol; Female; Finland; Humans; Middle Aged; Pentosyltransferases; Urinary Calculi

The effect of combining therapy with hydrochlorothiazide, allopurinol and systemic alkalization for urolithiasis with lower urinary pH was examined. A total of 90 patients were followed up for 1 to 3 years, the average follow up period being 18 months. The total stone disappearance rate was 60% (kidney stone), 74% (ureter stone) and 20% (bladder stone). Large amounts of thiazide diuretics, potassium and magnesium were intravenously administered to a patient with systemic alkalization at slow infusion speed, neither serious side effects nor complication occurred. This method is simple and an effective remedy. It is also very practical in the developing countries of the third world.

Topics: Adult; Aged; Allopurinol; Bicarbonates; Drug Therapy, Combination; Female; Humans; Hydrochlorothiazide; Hydrogen-Ion Concentration; Lactates; Lactic Acid; Male; Middle Aged; Sodium; Sodium Bicarbonate; Urinary Calculi

Topics: Allopurinol; Calcium Oxalate; Drug Evaluation; Female; Humans; Male; Urinary Calculi

Topics: Allopurinol; Calcium Oxalate; Humans; Urinary Calculi

Uric acid stone disease is dependent on three pathogenetic factors: acid urine pH, low urine volume, and hyperuricosuria. The management of nonobstructing uric acid calculi should include maintenance of an alkaline urine, an increase in urine volume, and reduction in urinary uric acid excretion. It appears that potassium alkali may avoid the complication of calcium stone formation in patients with uric acid stones. In patients with obstructing uric acid calculi, more rapid dissolution may be accomplished with intravenous alkalinization or direct irrigation of the stone with an alkaline solution.

Topics: Allopurinol; Citrates; Citric Acid; Dietary Proteins; Fluid Therapy; Humans; Methionine; Uric Acid; Urinary Calculi

Topics: Adult; Aged; Allopurinol; Arthritis; Colchicine; Coronary Disease; Gout; Humans; Hypertension; Middle Aged; Probenecid; Uric Acid; Urinary Calculi

Among patients with urolithiasis, the recurrence rate is 10-23% per year. We have applied guidelines for critical appraisal to 46 publications addressing the efficacy of thiazides, orthophosphates, cellulose phosphate, allopurinol, magnesium and citrate as prophylaxis against recurrent urolithiasis. The 34 studies which do not have a randomly allocated control group are subject to methodologic deficiencies such as co-intervention, variable outcome measures, variable natural history, statistical regression to the mean, selection bias and incomplete follow-up of patients. These deficiencies make conclusions regarding the efficacy of an intervention suspect. Among the 12 randomized clinical trials are 5 thiazide, 2 orthophosphate, 4 allopurinol and 1 magnesium intervention. The methodologic and statistical questions addressed were: adequacy of randomization, clinical relevance of outcomes, description of patients, clinical and statistical significance, and completeness of follow-up. Based on these methodologic considerations, one could not conclude that orthophosphates, cellulose phosphate, magnesium or citrate were efficacious in preventing recurrent urolithiasis. Two of the 5 thiazide and 1 of the 4 allopurinol randomized clinical trials demonstrate convincing evidence for efficacy of these interventions. With the exception of pilot studies of new interventions, conclusions about efficacy of interventions claimed to decrease the urolithiasis recurrence rate should be based on methodologically sound randomized clinical trials.

Topics: Allopurinol; Benzothiadiazines; Calcium; Cellulose; Citrates; Citric Acid; Diuretics; Humans; Magnesium; Recurrence; Sodium Chloride Symporter Inhibitors; Urinary Calculi

The urinary excretion levels of oxalic acid, calcium, kynurenic, and xanthurenic acids and serum pyridoxal and pyridoxal phosphate concentrations were determined for nonbilharzial and bilharzial hyperoxaluric patients with or without urinary stones. The effects of pyridoxine and allopurinol treatment were also studied. The different groups studied showed elevated levels of urinary oxalic acid, calcium, kynurenic, and xanthurenic acids as well as decreases in serum pyridoxal and pyridoxal phosphate concentrations. These data indicate that nonbilharzial hyperoxaluric patients suffer from dietary B6 deficiency, whereas bilharzial hyperoxaluric patients may suffer from impaired pyridoxine phosphokinase activity. Pyridoxine supplementation is recommended for the treatment of nonbilharzial hyperoxaluric patients. Allopurinol may be the proper drug in the treatment of oxaluria and stone formation or of bilharzial patients.

Topics: Adult; Alanine Transaminase; Alkaline Phosphatase; Allopurinol; Aspartate Aminotransferases; Calcium; Creatinine; Humans; Male; Middle Aged; Oxalates; Pyridoxine; Reference Values; Schistosomiasis; Urea; Urinary Calculi

We have investigated the composition of plasma and urine in patients with recurrent calcium calculi treated with allopurinol alone, thiazide alone, and both agents together for more than 18 months, and compared the results with those of patients receiving no treatment. In patients treated with allopurinol, both plasma and urinary uric acid were decreased, and plasma parathyroid hormone (PTH) and urinary calcium were increased between 1 and 2 years after treatment. In patients treated with thiazide, plasma calcium was decreased 3 months after treatment but then increased gradually, although the pre-treatment level was not reached. Urinary calcium was decreased 3 months after treatment but returned to pre-treatment levels at 6 and 12 months. Plasma PTH was gradually increased. In patients treated with both allopurinol and thiazide, plasma and urinary uric acid, plasma potassium and urinary calcium were decreased during treatment. Plasma PTH increased gradually during treatment. In patients receiving no treatment, the composition of plasma and urine did not alter during follow-up. The reasons for the changes in urinary calcium and plasma PTH have been discussed.

Topics: Adult; Allopurinol; Benzothiadiazines; Calcium; Diuretics; Drug Therapy, Combination; Electrolytes; Humans; Male; Middle Aged; Parathyroid Hormone; Recurrence; Sodium Chloride Symporter Inhibitors; Time Factors; Uric Acid; Urinary Calculi

We showed previously that ingestion of a non-specific high purine diet by healthy subjects increased not only urinary uric acid levels but urinary oxalate as well. Both increments were reduced significantly during concomitant allopurinol therapy. The present study was undertaken to investigate these findings in more detail under carefully controlled dietary conditions where a single specific purine, guanosine, was used as an additive and several different methods for oxalate determination (GLC, HPLC, isotacophoresis) were compared with the enzymatic method used previously. Results obtained by two direct techniques of oxalate determination showed no significant alteration in oxalate levels during any dietary regime, suggesting that the earlier results derived from problems inherent in the experimental design and methodology employed. The study confirmed that one of the beneficial effects of allopurinol was to reduce dietary purine absorption. The results may thus provide a logical explanation for the reduced incidence of urolithiasis during allopurinol therapy in some idiopathic oxalate stone formers addicted to purine-rich foods and beverages.

Topics: Adult; Allopurinol; Chromatography, Gas; Diet; Female; Guanosine; Humans; Male; Oxalates; Oxalic Acid; Urinary Calculi

Topics: Allopurinol; Animals; Benzothiadiazines; Calcium; Diuretics; Humans; Recurrence; Sodium Chloride Symporter Inhibitors; Urinary Calculi

Allopurinol in a daily dose of 300 mg. was administered to 99 patients with calcium oxalate stone disease. Treatment was started irrespective of urine composition and was continued for up to 8 years. Only 43 per cent of the patients treated for 5 or more years remained free of further stone formation, a result not better than observations in untreated stone patients. When patients were subgrouped with respect to recurrent or nonrecurrent stone formation during treatment, the former group, besides being followed for longer intervals than the latter group, had a urine composition suggesting a higher crystallization risk. We concluded that with the possible exception of hyperuricosuria or hyperuricemia the indication for allopurinol treatment of recurrent calcium oxalate stone disease is weak. The results also demonstrate clearly the problems combined with evaluation of prophylactic medical therapy in patients with calcium stones. The necessity of long-term followup and analysis of the biochemical risk situation is emphasized.

Topics: Allopurinol; Calcium Oxalate; Female; Humans; Male; Recurrence; Urinary Calculi

Topics: Adolescent; Adult; Aged; Allopurinol; Benzothiadiazines; Calcium; Child; Diuretics; Female; Humans; Male; Middle Aged; Recurrence; Sodium Chloride Symporter Inhibitors; Urinary Calculi

We evaluated 113 patients with recurrent or multiple calcium urolithiasis at our outpatient stone clinic between 1980 and 1983. Diagnostic categories included hypercalciuria (36 patients), hyperoxaluria (35 patients), and hyperuricosuria (31 patients). Thiazides and/or allopurinol were administered to the hypercalciurics and hyperuricosurics, respectively for prevention of stone recurrence. Patients followed up for more than one year were 23 (male 16, female 7) in the thiazide group, and 15 (male 12, female 3) in the allopurinol group. The mean treatment interval was 2.49 years in the former, and 2.35 years in the latter. The remission rate (percentage of patients without formation of any new stones) was 82.6% in the thiazide group, and 73.3% in the allopurinol group. The group stone formation rate was reduced from 0.85 to 0.35/pt-yr in the thiazide group, and from 0.74 to 0.27/pt-yr in the allopurinol group. Efficacy of these two drugs for the prevention of calcium stone recurrence was observed in this selective therapy, but a careful double blind study should be carried out to draw a definite conclusion.

Topics: Allopurinol; Benzothiadiazines; Calcium; Diuretics; Female; Humans; Magnesium; Male; Oxalates; Oxalic Acid; Phosphates; Recurrence; Sodium Chloride Symporter Inhibitors; Urinary Calculi

Topics: Allopurinol; Animals; Chemistry; Coronary Disease; Gout; History, 20th Century; Humans; Hypertension; Leukemia, Myeloid; National Institutes of Health (U.S.); Nephritis, Interstitial; Purines; United States; Uric Acid; Urinary Calculi; Xanthine Oxidase

Topics: Adolescent; Adult; Aged; Allopurinol; Combined Modality Therapy; Female; Fluid Therapy; Humans; Male; Middle Aged; Retrospective Studies; Uric Acid; Urinary Calculi

Topics: Allopurinol; Benzothiadiazines; Calcium; Cellulose; Citrates; Diuretics; Humans; Ion Exchange; Oxalates; Prostaglandin Antagonists; Sodium Chloride Symporter Inhibitors; Urinary Calculi

In order to evaluate whether therapy can reduce relapses of urinary stone formation, we have retrospectively analysed the long-term follow-up of 55 recurrent stone former patients either treated with high fluid intake and moderate low calcium and low oxalate diet alone (Group A 18 patients), or with the same dietetic advice plus hydrocholorothiazide, amiloride and allopurinol (Group B 37 patients). In group A, stone recurrence was completely abolished in 14 patients without hypercalciuria and hyperuricuria, but not in the four patients with hypercalciuria and hyperuricuria. In group B, no relapses were observed in 19 hypercalciuric and hyperuricuric patients during a cumulative follow-up of 91 years. Even if the other 18 patients had relapses during a cumulative follow-up of 89 years, they showed a significant decrease in stone/patient and stone/year rates. It is concluded that high fluid intake and diet can actually prevent stone recurrence in patients without hypercalciuria and hyperuricuria, but in hypercalciuric and hyperuricuric patients treatment with diuretic and allopurinol is better.

Topics: Allopurinol; Benzothiadiazines; Calcium, Dietary; Diuretics; Drinking; Humans; Oxalates; Oxalic Acid; Recurrence; Sodium Chloride Symporter Inhibitors; Urinary Calculi

Topics: Allopurinol; Benzothiadiazines; Calcium; Diuretics; Drug Evaluation; Humans; Recurrence; Sodium Chloride Symporter Inhibitors; Urinary Calculi

Topics: Allopurinol; Calcium; Follow-Up Studies; Humans; Recurrence; Uric Acid; Urinary Calculi

We studied the effect of allopurinol on the prevention of stone recurrence in 134 patients with recurrent, idiopathic calcium nephrolithiasis. They consisted of 113 male patients and 21 female, between 16 and 72 years with an average age of 42.7. The patients were divided into two groups according to the type of stone occurrence; those with multiple stones without previous stone episodes (multiple stone group), and the those with recurrent stones (stone episode group). Twenty three patients belonged to the multiple stone group and 111 patients belonged to the stone episode group. The stones in 19 of the 23 patients in the multiple stone group remained stable throughout the study, while stones in 4 grew. Fifty-nine of the 111 patients in the stone episode group were free from recurrence, but the others showed recurrence. Statistical analyses was done on the stone episode group. The stone recurrence rate of all of the 111 cases showed significant decrease during prophylactic treatment with allopurinol (p less than 0.01), although the observation period before treatment was 73.0 +/- 65.8 months and that during and after treatment was 28.2 +/- 12.1 months. During the two years before and after prophylaxis 79 patients also showed a significantly decreased recurrence rate. Moreover, regarding 37 cases without any stones at the start of treatment, stone recurrence rate decreased significantly after the administration of allopurinol. Throughout this study, we used a new method for evaluating reasonable stone recurrence. It did not calculate the number of stones recurred, but the stone-forming circumstance in each kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adolescent; Adult; Aged; Allopurinol; Calcium Oxalate; Drug Evaluation; Female; Humans; Male; Middle Aged; Recurrence; Urinary Calculi

In 30 cases of recurring urinary calcium oxalate and calcium phosphate calculi, renal or absorptive hypercalciuria or hyperuricemia, long term controls of serum and urine electrolytes were made under hydrochlorothiazide and allopurinol therapy. By differentiating the type of hypercalciuria it could be determined, if thiazide-therapy is indicated in renal hypercalciuria only or in the absorptive cases as well. Statistic comparison of the patients with - and without increased urinary sodium excretion solved the question whether high sodium excretion diminishes or abolishes the hypocalciuric thiazide effect. The frequency of stones before and after treatment supports the efficacy of thiazide prophylaxis.

Topics: Adult; Allopurinol; Calcium Oxalate; Calcium Phosphates; Drug Therapy, Combination; Female; Humans; Hydrochlorothiazide; Long-Term Care; Male; Recurrence; Urinary Calculi

Topics: Allopurinol; Calcium; Cellulose; Cystinuria; Diet; Drug-Related Side Effects and Adverse Reactions; Humans; Hydrochlorothiazide; Kidney Calculi; Magnesium; Phosphates; Uric Acid; Urinary Calculi

Topics: Adult; Allopurinol; Calcium, Dietary; Follow-Up Studies; Humans; Hydrochlorothiazide; Time Factors; Urinary Calculi; Water

All urinary calculi should be thoroughly examined. Among 2 000 calculi analyzed by infra-red spectrophotometry, some were found to contain rare constituants and drugs which might be held responsible for urinary stone formation. These included glafenine, triamterene, co-trimoxazole, sulphaguanidine, allopurinol, phenazopyridine, flumequine and anti-acid powders containing aluminium, calcium and magnesium trisilicates and/or carbonates or bicarbonates. Considering that these drugs are widely used, the incidence of drug-induced urinary calculi appears to be very low.

Topics: Allopurinol; Antacids; Fluoroquinolones; Glafenine; Humans; Phenazopyridine; Quinolizines; Sulfonamides; Triamterene; Urinary Calculi

Urolithiasis resulting from inherited metabolic derangement is rare. Only 13 cases of 2,8-dihydroxyadenine stones resulting from a deficiency of the enzyme adenine phosphoribosyl transferase have been reported since 1974. Of these cases 9 have been in children with the homozygous trait. To date, 3 homozygous and 1 heterozygous adults with urolithiasis have been reported. This disease has not been associated with any other clinical or biochemical abnormalities. Treatment includes low purine diet and allopurinol. We herein report a case of complete adenine phosphoribosyl transferase deficiency associated with 2,8-dihydroxyadenine urolithiasis in the United States, bringing the total to 14 in the literature.

Topics: Adenine; Adenine Phosphoribosyltransferase; Allopurinol; Child; Heterozygote; Homozygote; Humans; Male; Metabolism, Inborn Errors; Pentosyltransferases; Purines; United States; Urinary Calculi

Topics: Allopurinol; Calcium Oxalate; Calcium, Dietary; Cellulose; Citrates; Citric Acid; Combined Modality Therapy; Fluid Therapy; Humans; Hydrochlorothiazide; Kidney Calculi; Magnesium; Oxalates; Phosphates; Urinary Calculi

Disturbances in purine metabolism with hyperuricaemia and/or hyperuricosuria are a risk factor in uric acid and Ca oxalate stone formation. By way of a competitive xanthine oxidase inhibition, the formation of uric acid is reduced by allopurinol. In investigations on two groups of patients, Milurit could be demonstrated to decrease the uric acid levels in serum and urine. No differences could be seen in the dosages of 3 x 100 mg or 1 x 300 mg Milurit. Therefore, in stone recurrence prevention, the administration of Milurit 300 is recommended.

Topics: Adolescent; Adult; Aged; Allopurinol; Calcium Oxalate; Female; Humans; Male; Middle Aged; Oxypurinol; Recurrence; Uric Acid; Urinary Calculi; Xanthine Oxidase

Urinary tract calculi composed primarily of xanthine are rare in adults and children. However, there is risk of xanthine calculi formation in children with hereditary xanthinuria and children on xanthine oxidase inhibitor therapy for hyperuricemia. We describe the clinical presentation and management of 2 children with the Lesch-Nyhan syndrome (a congenital disorder of purine metabolism) and xanthine calculi. Little information has been available to direct the urologic management of such patients. We have based a plan for management upon our clinical experience with these children, as well as upon in vitro dissolution studies of the calculi. We have had some clinical success using an alternating acid/base dissolution therapy developed in the laboratory.

Topics: Adolescent; Allopurinol; Child; Humans; Lesch-Nyhan Syndrome; Male; Urinary Calculi; Xanthines

29 patients (20 male and 9 female, average age 55 years), suffering from uric acid-urolithiasis were treated with Zyloric-U over a period of 8 to 20 months. Two of them had side effects (cutaneous symptoms). In all other cases the stones were dissolved or diminuated. Chemical analysis demonstrated a significant reduction of serum uric acid as well as a decrease of calcium secretion in the urine. Yet the urine-pH of 5 remained unchanged. In some cases, if the patients excreted gravel and if the level of uric acid was not lowered sufficiently the dose was raised to twice 300 mg. A report of the follow-up of these patients shall be published later.

Topics: Aged; Allopurinol; Female; Humans; Long-Term Care; Male; Middle Aged; Uric Acid; Urinary Calculi

Topics: Allopurinol; Calcium; Female; Humans; Hydrochlorothiazide; Male; Urinary Calculi

Topics: Adult; Allopurinol; Calcium; Female; Humans; Magnesium; Male; Middle Aged; Oxalates; Phosphates; Recurrence; Uric Acid; Urinary Calculi; Urinary Tract Infections

Purine nucleotide degradation refers to a regulated series of reactions by which human purine ribonucleotides and deoxyribonucleotides are degraded to uric acid in humans. Two major types of disorders occur in this pathway. A block of degradation occurs with syndromes involving immune deficiency, myopathy or renal calculi. Increased degradation of nucleotides occurs with syndromes characterized by hyperuricemia and gout, renal calculi, anemia or acute hypoxia. Management of disorders of purine nucleotide degradation is dependent upon modifying the specific molecular pathology underlying each disease state.

Topics: Adenosine Deaminase; Adenosine Monophosphate; Adenosine Triphosphate; AMP Deaminase; Anemia; Animals; Deoxyribonucleotides; Female; Gout; Humans; Hypoxia; Male; Nucleotidases; Phosphorylation; Purine Nucleotides; Purine-Nucleoside Phosphorylase; Purine-Pyrimidine Metabolism, Inborn Errors; Purines; Ribonucleotides; Uric Acid; Urinary Calculi; Xanthine Oxidase

Topics: Allopurinol; Aluminum Hydroxide; Follow-Up Studies; Humans; Kidney Calculi; Methods; Ureteral Calculi; Urinary Calculi

Topics: Adult; Allopurinol; Child; Female; Gout; Humans; Hypoxanthine Phosphoribosyltransferase; Male; Myeloproliferative Disorders; Neoplasms; Pedigree; Uric Acid; Urinary Calculi

The nucleation kinetics of calcium oxalate were studied in the presence and absence of sodium urate monohydrate crystalline material by three experimental measurements. These included analytical determinations of calcium and radiotracer analysis of oxalate in the metastable calcium oxalate solution phase and the independent detection of new crystal nuclei by solution turbidity measurements. None of the methods gave any evidence that sodium urate increases the induction time for nucleation of calcium oxalate, in contrast to previously published reports. These results are discussed in relation to the mechanisms advanced to explain the interdependency of hyperuricosuria and calcium oxalate urolithiasis.

Topics: Allopurinol; Calcium Oxalate; Humans; Kinetics; Nephelometry and Turbidimetry; Uric Acid; Urinary Calculi

Topics: Adenine; Adult; Allopurinol; Female; Humans; Kidney Calculi; Kidney Pelvis; Purine-Pyrimidine Metabolism, Inborn Errors; Urinary Calculi

The annual incidence of urolithiasis in the population is at least 0.1%. In rural areas, there are remarkably less actual stone formers than in urban districts, and also vegetarians show less stone diseases. Calcium carbonate as a urinary calculus compound is not in the strict sense impossible, but often an artifact. About 10% of homozygotic cystinuria patients never suffer an actual stone disease.. It is obvious that for stone formation urinary supersaturation alone is not sufficient. Besides the well-known inhibitors like citrate, magnesium and pyrophosphate there have to be other important urinary constituents. Risk factors are high protein or glucose intakes and, in general, hyperalimentation, simply because any food has to be deplenished somehow and increases the urine concentration. A special cause may be found in alterations of the renal tubuli. Diagnostic: For the quite difficult oxalate analysis, an enzymatic test is commercially available. Up to now, the most important analytical task in urolithiasis is still the correct analysis of urinary calculi. Qualitative chemical analysis shows up to 50% erroneous results, leading to false therapies. To determine the calculus compounds the best appropriate method is by far the X-ray diffraction analysis.. The results with adsorption medicines are contradictory. Satisfactory therapies are given for uricosuria with allopurinol and for oxaluria with pyridoxine. A new therapy for cystinuria may be the combined application of ascorbic acid and sodium hydrogen carbonate.

Topics: Allopurinol; Ascorbic Acid; Carbonates; Diet; Humans; Pyridoxine; Risk; Urinary Calculi

A review of the current management of urinary tract stones as applied to the University Department of Surgery is presented. The use of allopurinol and alkalinisation of urine is effective in dissolution and prevention of uric acid stones. Cellulose phosphate and thiazide therapy for calcium stone formers have a limited place, as we are still unable to identify those who will benefit from such therapy in the local population. Antegrade pyelogram and percutaneous nephrostomy have useful roles to play in investigation and also management of patients with calculous anuria. The use of regional renal hypothermia has enabled us to operate with more confidence on branched or multiple renal calculi. With better visual lithotrite, more and bigger stones in the lower urinary tract can now be removed endoscopically.

Topics: Allopurinol; Anuria; Bicarbonates; Cystoscopy; Endoscopy; Female; Humans; Hypothermia, Induced; Kidney; Middle Aged; Radiography; Urinary Calculi

Complete lack of adenine phosphoribosyltransferase (APRT) is a not uncommon cause of urinary lithiasis in young children. The calculi are made up of a very poorly soluble substance, 2,8-dihydroxyadenine, which results from the oxidation of adenine by xanthinoxidase. A study of the 7 cases of APRT deficiency hitherto published (including 5 cases with lithiasis) shows that the diagnosis is rarely made, since the conventional methods of urinary stone analysis are unable to distinguish dihydroxyadenine from uric acid. This form of lithiasis can be prevented by inhibiting xanthinoxidase with allopurinol. The remarkable efficacy of this treatment and the frequent severity of the disease should raise the possibility of 2,8-dihydroxyadenine lithiasis in very case of alleged uric acid lithiasis in young children.

Topics: Adenine; Adenine Phosphoribosyltransferase; Adolescent; Allopurinol; Child; Child, Preschool; Erythrocytes; Female; Humans; Male; Pentosyltransferases; Urinary Calculi; Xanthine Oxidase

Topics: Allopurinol; Benzbromarone; Benzothiadiazines; Diuretics; Gout; Humans; Purines; Sodium Chloride Symporter Inhibitors; Uric Acid; Urinary Calculi

Twelve male patients with urolithiasis were treated with 300 mg allopurinol daily. Urinary urate decreased from 251 +/- 55 to 156 +/- 19 (mean +/- SD) mmol per mol creatinine. The inhibition of calcium oxalate crystal growth was measured in an in vitro system and the inhibition index increased from 0.51 +/- 0.06 to 0.57 +/- 0.08 (mean +/- SD). Urinary citrate excretion was unaffected by the treatment.

Topics: Allopurinol; Calcium Oxalate; Crystallization; Humans; Male; Uric Acid; Urinary Calculi

We report on experiences with dispensary care of patients with uric acid calculi who were metaphylactically treated alkylsing the urine with blemares or the xanthine oxydase inhibitor milurite and in combination of these two. The share of recidivations in 168 metaphylactically treated patients is about 20--26% according to the kind of therapy. One of the main reasons for the high share of recidivations is the untrustworthiness of the patients in observing the metaphylactic measures.

Topics: Allopurinol; Female; Humans; Male; Outpatients; Urinary Calculi

Topics: Acetazolamide; Adult; Aged; Allopurinol; Antacids; Calcium; Diuretics; Female; Humans; Male; Middle Aged; Piperazines; Tromethamine; Uric Acid; Uricosuric Agents; Urinary Calculi; Urography

Topics: Allopurinol; Colchicine; Diabetes Complications; Gout; Humans; Hypertension; Indomethacin; Kidney Diseases; Obesity; Proteinuria; Socioeconomic Factors; Synovial Fluid; Uric Acid; Urinary Calculi

Topics: Allopurinol; Calcium Phosphates; Humans; Magnesium; Uric Acid; Urinary Calculi

Topics: Aged; Allopurinol; Bicarbonates; Female; Humans; Hydrogen-Ion Concentration; Male; Uric Acid; Urinary Calculi

In patients with urate calculi as well as in endangered persons--formation of calculi in the anamnesis, excretion of calculi or sand, urate diathesis--a regular permanent control and care is also of importance as in every other patient suffering from a chronic renal disease. It would be desirable to establish the actual frequency of urolithiasis by introducing the duty of notification. On this way a network of care units could be established within the leading regional institutions, which would further the elaboration of unitary directives for the examination and treatment of patients.

Topics: Allopurinol; Citrates; Diet Therapy; Fluid Therapy; Humans; Hydrogen-Ion Concentration; Magnesium; Pyridoxine; Solubility; Uric Acid; Urinary Calculi; Urine

APRT deficiency, a new cause of supposed "uric acid" stones in young children may be benign or life threatening. This stresses the importance of early recognition and diagnosis. The renal failure, severe in some instances, is preventable because 2,8-DHA formation, the precipitating factor in all, may be controlled by allopurinol preferably without alkali. A low purine diet is advised. "Uric acid" stones in children should always be subjected to sophisticated analysis, and regarded with suspicion in young adults. Diagnosis from red cell APRT activity will be impossible in transfused subjects.

Topics: Adenine Phosphoribosyltransferase; Allopurinol; Child; Diet Therapy; Female; Homozygote; Humans; Male; Pentosyltransferases; Purines; Solubility; Uric Acid; Urinary Calculi

Some common conservative treating methods of urolithiasis are critically discussed. Based on physico-chemical relationships of solubility and cristallisation of stone-forming compounds our own methods of conservative treatment of urolithiasis is presented.

Topics: Allopurinol; Aluminum Hydroxide; Calcium; Cystine; Humans; Ion Exchange; Magnesium; Oxalates; Phosphates; Pyridoxine; Quaternary Ammonium Compounds; Succinimides; Uric Acid; Urinary Calculi

Topics: Aged; Allopurinol; Female; Humans; Piperazines; Uric Acid; Urinary Calculi

The present paper adopts a definite attitude to the differentiated therapy of the disturbances of the uric acid metabolism. This demands an exacter subdivision of the kind of the metabolic disturbance (types Ia, Ib, IIa, IIb, and III). On the basis of this classification in types an individually adapted therapy is possible. It might form the prerequisite of a still more effective meeting of the nephrogenic complications of the gout and of the reduction of the side effects of the necessary permanent therapy.

Topics: Allopurinol; Arteriosclerosis; Citrates; Gout; Humans; Hypertension; Kidney Diseases; Obesity; Phenylbutazone; Uric Acid; Urinary Calculi

Topics: Alkalies; Citrates; Diuresis; Fluid Therapy; Gout; Humans; Hydrogen-Ion Concentration; Recurrence; Uric Acid; Urinary Calculi; Xanthine Oxidase

Topics: Allopurinol; Humans; Male; Oxalates; Urinary Calculi

Topics: Allopurinol; Gout; Humans; Hypoxanthine Phosphoribosyltransferase; Male; Urinary Calculi; Xanthines

Xanthinuria, described in 1954 by Dent and Philpot, is a rare metabolic disorder, characterised by a deficiency in xanthine-oxidase, a key enzyme in the synthesis of uric acid. It results in hypouricaemia and hypouricuria, the urinary excretion of products of purine synthesis taking place in the form of uric acid precursors: hypoxanthine and xanthine. By virtue of the very slight solubility of xanthine, this xanthinuria may cause urinary lithiasis, in general occurring early. More often, however, the disease is asymptomatic and diagnosed following the chance discovery of hypouricaemia. We report 6 recent cases.

Topics: Adolescent; Adult; Child; Female; Humans; Male; Purine-Pyrimidine Metabolism, Inborn Errors; Uric Acid; Urinary Calculi; Xanthine Oxidase; Xanthines

A variety of substances have been used to prevent recurrence of stone disease. Recently there has been considerable interest in the ability of allopurinol to prevent stone recurrence. This article discusses the effect of allopurinol on the urinary oxalate in a group of stone formers. A significant reduction was obtained especially in subjects in whom the blood urate levels exceeded 300 mumol./L. Possible mechanisms explaining the mode of action of the drug are discussed.

Topics: Adult; Aged; Allopurinol; Calcium; Female; Humans; Male; Middle Aged; Oxalates; Urinary Calculi

Allopurinol is a drug which could be valuable in the treatment of stone patients. In 29 subjects treated with 300 mg of the drug per day it has been found that there was a significant fall in urine oxalate excretion if the blood urate was above 330 mumol/l. In 10 subjects followed for 1 year the urine oxalate was significantly reduced and maintained at a lower level than the original.

Topics: Allopurinol; Female; Follow-Up Studies; Humans; Male; Oxalates; Uric Acid; Urinary Calculi

Topics: Allopurinol; Citrates; Cystine; Humans; Hydrogen-Ion Concentration; Uric Acid; Urinary Calculi; Urine

In this study of 17 renal transplant recipients with hyperuricemia the effects of allopurinol vs. benzbromarone were compared. Both drugs effectively lowered serum uric acid concentrations by 19 vs. 35% of pretreatment values. Adverse reaction to allopurinol consisted in augmenting of azathioprin toxicity for bone marrow, with occurrence of an isolated fall in the hematocrit in several patients. With benzbromarone no drug interactions were observed. However, one patient exhibited uric acid stone formation in the damaged kidney.

Topics: Allopurinol; Azathioprine; Benzbromarone; Creatinine; Drug Interactions; Female; Humans; Kidney Transplantation; Male; Transplantation, Homologous; Uric Acid; Urinary Calculi

Topics: Allopurinol; Calcium; Humans; Oxalates; Urinary Calculi

Topics: Acute Kidney Injury; Adult; Aged; Allopurinol; Child; Female; Humans; Kidney Calculi; Male; Middle Aged; Ureteral Calculi; Urinary Calculi

Since 1973 we have used allopurinol in the prevention and aftercare of recurrent urolithiasis. We give indications for the administration of allopurinol for patients with chronically recurring calcium oxalate lithiasis. Special attention is given to the urinary stone analysis as well as to metabolic disorders as for example hyperuricaemia, hyperuricuria or idiopathic hypercalciuria. In 15 patients with calcium oxalate lithiasis the stone/patient/year ratio could be decreased to 38%. In 19 patients with uric acid/calcium oxalate calculi or alternating stone formations from uric acid and calcium oxalate we succeeded in decreasing this ratio from 1.72 to 0.47 or 27%.

Topics: Allopurinol; Calcium; Humans; Oxalates; Recurrence; Urinary Calculi

Topics: Alcohol Drinking; Allopurinol; Blood Proteins; Body Weight; Coronary Disease; Diabetes Complications; Female; Gout; Humans; Hypertension; Lead Poisoning; Male; Protein Binding; Risk; Uric Acid; Urinary Calculi

We studied the clinical and biochemical manifestations of complete adenine phosphoribosyltransferase deficiency in the kindred of a male homozygous child excreting stones of 2,8-dihydroxyade-nine. Abnormal amounts of adenine, 8-hydroxyade-nine and 2,8-dihydroxyadenine (25 per cent of total purine metabolites) appeared in the urine of the propositus and his clinically normal brother, but not in heterozygotes or a control. Adenine phosphoribosyl-transferase activity in erythrocytes was less than 1 per cent of normal in both homozygotes and varied from 20 to 57 per cent of normal in six heterozygotes. Heterozygotes exhibited neither hyperuricemia nor gout. Treatment of the propositus with allopurinol and a low purine diet stopped stone formation. In addition, excretion of 2,8-dihydroxyadenine decreased. An autosomal recessive mode of inheritance with variable expression in the phenotype is indicated. Homozygotes may be detected by their raised urinary adenine levels or absence of detectable erythrocyte adenine phosphoribosyltransferase activity (or both).

Topics: Adenine; Adenine Phosphoribosyltransferase; Allopurinol; Child; Child, Preschool; Crystallization; Female; Heterozygote; Homozygote; Humans; Infant; Male; Pedigree; Pentosyltransferases; Purine-Pyrimidine Metabolism, Inborn Errors; Purines; Uric Acid; Urinary Calculi

Topics: Adult; Aged; Allopurinol; Female; Humans; Male; Middle Aged; Uric Acid; Urinary Calculi

Topics: Allopurinol; Humans; Infant; Male; Uric Acid; Urinary Calculi

Topics: Allopurinol; Humans; Uric Acid; Urinary Calculi

Topics: Allopurinol; Child; Crystallization; Humans; Male; Pyrazoles; Pyrimidines; Spectrophotometry, Infrared; Urinary Calculi; Xanthine Oxidase

Topics: Allopurinol; Citrates; Humans; Male; Middle Aged; Recurrence; Solubility; Urinary Calculi

Topics: Allopurinol; Female; Gout; Humans; Pregnancy; Uricosuric Agents; Urinary Calculi

Topics: Adolescent; Adult; Aged; Allopurinol; Female; Humans; Male; Middle Aged; Oxalates; Recurrence; Uric Acid; Urinary Calculi

Topics: Allopurinol; Aluminum; Ammonium Chloride; Ascorbic Acid; Citrates; Glycine; Humans; Magnesium; Penicillamine; Phosphates; Pyridoxine; Recurrence; Urinary Calculi

Topics: Allopurinol; Calcium; Humans; Kidney; Long-Term Care; Oxalates; Uric Acid; Urinary Calculi

Topics: Acute Kidney Injury; Allopurinol; Calcium; Humans; Uric Acid; Urinary Calculi

Topics: Adrenocorticotropic Hormone; Allopurinol; Colchicine; Diet; Extracellular Space; Gout; Humans; Indomethacin; Kidney Concentrating Ability; Pentosyltransferases; Phenylbutazone; Purines; Synovial Fluid; Uric Acid; Uricosuric Agents; Urinary Calculi

Topics: Allopurinol; Animals; Dermatitis; Dog Diseases; Dogs; Female; Uric Acid; Urinary Calculi

Topics: Adult; Child, Preschool; Female; Humans; Liver; Male; Metabolism, Inborn Errors; Middle Aged; Uric Acid; Urinary Calculi; Xanthine Oxidase; Xanthines

Topics: Allopurinol; Anemia; Anti-Bacterial Agents; Humans; Infant; Intellectual Disability; Lesch-Nyhan Syndrome; Neurologic Manifestations; Uric Acid; Urinary Calculi; Urinary Tract Infections

Topics: Adult; Allopurinol; Calcium; Gout; Humans; Male; Oxalates; Urinary Calculi

Topics: Allopurinol; Child; Diet; Humans; Male; Metabolism, Inborn Errors; Purinones; Urinary Calculi; Xanthines

Topics: Allopurinol; Animals; Blood Glucose; Body Fluids; Carbohydrates; Chromatography, Ion Exchange; Dogs; Male; Ultraviolet Rays; Urinary Calculi

Topics: Adult; Allopurinol; Humans; Magnesium; Male; Urinary Calculi

Topics: Allopurinol; Colchicine; Diabetes Complications; Diabetes Mellitus; Female; Gout; Humans; Male; Uric Acid; Urinary Calculi

Topics: Allopurinol; Diet Therapy; Humans; Male; Middle Aged; Radionuclide Imaging; Uric Acid; Urinary Calculi; Urography; Xanthine Oxidase

Topics: Alginates; Allopurinol; Calcium; Diet Therapy; Diuretics; Female; Humans; Ion Exchange Resins; Magnesium; Male; Methylene Blue; Oxalates; Phosphates; Pyridoxine; Sodium; Urinary Calculi

Topics: Adolescent; Adult; Aged; Child, Preschool; Female; Humans; Male; Middle Aged; Pedigree; Purine-Pyrimidine Metabolism, Inborn Errors; Urinary Calculi; Xanthine Oxidase; Xanthines

Topics: Administration, Oral; Allopurinol; Cystine; Humans; Magnesium; Oxalates; Penicillamine; Phosphates; Pyridoxine; Quaternary Ammonium Compounds; Urinary Calculi

Topics: Allopurinol; Citrates; Humans; Uric Acid; Urinary Calculi; Urography

Topics: Adult; Allopurinol; Humans; Male; Middle Aged; Uric Acid; Urinary Calculi; Urography

Topics: Acidosis; Adolescent; Adult; Alkalies; Allopurinol; Child; Colectomy; Colitis, Ulcerative; Dehydration; Female; Humans; Ileostomy; Male; Postoperative Complications; Uric Acid; Urinary Calculi

Topics: Adolescent; Allopurinol; Athetosis; Child; Humans; Hypoxanthines; Intellectual Disability; Lesch-Nyhan Syndrome; Male; Probenecid; Purine-Pyrimidine Metabolism, Inborn Errors; Pyelonephritis; Self Mutilation; Uric Acid; Urinary Calculi; Xanthines

Topics: Carbonates; Humans; Kidney Tubules; Oxalates; Phosphates; Uric Acid; Urinary Calculi; Xanthine Oxidase

Topics: Adolescent; Adult; Alcohol Oxidoreductases; Child; Glycolates; Glyoxylates; Humans; Kidney; Ligases; Liver; Metabolism, Inborn Errors; Nephrocalcinosis; Oxalates; Oxidoreductases; Urinary Calculi; Vitamin B 6 Deficiency; Xanthine Oxidase

Topics: Administration, Oral; Allopurinol; Animals; Dog Diseases; Dogs; Uric Acid; Urinary Calculi

Topics: Adolescent; Allopurinol; Child; Humans; Infant; Penicillamine; Radiography; Urinary Calculi

Topics: Allopurinol; Bicarbonates; Citrates; Humans; United States; Uric Acid; Urinary Calculi

Topics: Allopurinol; Child; Child, Preschool; Female; Humans; Leukemia; Male; Purines; Uric Acid; Urinary Calculi

Topics: Colitis, Ulcerative; Humans; Hydrogen-Ion Concentration; Ileostomy; Kidney Function Tests; Parenteral Nutrition; Postoperative Care; Postoperative Complications; Uric Acid; Urinary Calculi; Water-Electrolyte Balance; Xanthine Oxidase

Topics: Allantoin; Animals; Dogs; Infrared Rays; Metabolism, Inborn Errors; Purines; Spectrum Analysis; Ultraviolet Rays; Uric Acid; Urinary Calculi; X-Ray Diffraction; Xanthine Oxidase; Xanthines

Topics: Allopurinol; Female; Gout; Humans; Male; Uric Acid; Urinary Calculi

Topics: Adolescent; Adult; Aged; Child; Child, Preschool; Diet Therapy; Female; Humans; Hypoxanthines; Male; Middle Aged; Renal Tubular Transport, Inborn Errors; Sex Factors; Urinary Calculi; Xanthine Oxidase; Xanthines

Topics: Adolescent; Allopurinol; Chromatography; Depression, Chemical; Erythrocytes; Fibroblasts; Humans; Leukocytes; Male; Psychomotor Disorders; Purine-Pyrimidine Metabolism, Inborn Errors; Purines; Transferases; Uric Acid; Urinary Bladder Calculi; Urinary Calculi; Xanthines

Topics: Adolescent; Allopurinol; Humans; Urinary Calculi; Xanthines

Topics: Allopurinol; Child; Humans; Urinary Calculi; Xanthines

Topics: Allopurinol; Apatites; Calcium; Creatinine; Female; Humans; Hyperparathyroidism; Male; Sex Factors; Uric Acid; Urinary Calculi

Topics: Aged; Allopurinol; Antineoplastic Agents; Humans; Leukemia, Lymphoid; Tablets; Uric Acid; Urinary Calculi

Topics: Allopurinol; Citrus; Flavonoids; Gout; Humans; Male; Middle Aged; Piperazines; Purines; Uric Acid; Urinary Calculi

Topics: Adult; Allopurinol; Child, Preschool; Cystinuria; Female; Humans; Penicillamine; Uric Acid; Urinary Calculi

Topics: Allopurinol; Colchicine; Follow-Up Studies; Gout; Humans; Lymphoma, Non-Hodgkin; Male; Middle Aged; Uric Acid; Urinary Calculi

Topics: Adult; Aged; Allopurinol; Blood Urea Nitrogen; Colchicine; Enzyme Therapy; Female; Gout; Humans; Indomethacin; Male; Middle Aged; Phenylbutazone; Uric Acid; Urinary Calculi; Xanthine Oxidase

Topics: Adolescent; Allopurinol; Blood Urea Nitrogen; Enzyme Therapy; Humans; Male; Uric Acid; Urinary Calculi; Xanthine Oxidase

Topics: Adult; Aged; Allopurinol; Arthritis; Enzyme Therapy; Enzymes; Female; Humans; Male; Middle Aged; Uric Acid; Urinary Calculi

Topics: Humans; Infant; Male; Urinary Calculi; Xanthine Oxidase; Xanthines

Topics: Allopurinol; Bicarbonates; Enzyme Therapy; Humans; Penicillamine; Urinary Calculi; Xanthine Oxidase

Topics: Allopurinol; Enzyme Therapy; Humans; Kidney Calculi; Male; Middle Aged; Urinary Calculi; Xanthine Oxidase; Xanthines

Topics: Adult; Aged; Allopurinol; Female; Gout; Humans; Hypoxanthines; Male; Metabolic Diseases; Middle Aged; Uric Acid; Uricosuric Agents; Urinary Calculi; Xanthine Oxidase; Xanthines

Topics: Aged; Allopurinol; Female; Gout; Humans; Male; Middle Aged; Uric Acid; Urinary Calculi

Topics: Adult; Aged; Allopurinol; Female; Gout; Humans; Hyperparathyroidism; Kidney Tubules; Male; Middle Aged; Uric Acid; Uricosuric Agents; Urinary Calculi

Topics: Allopurinol; Gout; Humans; Joint Diseases; Kidney Calculi; Orotic Acid; Time Factors; Uric Acid; Urinary Calculi

Topics: Adolescent; Animals; Female; Humans; Male; Metabolism, Inborn Errors; Rats; Uric Acid; Urinary Calculi; Xanthine Oxidase; Xanthines

Topics: Adrenocorticotropic Hormone; Colchicine; Enzyme Therapy; Enzymes; Gout; Humans; Indomethacin; Probenecid; Sulfinpyrazone; Urinary Calculi; Xanthine Oxidase

Topics: Adolescent; Adult; Aged; Antineoplastic Agents; Blood; Bone Marrow Diseases; Child, Preschool; Colonic Neoplasms; Enzyme Therapy; Female; Humans; Leukemia; Lymphoma; Male; Middle Aged; Mycosis Fungoides; Polycythemia Vera; Pyrimidines; Sarcoma; Uric Acid; Urinary Calculi; Xanthine Oxidase

Allopurinol (4-hydroxypyrazolo (3,4-d)-pyrimidine) is a potent xanthine oxidase inhibitor which inhibits the oxidation of naturally occurring oxypurines, thus decreasing uric acid formation. The clinical and metabolic effects of this agent were studied in 80 subjects with primary and secondary gout and other disorders of uric acid metabolism. Allopurinol has been universally successful in lowering the serum uric acid concentration and uric acid excretion to normal levels, while not significantly affecting the clearance of urate or other aspects of renal function. Oxypurine excretion increased concomitantly with the fall in urine uric acid. The agent is particularly valuable in the management of problems of gout with azotemia, acute uric acid nephropathy and uric acid urolithiasis. The minor side effects, clinical indications and theoretical complications are discussed.

Topics: Aged; Colchicine; Diet; Enzyme Therapy; Female; Gout; Humans; Male; Middle Aged; Sulfinpyrazone; Uric Acid; Urinary Calculi; Urobilin; Xanthine Oxidase

Topics: Adolescent; Adult; Aged; Child; Child, Preschool; Enzyme Therapy; Female; Gout; Humans; Kidney Diseases; Leukemia; Lymphoma; Male; Middle Aged; Uric Acid; Urinary Calculi; Xanthine Oxidase

Topics: Adult; Aged; Blood; Enzymes; Female; Gout; Humans; Male; Probenecid; Uric Acid; Urinary Calculi; Urine; Xanthine Oxidase

Topics: Child, Preschool; Chromosome Aberrations; Chromosome Disorders; Enzyme Therapy; Hematuria; Humans; Male; Metabolism, Inborn Errors; Self Mutilation; Uric Acid; Urinary Calculi; Xanthine Oxidase

Topics: Allopurinol; Arthritis; Blood; Bone Marrow Diseases; Drug Therapy; Enzyme Inhibitors; Fluids and Secretions; Gout; Humans; Metabolism; Pharmacology; Polycythemia Vera; Pyrazoles; Pyrimidines; Toxicology; Uric Acid; Uricosuric Agents; Urinary Calculi; Urine; Xanthine Oxidase