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PubMed1997

Urinary excretion of minerals, oxalate, and uric acid in north Indian children.

Urinary excretion of calcium, magnesium, phosphate, uric acid, oxalate, and creatinine was measured in 208 children (aged 8-15 years, 124 boys, 84 girls), living in a residential school near New Delhi. Levels were reduced compared with those reported from developed countries. The 95th percentile value of 24-h creatinine excretion was 33.4 mg/kg, calcium 2.2 mg/kg, magnesium 2.9 mg/kg, phosphate 9.4 mg/kg, uric acid 4.4 mg/kg, and oxalate 1.5 mg/kg. The 95th percentile value of the urine calcium/creatinine ratio was 0.15 and oxalate/creatinine 0.06. The dietary intake of proteins, calcium, and other nutrients in these children was less than recommended and explained the reduced urinary excretion observed. Physicians need to be aware of the regional patterns of normal urinary excretion of these constituents.

Adolescent↗
PubMed1987

Urothelial injury to the rabbit bladder from alkaline irrigants useful in the treatment of uric acid stones.

Irrigation of the urinary tract with alkaline solutions may be used appropriately in some clinical situations to dissolve uric acid stones. Since in vitro studies have suggested that tham-E (pH 10.6) is somewhat more effective than tham (pH 8.6) in promoting dissolution of uric acid, these studies were undertaken to assess the relative toxicities of these two irrigating solutions to the urothelium. Rabbit bladders were irrigated antegrade via a ureterotomy for twenty hours. Tham E produced considerably more mucosal injury than did tham (p = 0.0001). The minimal advantage in rapidity of stone dissolution offered by tham E over tham is more than offset by the considerably increased potential for toxic side effects. The results suggest tham and not tham E should be used for irrigation to dissolve uric acid stones.

Animals↗
PubMed2006

Completing the uric acid degradation pathway through phylogenetic comparison of whole genomes.

Mammals that degrade uric acid are not affected by gout or urate kidney stones. It is not fully understood how they convert uric acid into the much more soluble allantoin. Until recently, it had long been thought that urate oxidase was the only enzyme responsible for this conversion. However, detailed studies of the mechanism and regiochemistry of urate oxidation have called this assumption into question, suggesting the existence of other distinct enzymatic activities. Through phylogenetic genome comparison, we identify here two genes that share with urate oxidase a common history of loss or gain events. We show that the two proteins encoded by mouse genes catalyze two consecutive steps following urate oxidation to 5-hydroxyisourate (HIU): hydrolysis of HIU to give 2-oxo-4-hydroxy-4-carboxy-5-ureidoimidazoline (OHCU) and decarboxylation of OHCU to give S-(+)-allantoin. Urate oxidation produces racemic allantoin on a time scale of hours, whereas the full enzymatic complement produces dextrorotatory allantoin on a time scale of seconds. The use of these enzymes in association with urate oxidase could improve the therapy of hyperuricemia.

Allantoin↗
PubMed1979

[Effect of uric acid lowering drugs in low dosage in patients with hyperuricemia and hypertriglyceridemia in a randomized group study].

The serum uric acid lowering effects of 100 mg Allopurinol (A), 20 mg Benzbromarone (B) and the combination of both were tested in a randomized block-trial in 12 male patients suffering from hyperuricemia and hyperlipoproteinemia type IIb/IV. Therapy periods lasted 4 weeks each. Allopurinol lowered the uric acid concentrations from 7,54 mg/100 ml to 5,95 mg/100 ml, Benzbromarone from 7,54 mg/100 ml to 6,11 mg/100 ml and the combination from 7,54 mg/100 ml to 4,90 mg/100 ml, all three significantly. The difference between the effect of the combination drug and Allopurinol and Benzbromarone respectively was also significant. An additive effect of both components is evident. Serum creatinin concentration remained constant. Uric acid and creatinin excretion could not be evaluated because of failure of patient compliance in the collecting of urine.

Adult↗
PubMed1986

Uric acid protects membranes and linolenic acid from ozone-induced oxidation.

Aqueous preparations of linolenic acid, bovine serum albumin, and bovine erythrocyte membrane fragments were bubbled with ozone in the presence or absence of uric acid. Ozonation of the membrane fragments or the bovine serum albumin did not result in protein degradation. After 15 min of ozonation, the absorbance of the thiobarbituric acid-reactive material increased by 0.34 in the linolenic acid preparation and by 0.08 in the suspension of membrane fragments. In the presence of uric acid, these changes in absorbance were reduced to 0.14 for the fatty acid and to 0.01 for the membrane fragments. This result indicates that uric acid protects lipids from ozone-induced oxidation.

Animals↗
PubMed1993

Uric acid level increases in humans engaged in gambling: a preliminary report.

The effect of gambling and gaming on plasma levels of uric acid was studied. Blood samples were obtained from normal subjects while they gambled for money or while they played checkers without betting. There was an interaction of time and activity reflecting primarily an association of increased uric acid levels during gambling over time, compared with gaming and relaxation. This indicates that gambling can increase plasma levels of uric acid.

Adult↗
PubMed1988

Inherited superactivity of phosphoribosylpyrophosphate synthetase: association of uric acid overproduction and sensorineural deafness.

PURPOSE: Superactivity of 5-phosphoribosyl 1-pyrophosphate (PP-Rib-P) synthetase, inherited as an X chromosome-linked trait, has been reported in nearly 20 families in which overproduction of uric acid is invariably present in hemizygous affected males. Clinical manifestations of PP-Rib-P synthetase superactivity are mainly limited to gout in early adulthood. Neurologic deficits, including sensorineural deafness, have rarely been described. We herein document the association of PP-Rib-P synthetase superactivity, gout with excessive uric acid synthesis, and sensorineural deafness in an additional family. PATIENTS AND METHODS: Two members of a Spanish family were studied: an eight-year-old boy (Patient 1) with tophaceous gout, purine nucleotide and uric acid overproduction, and sensorineural deafness, and his 27-year-old mother (Patient 2), who had gout. Fibroblast cultures were initiated from skin biopsy specimens, and measurements of PP-Rib-P and purine nucleotide metabolism in the fibroblasts were performed. RESULTS: A labile but superactive PP-Rib-P synthetase was demonstrated in the fibroblasts cultured from both Patients 1 and 2. The kinetic basis of PP-Rib-P synthetase superactivity in this family was resistance to purine nucleotide inhibition of enzyme activity. More severe derangements in the enzyme and in PP-Rib-P and purine synthesis in Patient 1's cells than in Patient 2's cells suggest that Patient 1 is hemizygous and Patient 2 is heterozygous for an X chromosome-linked genetic defect. Limited pedigree data support this view. Compared with affected members of seven other families with PP-Rib-P synthetase superactivity, these patients are intermediate in the range of clinical expression and in the severity of the enzyme defect as measured by the degree of aberration of PP-Rib-P and purine nucleotide synthesis in fibroblasts. Metabolic abnormalities were more severe in Patient 1's cells than in the cells of most male patients (in whom clinical expression is limited to early adult-onset gout) but were less severe than in the cells of two patients in whom more complex enzyme defects were associated with uric acid overproduction and neurodevelopmental abnormalities (including deafness) in male children and adult women. CONCLUSION: Certain defects resulting in PP-Rib-P synthetase superactivity may be causally related to neurologic impairment, most commonly sensorineural deafness.

Adult↗
PubMed1994

Evaluation of serum uric acid to creatinine ratio in fulminant hepatitis.

Of the eight patients with fulminant hepatitis placed under total parenteral nutrition with an amino acid solution rich in branched chain amino acids and treated by plasma exchange, four survived and four died from hepatic failure. Serum uric acid levels in the non-survived group were significantly lower on days 1-6 compared with the survived group. The concentration ratios of uric acid to creatinine and prothrombin time were significantly lower on days 5-8 and days 3-8, respectively, in a similar comparison. Thus, the uric acid to creatinine ratio, which corrects for the possible renal dysfunction associated with acute hepatic failure, may serve as a clinically useful prognostic indicator for patients with fulminant hepatitis.

Adolescent↗
PubMed2002

Determination of uric acid in human serum by capillary electrophoresis with polarity reversal and electrochemical detection.

Capillary zone electrophoresis (CE) under conditions of reversed polarity is used in conjunction with electrochemical detection (EC) at carbon fiber microcylinder electrodes for the selective and sensitive determination of uric acid in human blood serum. Comigration of anions with the electroosmotic flow is accomplished with reversed polarity and the buffer additive cetyltrimethylammonium bromide (CTAB) in a 2-(N-morpholino)ethanesulfonic acid (MES) buffer system, giving rise to rapid and sensitive analyses. Optimal buffer conditions (pH 7.0), detection potential (0.80 V vs. Ag/AgCl), and electrokinetic injection are employed to allow for maximal resolution and signal intensity. Amperometric end-column detection with a carbon fiber microcylinder electrode results in lower limits of detection for uric acid of about 25 nM (ca. 140 amol injected) without the need for decoupling. Linear calibration plots using uric acid standards in water and serum are obtained over a linear range from 5.00 x 10(-4) M to 2.50 x 10(-7) M. Uric acid concentrations obtained for human sera using the CE-EC approach described here are shown to compare favorably to the accepted laboratory values.

Calibration↗
PubMed2000

Hypoxanthine, uric acid and allantoin as indicators of in vivo free radical reactions. Description of a HPLC method and human brain microdialysis data.

A practical one-step high performance liquid chromatography (HPLC) method was developed for the simultaneous determination of hypoxanthine, uric acid and allantoin in small (4 microL) microdialysis samples. The rationale for this work was the current interest in hypoxanthine as a marker for energy perturbation in hypoxia/ ischemia, in uric acid as an endogenous antioxidant, and in allantoin as a marker for in vivo formation of reactive oxygen species (ROS). The method is based on ion pairing reversed phase chromatography and UV detection. The coefficient of variance for within and between run imprecision was generally below 5%, somewhat higher for concentrations close to the detection limit (0.4-1.0 pmoles). Recoveries ranged from 89 to 102% and linearity was observed in the concentration range from 0.25 to 25.0 mmol/L. There was an excellent correlation between the present method and available reference methods. The method was applied to cerebral microdialysis samples from a patient with severe subarachnoid haemorrhage complicated by secondary ischemia leading to cerebral infarction. The secondary ischemia was associated with an increase of hypoxanthine followed by increasing allantoin and uric acid levels. We submit that this pattern of chemical changes indicates increased ROS formation produced by secondary ischemia. The HPLC method appears to be a useful tool for studying changes of hypoxanthine, uric acid and allantoin levels in microdialysis samples.

Allantoin↗
PubMed1985

The association between plasma cholesterol, high-density-lipoprotein cholesterol, triglycerides and uric acid in ethanol consumers.

The relationship between the concentrations of plasma cholesterol, high-density-lipoprotein (HDL) cholesterol, triglycerides and uric acid has been studied in relation to alcohol consumption in men attending a health-screening centre. Although it has been suggested that these metabolites are associated with each other by environmental factors, including ethanol consumption, the only correlation we have found between the variables which is statistically significantly related to alcohol consumption is that between total cholesterol and uric acid. A comparison of these correlations with epidemiological data suggests that assessment of cardiovascular risk is best done by using plasma cholesterol and uric acid levels, corrected for alcohol consumption. The correlation between HDL-cholesterol and the remaining fractions of plasma cholesterol is constant over all levels of alcohol consumption, and therefore the division of cholesterol between these fractions is apparently independent of both alcohol consumption and cholesterol synthesis.

Alcohol Drinking↗
PubMed1996

[Exercise-induced acute renal failure observed in a boy with idiopathic renal hypouricemia caused by postsecretary reabsorption defect of uric acid].

Acute renal failure without oliguria developed in an 11-year boy after running exercise. With improvement of his renal function, marked hypouricemia became apparent (0.8-0.9 mg/dl). Increased excretion of uric acid into the urine, increased clearance ratio of uric acid against creatinine (CUA/CCr), normal concentration of plasma xanthine and hypoxanthine, and suppression of CUA/CCr ratio by pyrazinamide loading but not by probenecid, were observed in the patient and his two siblings, suggesting that hereditary abnormalities of reabsorption of uric acid after secretion from the renal tubules resulted in the hypouricemia. The mechanism of acute renal failure in this disease remains unknown.

Absorption↗
PubMedDate not supplied

Renal handling of uric acid in patients with type 1 diabetes in relation to glycemic control.

BACKGROUND: The aim of the study was to compare the renal handling of uric acid (UA) in 16 patients with type 1 diabetes without renal failure (age 34.8 +/- 13.3 years) and in 15 healthy subjects (age 34.9 +/- 12.6 years). METHODS: Creatinine clearance (Cr-Cl), clearance of uric acid (UA-Cl), fractional excretion of uric acid (UA-FE), and 24-h urinary UA excretion (UA-U) were determined. Glycemic control was assessed using fasting glucose, glycated hemoglobin and fructosamine tests. RESULTS: Patients with diabetes had significantly (p < 0.0001) lower serum UA concentrations compared to control group (2.8 +/- 0.7 vs. 5.7 +/- 0.8 mg/dl), and higher urinary UA excretion (813 +/- 107 vs. 423 +/- 40 mg/day), UA clearance (21.9 +/- 7.1 vs. 5.2 +/- 0.9 mL/min) and fractional UA excretion (17.1 +/- 5.5 vs. 4.8 +/- 1.3%), with higher creatinine clearance (129 +/- 16 vs. 111 +/- 12 mL/min, p < 0.005). In patients with diabetes there was a strong negative correlation between serum UA concentration and UA 24-h excretion (R = -0.79; p < 0.001). Fractional UA excretion correlated with fasting glycemia and HbA1c (R = +0.51 and +0.53; p < 0.05). CONCLUSIONS: In type 1 diabetes there is significant UA renal clearance increase, which is higher with poor glycemic control. It leads to hypouricemia despite an approximately twofold UA excretion increase and therefore despite increased UA synthesis.

Adult↗
PubMed1985

Renal uric acid handling is not affected by beta-adrenoceptor blockade in normotensive subjects.

Nine normotensive healthy females received timolol 5 mg daily for a 4-day period and subsequently 20 mg daily for another 4-day period. None of the two dosages of timolol caused significant changes in serum uric acid or 24-h urinary fractional excretion of uric acid. Thus the increments of serum uric acid previously found in hypertensive patients is not likely to be caused by beta-adrenoceptor blockade per se.

Adrenergic beta-Antagonists↗
PubMed2005

Effect of ethanol on metabolism of purine bases (hypoxanthine, xanthine, and uric acid).

There are many factors that contribute to hyperuricemia, including obesity, insulin resistance, alcohol consumption, diuretic use, hypertension, renal insufficiency, genetic makeup, etc. Of these, alcohol (ethanol) is the most important. Ethanol enhances adenine nucleotide degradation and increases lactic acid level in blood, leading to hyperuricemia. In beer, purines also contribute to an increase in plasma uric acid. Although rare, dehydration and ketoacidosis (due to ethanol ingestion) are associated with the ethanol-induced increase in serum uric acid levels. Ethanol also increases the plasma concentrations and urinary excretion of hypoxanthine and xanthine via the acceleration of adenine nucleotide degradation and a possible weak inhibition of xanthine dehydrogenase activity. Since many factors such as the ALDH2*1 gene and ADH2*2 gene, daily drinking habits, exercise, and dehydration enhance the increase in plasma concentration of uric acid induced by ethanol, it is important to pay attention to these factors, as well as ingested ethanol volume, type of alcoholic beverage, and the administration of anti-hyperuricemic agents, to prevent and treat ethanol-induced hyperuricemia.

Acetyl Coenzyme A↗
PubMed1996

Cerebral uric acid increases following experimental traumatic brain injury in rat.

Following traumatic brain injury (TBI), cortical and thalamic areas were analyzed histologically and by high-performance liquid chromatography with electrochemical detection for uric acid at various survival times. Following TBI, cortical uric acid was elevated by ten-fold at 24 and 48 h, but not at 1 h post-TBI. Histological evidence of neurodegeneration was found not only in cortex but also in the anteroventral thalamus. These data suggest that as in stroke, uric acid measurements may be a convenient and sensitive method for measuring peroxidative status in TBI.

Animals↗
PubMed1996

Serum uric acid, insulin secretion and resistance in nonhyperuricemic and hyperuricemic obese female subjects.

In order to study the relationships between obesity, serum uric acid, insulin secretion and insulin resistance in female subjects, we evaluated serum C-peptide and glucose-induced insulin utilization (euglycemic hyperinsulinemic clamp) in 16 obese (8 nonhyperuricemic and 8 hyperuricemic) and 10 nonobese control subjects. Baseline C-peptide levels were significantly higher in hyperuricemic compared to both nonhyperuricemic obese subjects and controls (P < 0.001). M values, a measure of glucose disposal and insulin sensitivity, were significantly lower in hyperuricemic obese compared to nonhyperuricemic obese subjects and controls (P < 0.001) and, for all subjects were inversely correlated with the serum uric acid values (r = -0.821, P < 0.001). In conclusion, in this group of subjects the serum uric acid values were directly related to insulin resistance independently of age, sex, excess body weight, fat distribution and blood pressure.

Adult↗
PubMed1999

Uric acid as a cardiovascular risk factor in arterial hypertension.

BACKGROUND: Increased serum urate concentrations is a frequent finding in patients with hypertension. Since hyperuricaemia is associated with obesity, renal disease, hyperlipidaemia, and atherosclerosis the question as to whether serum urate is a cardiovascular risk factor per se has remained elusive. In considering the relationship between uric acid and hypertension three aspects should be answered: (a) the significance of hyperuricaemia; (b) the pathophysiological mechanism of the association; and (c) whether hyperuricaemia is deleterious. SIGNIFICANCE OF HYPERURICAEMIA: Several arguments favour the concept that increased serum urate in hypertensive patients most likely reflects renal vascular involvement. PATHOPHYSIOLOGICAL MECHANISM: Hyperuricaemia is accompanied by a relatively diminished uric acid excretion rate in hypertensive patients. Selective insulin resistance and hyperinsulinism estimulates the tubular sodium-hydrogen exchanger and facilitates the active reabsorption of urate. IS HYPERURICAEMIA DELETERIOUS?: In addition to the renal (urolithiasis) and articular disturbances that hyperuricaemia may cause, vascular damage due to arterial hypertension may limit the availability of oxygen for ATP synthesis. Tissue hypoxia determines increased adenine nucleotide degradation which ends in uric acid overproduction. The formation of uric acid is accompanied by an enhanced synthesis of reactive oxygen species which play a significant role in tissue damage. The hypothesis that hyperuricaemia indicates hypertensive vascular damage is plausible and if unequivocally demonstrated may contribute to delineate evidence-based therapeutic strategies for hypertensive-hyperuricaemic patients.

Humans↗