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PubMed1999

[Association of blood uric acid with other cardiovascular risk factors in the male working population in Valencia].

BACKGROUND: Serum uric acid has been reported to be a risk factor for cardiovascular disease (CVD). The objective of the present work was to determine the prevalence of hyperuricemia in a large size sample of a healthy male population, as well as the association between uric acid and other cardiovascular risk factors. PATIENTS AND METHODS: A cross-sectional study was conducted in a randomly selected sample of 1,564 healthy men in Valencia (Spain), aged 20-67 years, working in the automobile industry. Serum values of uric acid, cholesterol, and glucose were obtained, as well as blood pressure and body mass index measurements. An assessment was made of socio-economic data, drug therapy, and smoking. RESULTS: The overall prevalence of hyperuricemia was 5.10%; it increased with age. A marked increase (p < 0.01) of hyperuricemic individuals was observed with increased prevalence of other cardiovascular risk factors (from 1.8% with hyperuricemia alone up to 28% among individuals with four simultaneous risk factors). By means of a multivariate logistic regression analysis, the OR of hyperuricemia associated with each factor were calculated: increased serum glucose was the variable with a stronger association (OR: 2.69; 95%CI: 1.21-5.99), obesity ranking next (OR: 2.50; 95%CI: 1.42-4.49). Statistically significant associations were also observed for increased serum cholesterol, increased blood pressure, and smoking. CONCLUSIONS: The prevalence of hyperuricemia varies with the simultaneous presence of other classical cardiovascular risk factors. Even in this healthy mediterranean population, uric acid is significantly associated with several components in the plurimetabolic syndrome.

Adult↗
PubMedDate not supplied

[Pseudouridine and uric acid excretion in patients with viral hepatitis].

Daily excretion of pseudouridine and uric acid with urine was studied in healthy persons and in patients with viral hepatitis during various periods of the disease. Excretion of pseudouridine was increased 2.5-fold and of uric acid--2-fold within the acute period of the disease. The degree of impairment in nucleic acids metabolism could be estimated by measuring of excretion of pseudouridine and uric acid and by calculation of their ratio during various periods of the disease.

Hepatitis A↗
PubMed1978

New enzymatic method for serum uric acid at 500 nm.

We describe a manual method, well suited to mechanization, for quantitating serum uric acid at 500 nm. In the assay mixture (0.10 ml of sample and 3.00 ml of reagent) the hydrogen peroxide produced from uric acid by uricase is coupled with p-hydroxybenzoate and 4-aminoantipyrine in the presence of peroxidase to form a colored complex, which is measured. A separate sample blank is obviated by taking an initial absorbance measurement 20 s after the sample is added. The reaction is complete within 5 min; its sensitivity is 0.001 deltaA/mg per liter. Absorbances are linearly related to uric acid concentrations up to 120 mg/liter. Many substances that may be present in normal serum do not interfere, but bilirubin in moderately above-normal concentrations will interfere. The procedure can be modified to largely correct for this, when necessary. The proposed method (y) correlated well (r = 0.979) with the uric acid 293 nm reference method (x) and the relation is described by the equation y = 0.998x + 2.42.

Humans↗
PubMed1965

INBORN ENZYMATIC DEFECT AS THE PROBABLE CAUSE OF THE FORMATION OF RENAL STONES CONSISTING OF URIC ACID.

In four persons of one family the existence of an enzymatic defect, presumably consisting of a deficiency of glutaminase in the cells of the renal tubules, is postulated, and is implied by a reduced elimination of ammonia in the urine, by a relatively low urinary pH, and by its increased titratable acidity. The most characteristic clinical symptom is irritation of the distal part of the urinary tract, connected with numerous crystals of uric acid appearing in the urinary sediment. The elimination of uric acid is normal, or even reduced, and the level of uric acid in the blood serum is also within normal limits. After the administration of glutaminic acid elimination of ammonia is further decreased and the quantity of uric acid crystals is increased. Loading with glutaminic acid may also cause an attack of renal pain in the individual suffering from this defect but the administration of ammonium chloride does not cause any increase in ammonia production. It seems probable that the enzymatic defect is connected with the presence of antigen B in the erythrocytes and that it is inherited as a dominant autosomal feature. A suitable diet to make the urine alkaline allows kidneys to function efficiently in individuals suffering from this defect.

Erythrocytes↗
PubMed1989

[Changes in xanthine and uric acid in rat brain after middle cerebral artery occlusion].

Xanthine and uric acid, products of purine metabolism, were measured by reversed-phase high-performance liquid chromatography (HPLC) with electrochemical detection in rat forebrain following focal cerebral ischemia. Focal cerebral ischemia was induced in the rat by permanent occlusion of the left middle cerebral artery (MCA). Sprague-Dawley rats were anesthetized with halothane inhalation and left MCA was occluded via trans-retro-orbital approach. Normal and sham-operated rats were used as control animals. The animals were decapitated 2 (MCA = 5, Sham = 5), 4 (MCA = 7, Sham = 6), 8 (MCA = 5, Sham = 5), and 16 (MCA = 6, Sham = 6) hours or 1 (MCA = 5, Sham = 5), 2 (MCA = 6, Sham = 6), 7 (MCA = 7, Sham = 6), 14 (MCA = 6, Sham = 5), and 28 (MCA = 7, Sham = 5) days after the operation. The brains were removed and divided into right and left hemisphere. Each hemisphere was homogenized and centrifuged. The supernates were filtered with membrane filter. An aliquot of the filtrate was used for measurement of xanthine and uric acid in both of the ischemic and contralateral hemisphere by a HPLC system. In the normal group, xanthine and uric acid in the brain was 12.4 +/- 0.4 and 2.2 +/- 0.1 nmol/g tissue (mean +/- SEM), respectively. In the ischemic hemisphere, xanthine increased up to 57.7 +/- 5.2 nmol/g tissue 2 hours after MCA occlusion and reached a maximum value of 59.42 +/- 4.91 nmol/g tissue 4 hours following the induction of ischemia. Xanthine level was still high 8 hours after ischemia and then rapidly decreased to the normal value at day 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Epitaxial relationships between uric acid crystals and mineral surfaces: a factor in urinary stone formation.

Uric acid (C5H4N4O3) is one of the final products of purine metabolism. Its concentration balance is maintained in the kidneys, but compromised kidney function can result in its crystallization either in the renal tract or in the interstitial fluid of joints. In physiological deposits, crystalline uric acid is most frequently found either in a protonated state (anhydrous or dihydrate phases) or as a deprotonated urate ion (sodium or ammonium salts). Often these precipitates are found in association with a number of mineral phases (e.g., calcium oxalates, calcium phosphates, and magnesium phosphates). Their frequent and common coexistence suggests that synergistic relationships between these crystalline phases may exist. A comprehensive list of different heterogeneous uric acid/uric acid and uric acid/mineral interfaces that are epitaxially matched was generated with the lattice-matching program EpiCalc. Two hundred twenty-five coincident epitaxial matches and four commensurate epitaxial matches were identified using this screening procedure.

Crystallization↗
PubMed2003

The significance of serum uric acid, creatinine and urinary microprotein levels in predicting pre-eclampsia.

The object of this study was to determine whether serum uric acid, serum creatinine and urinary microprotein levels could be used to identify women who might subsequently develop pre-eclampsia during pregnancy. This is a cross-sectional descriptive study performed on women attending the University antenatal clinic in Colombo South Teaching Hospital, Sri Lanka. Serum uric acid, creatinine and microproteinuria levels were determined in 256 women attending the antenatal clinic at 28 weeks of pregnancy. Subsequently they were followed-up at 2-weekly intervals until 36 weeks and weekly thereafter until delivery. At each visit blood pressure was recorded and serum uric acid, creatinine and microprotein levels were determined. Fifty-nine women developed blood pressures of 140/90 mmHg or more during the study period. Serum uric acid and serum creatinine levels did not show any significant difference before the elevated blood pressures were recorded. Microprotenuria levels of more than 375 mg/l were recorded in 43 women before elevation of their blood pressure. Sixty-five women of 197 who remained normotensive had microproteinuria levels of more than 375 mg/l. The sensitivity and specificity of microproteinuria levels of more than 375 mg/l as a screening test for prediction of pre-eclampsia was 73% and 67%, respectively. Therefore, microproteinuria of more than 375 mg/l may be used as a cut-off value and as a screening test for the early detection of women at risk of developing pre-eclampsia. Serum uric acid and creatinine had no predictive value as a screening test for pre-eclampsia.

Biomarkers↗
PubMed1993

Uric acid metabolism and tubular sodium handling. Results from a population-based study.

OBJECTIVE: To define the relationship, if any, between uric acid metabolism (serum and urinary levels) and proximal tubular sodium handling in a sample of general male population. DESIGN: Cross-sectional survey of a sample of the male working population conducted as part of a nationwide survey of the prevalence of cardiovascular risk factors. SETTING: The Olivetti factory in Pozzuoli, a suburb of Naples, Italy. PARTICIPANTS: Five hundred sixty-eight untreated male workers aged 21 to 68 years (90.8% of those eligible). MEASUREMENTS: Anthropometry, blood pressure, blood tests, a detailed questionnaire, and urinary measurements on a fasting timed collection after a 300-mg lithium carbonate capsule was taken the night before the investigation. RESULTS: Serum uric acid level was inversely and significantly associated with the fractional excretion of lithium (r = -.22, P < .001), ie, the higher the serum uric acid level, the greater the amount of sodium reabsorbed at nephron sites proximal to the distal tubule. The association was graded and independent of possible confounders such as age, body mass, smoking, wine consumption, blood pressure, fractional excretion of sodium, and serum creatinine (R2 = .34, P < .001). CONCLUSIONS: High serum uric acid levels are independently associated with increased proximal tubular sodium reabsorption in men. This relationship suggests an altered tubular sodium handling and uric acid metabolism consistent with hyperinsulinemia, insulin resistance being the possible pathophysiological link.

Adult↗
PubMed1990

Uric acid crystal binding to renal inner medullary collecting duct cells in primary culture.

Attachment of microcrystals to cellular membranes may be an important component in the pathophysiology of urolithiasis. This study characterizes the concentration-dependent binding of uric acid crystals to rat renal inner medullary collecting duct cells in primary culture. Collecting duct cell cultures grew as monolayers with interspersed aggregates of rounded cells. Cultures were incubated with 14C-uric acid crystals, and the crystals that bound were quantitated by adherent radioactivity. Uric acid crystal adherence demonstrated concentration dependent saturation with a 1/alpha value (maximum micrograms of crystals adhering to 1 cm2 of binding area) of 645 micrograms/cm2. The beta values (fraction of cross-sectional area which bound crystals) of uric acid (mean = 0.15) and calcium oxalate monohydrate (mean = 0.13) crystals did not differ significantly. Uric acid crystal binding was inhibited by pre-bound calcium oxalate monohydrate crystals in a concentration dependent manner. These data suggest that uric acid and calcium oxalate crystals exhibit similar binding patterns to rat renal inner medullary collecting duct cells in primary culture.

Animals↗
PubMed1997

Uric acid changes in serum during different forms of hepatic vascular inflow occlusion.

The present study was conducted to develop an efficient marker which can evaluate the influence of the occlusion of hepatic vascular inflow, which technique is commonly used in major liver surgery or in liver transplantation. Serum samples from the rats induced by hepatic vascular inflow occlusion were analyzed with high performance liquid chromatography with the electrochemical detection, and a substance which changed in accordance with the duration of the occlusion was obtained. Both the retention time and the ultraviolet absorption spectra of the substance completely agreed with those of an authentic uric acid and the substance was ultimately determined to be uric acid. To evaluate the changes in serum uric acid during different forms of hepatic vascular inflow occlusion we devised the four types of experimental model, viz. the occlusion of hepatic artery, portal vein, both hepatic artery and portal vein and both hepatic artery and portal vein of left hepatic lobes. From the device of experiments our results indicated that in the early stage of hepatic vascular inflow occlusion the high values of serum uric acid did not reflect the damage of hepatic circulation but rather responded to the intestinal congestion. Our results also indicated that even after the declamping of hepatic vascular inflow if high values of serum uric acid are prolonged it means the deterioration of the portocaval circulation including both intestinal and hepatic circulation. So that the evaluation of the severity of injured liver due to hepatic vascular inflow occlusion should be done with the caution especially in vivo study when uric acid values are used as a marker.

Animals↗
PubMed1988

Family resemblance for serum uric acid in a Jerusalem sample of families.

Familial aggregation of serum uric acid was studied in a sample of families examined in the Jerusalem Lipid Research Clinic. We first examined homogeneity of familial correlations across the major origin groups in the Israeli population sample. In general correlations were homogeneous across origin groups, except for spouse pairs. Pooled correlations among biological relatives across the origin groups were all statistically significant. Spouse correlation upon adjustment for concomitant variables was moderately positive (r = 0.115), yet significantly different from zero. Genetic and cultural determinants of uric acid were estimated utilizing a path model with 10 parameters to be estimated from a total of 16 correlations. Under a reduced model, genetic heritability (h2) was estimated to be 0.47 +/- 0.05 and cultural heritability (c2) was 0.11 +/- 0.03. However, our data gave suggestive evidence that cultural heritability was higher in parents (c2 = 0.28) than in children (c2 = 0.10). Commingling analysis and segregation analysis were also performed, and our findings imply that in the Israeli population there is no evidence for a major gene for high uric acid levels segregating in families.

Adult↗
PubMed2006

Relationship between serum uric acid, creatinine, albumin and gestational diabetes mellitus.

BACKGROUND: During normal pregnancy, plasma concentrations of creatinine and uric acid normally decrease as a consequence of their increased glomerular filtration. Hyperuricemia in pregnant women has been associated with several pregnancy complications. We researched the relationship between serum uric acid, creatinine and albumin levels in pregnant women with normal glucose tolerance and gestational diabetes mellitus. METHODS: A total of 112 patients were evaluated, 56 of whom had gestational diabetes. All of the patients had single estimations of serum uric acid, creatinine, albumin and liver enzymes carried out on booking between the 24th and 28th gestational weeks. The women were followed up throughout pregnancy. RESULTS: Significant differences were found between the two groups for maternal age, gravida, parity and maternal weight gain during pregnancy, but not for body mass index or blood pressure. Creatinine levels were significantly higher in the diabetic group than in the control group [0.6+/-0.15 vs. 0.43+/-0.1 mg/dL (53.04+/-13.26 micromol/L vs. 38.01+/-8.84 micromol/L), p<0.001]. Uric acid levels were also higher in the diabetic patients, but this elevation was not statistically significant [4.42+/-1.09 vs. 4.1+/-0.84 mg/dL (260.78+/-64.31 micromol/L vs. 241.49+/-49.56 micromol/L), p>0.05]. There were no differences in mean albumin concentrations or liver function tests. CONCLUSIONS: In this prospective study of Turkish women, we found that patients with gestational diabetes had significantly higher levels of creatinine than normal pregnant women.

Adult↗
PubMed1988

Mechanism of hypouricemia in Hodgkin's disease. Isolated defect in postsecretory reabsorption of uric acid.

We present a patient with hypouricemia associated with Hodgkin's disease. Serum uric acid level ranged from 1.4 to 2.2 mg/dl and fractional excretion of uric acid was 26.5%. No other renal tubular abnormalities were found. The pyrazinamide suppression test came off normal. However, during the benzbromarone test, the uricosuric response was reduced. The abnormal renal handling of urate became normal following therapy of Hodgkin's disease. The findings suggest that hypouricemia in Hodgkin's disease is caused by an impairment of postsecretory tubular reabsorption of uric acid.

Female↗
PubMed1980

[Study of the binding between uric acid and plasma proteins (author's transl)].

The Authors have analyzed the complex problems of the possible binding between uric acid and plasma proteins using two methods consisting of serum ultrafiltration at 22 degrees C or electrophoresis on different supports with successive specific coloration of the free and bound uric acid. The percentage of free and bound uric acid was established in serum from normal subjects, patients with primary gout, patients with renal insufficiency treated by dialysis and subjects with type IV dyslipidemia. The Authors discuss the results obtained as regards the possible role played by urate-plasma proteins binding in the interpretation of a genetic defect present in gouty patients involving a diminished uric acid binding capacity of plasma proteins.

Blood Proteins↗
PubMed1994

L-dopa induced increases in brain uric acid in an animal model of Parkinson's disease: a relationship to behavioral activation.

Rats with severe unilateral dopamine denervation (> or = 95% dopamine deficit), produced by intracerebral injection of 6-hydroxydopamine (6-OHDA) into the ventral tegmentum nigrostriatal dopamine neurons, were administered 25 mg/kg L-dopa (3,4-dihydroxyphenylalanine) methyl ester/2 mg/kg carbidopa. The neurochemical effects of the L-dopa treatment on uric acid in the cortex and striatum of the intact and 6-OHDA hemisphere were measured. In comparison to saline animals, uric acid concentrations in brain were increased in the L-dopa treated animals. There were no interhemispheric differences in the uric acid concentrations either in the L-dopa or in the saline treated animals. Interhemispheric differences were, however, observed in terms of the correlations obtained between L-dopa and uric acid concentrations in the intact vs. the 6-OHDA hemisphere. Statistically significant correlation coefficients were found in the striatal and cortex samples obtained from the 6-OHDA hemisphere. Furthermore, high correlation coefficients were observed between contralateral rotation frequencies and uric acid concentrations in the cortex and striatum of the 6-OHDA hemisphere. In contrast, only low and statistically non significant correlations were observed in the tissue samples obtained from the intact hemisphere. These observations suggest that L-dopa activation of the dopamine supersensitive receptors of the DA denervated hemisphere and the associated metabolism of purines with high energy phosphate bonds (e.g. ATP and GTP) increases uric acid as an end-product of purine metabolism. These findings are consistent with other findings indicating that uric acid in the brain can provide an index of metabolic activation in brain tissue.

Animals↗
PubMed2007

The role of uric acid in pediatric hypertension.

Over the past few years, increasing evidence has supported the possible role of uric acid as a mediator of high blood pressure. Both animal model data and tissue culture experiments suggest that uric acid might cause increased blood pressure through a 2-phase process. The first phase is dominated by a uric acid-mediated vasoconstriction followed by induction of renal afferent arteriolosclerosis and altered pressure natriuresis, leading to sodium-dependent hypertension. We have assessed children with newly diagnosed essential hypertension through cross-sectional studies and clinical trials. Elevated uric acid is closely associated with new-onset essential hypertension in children, and preliminary data suggest that lowering of uric acid can lower blood pressure in some patients. Future studies will be needed to determine whether the mechanisms shown in animal models can be extrapolated to children.

Adolescent↗
PubMed1991

Use of the o-phenylenediamine fluorescence system in the enzymatic assay of serum uric acid.

A manual enzymatic method is described for sensitive fluorometric determination of uric acid in human serum. This method is based on an enzymatic reaction with uricase to form hydrogen peroxide from uric acid and the following oxidation of o-phenylenediamine with peroxidase and hydrogen peroxide for the production of a fluorescence compound. The specificity and the selectivity in the method are due to the uricase reaction and the fluorometry, respectively. The formed fluorescence in the reaction mixture is measured at 410 nm (an excitation) and 550 nm (an emission). This enzymatic method can determine uric acid at 30-1000 microM, with a between-assay relative standard deviation of 4.35% or less. A good correlation is obtained between the present method and the colorimetric kit method.

Ascorbate Oxidase↗