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PubMed1979

Improved automated kinetic determination of uric acid in serum by use of uricase/catalase/aldehyde dehydrogenase.

The enzymatic determination of serum uric acid by use of uricase, catalase, and aldehyde dehydrogenase according to Haeckel [J. Clin. Chem. Clin Biochem. 14, 101 (1976)] showed interferences from ethanol-converting enzymes, which are present in some patients' sera. We have identified these enzymes as alcohol dehydrogenase isoenzymes. Among other substances, a mixture of pyrazole and oxalate can be used to eliminate these interferences. This inhibitor system gives good results when used in the automated kinetic uric acid determination, as is shown by a comparison with the manual assay for uric acid according to Kageyama [Clin. Chim. Acta 31, 421 (1971)].

Aldehyde Oxidoreductases↗
PubMed1997

Effect of diltiazem on plasma concentrations of oxypurines and uric acid.

To determine the clinical effect of diltiazem on the metabolism of adenosine, and its importance in ischemic heart disease, arterial plasma concentrations of the purine metabolites were determined in 21 healthy volunteers (10 female and 11 male) and 19 patients with effort angina (8 female and 11 male) before, during, and immediately after standard treadmill exercise tests conducted before and after they had taken 60 mg diltiazem (Cardizem; Hoechst Marion Roussel, Laval, QC, Canada) four times a day for 1 week. The results showed that the cardiac patients had significantly lower mean plasma concentrations of uric acid (46.82 +/- 25.51 versus 95.47 +/- 35.41 micrograms/ml, p 0.05), inosine (0.25 +/- 0.19 versus 0.84 +/- 0.17 microgram/ml, p < 0.05), and hypoxanthine (0.28 +/- 0.35 versus 0.50 +/- 0.27 microgram/ml, p < 0.05). Diltiazem decreased the mean resting plasma concentrations of uric acid in patients (uric acid 43.47 +/- 22.26 versus 46.82 +/- 25.51 micrograms/ml, p < 0.05) and healthy volunteers (uric acid 85.68 +/- 26.71 versus 95.47 +/- 35.41 micrograms/ml, p < 0.05). There was no statistically significant change in the plasma concentrations of the purine metabolites during exercise (p < 0.05). Female subjects had significantly lower plasma concentrations of uric acid than males (patients, 34.87 +/- 26.93 versus 55.78 +/- 21.25 micrograms/ml; healthy volunteers, 84.79 +/- 32.07 versus 104.22 +/- 37.05 micrograms/ml; p < 0.05 for both). Results of the study suggest that normal therapeutic doses of diltiazem may modulate the metabolism of adenosine and that some of the purine metabolites may be useful markers for specific types of ischemic heart disease.

Adenosine↗
PubMed2001

Identification of a new candidate locus for uric acid nephrolithiasis.

Renal stone formation is a common multifactorial disorder, of unknown etiology, with an established genetic contribution. Lifetime risk for nephrolithiasis is approximately 10% in Western populations, and uric acid stones account for 5%-10% of all stones, depending on climatic, dietary, and ethnic differences. We studied a small, isolated founder population in Sardinia, characterized by an increased prevalence of uric acid stones, and performed a genomewide search in a deep-rooted pedigree comprising many members who formed uric acid renal stones. The pedigree was created by tracing common ancestors of affected individuals through a genealogical database based on archival records kept by the parish church since 1640. This genealogical information was used as the basis for the study strategy, involving screening for alleles shared among affected individuals, originating from common ancestors, and utilization of large pedigrees to obtain greater power for linkage detection. We performed multistep linkage and allele-sharing analyses. In the initial stage, 382 markers were typed in 14 closely related affected subjects; interesting regions were subsequently investigated in the whole sample. We identified two chromosomal regions that may harbor loci with susceptibility genes for uric acid stones. The strongest evidence was observed on 10q21-q22, where a LOD score of 3.07 was obtained for D10S1652 under an affected-only dominant model, and a LOD score of 3.90 was obtained using a dominant pseudomarker assignment. The localization was supported also by multipoint allele-sharing statistics and by haplotype analysis of familial cases and of unrelated affected subjects collected from the isolate. In the second region on 20q13.1-13.3, multipoint nonparametric scores yielded suggestive evidence in a approximately 20-cM region, and further analysis is needed to confirm and fine-map this putative locus. Replication studies are required to investigate the involvement of these regions in the genetic contribution to uric acid stone formation.

Alleles↗
PubMed1988

Definitive characterization of uric acid as an interferent in peroxidase indicator reactions and a proposed mechanism of action.

We have characterized and identified uric acid as an interferent to peroxidase catalyzed reactions where hydrogen peroxide is generated at relatively low concentrations. The implications of these findings are important for those utilizing peroxidase as an indicator reaction where low primary substrate concentrations require their preliminary extraction or chemical modification. We have shown that the elimination of uric acid as an interferent from biologic fluid obviates the necessity for such treatment. In amniotic fluid, our data suggests that uric acid represents the only interference to peroxidase-catalyzed reactions, especially when using p-substituted phenols as proton donors. The removal of uric acid has been shown to eliminate hydrogen peroxide reduction and should allow for an increase in sensitivity and specificity for measurements incorporating a peroxidase-coupled indicator reaction, hence, more effective use of these reaction sequences. To our knowledge, this is the first report of a mechanism to eliminate hydrogen peroxide reduction in amniotic fluid.

Amniotic Fluid↗
PubMed1980

Oral purine loading for evaluation of uric acid excretion in patients with urinary calculi.

We present a model for oral uric acid loading which may be used to study the relapsing tendency of stone-formers. The oral administration of 2 g of guanosine was associated with two different response patterns of urinary uric acid excretion in patients with urolithiasis. The two groups also had considerably different relapse rates. The relapsing tendency in the group with the comparatively decreased reaction of urate excretion was less pronounced than in the group with enhanced uric acid excretion after oral purine loading.

Administration, Oral↗
PubMed1983

A simple spectrophotometric method for the direct determination of uric acid in avian excreta.

A procedure was developed for the direct quantitation of uric acid in poultry excreta. It involved the determination of the absorbance of a perchloric acid extract of excreta at 285 nm. Interference from other ultraviolet absorbing material was shown to be negligible. The correlation (r) between this procedure and a recently developed high-performance liquid chromatographic procedure for uric acid content of excreta from birds fed different diets was .993 (P less than .01). It was concluded that this procedure provides a simple and reliable method for the quantitation of uric acid in avian excreta.

Animals↗
PubMed1977

[Extracorporeal uric clearance for the demonstration of in vivo bound uric acid].

Although numerous in vitro experiments demonstrated a variable degree of urate bound to human serum albumin and other macromolecules of human plasma, only few data are available on in vivo bound urate. Extracorporal clearances of uric acid, urea nitrogen, creatinine and phosphorus were performed at the beginning, the midtime and the end of 10 hours of hemodialysis. A continuous decrease of uric acid clearance was observed in ratio with the capacity of the artificial kidney used. In contrast to uric acid the clearances of urea nitrogen, creatinine and phosphorus remained constant during the time of dialysis. From the fall of uric acid clearance, the authors conclude a partial binding of uric acid in human plasma.

Adult↗
PubMed1987

A new diuretic that does not reduce renal handling of uric acid in rats, S-8666.

The uric acid-retaining effects of diuretics were studied using sodium-restricted spontaneously hypertensive rats. Test agents were administered orally once a day for two weeks. Diuretic thiazides such as trichlormethiazide and hydrochlorothiazide and loop diuretics such as furosemide and indacrinone clearly reduced the renal function for uric acid excretion in treatment which produced major effects such as diuresis, saluresis and hypotension. However, a new diuretic with uricosuric activity, S-8666, developed in our laboratories, had no effect on the renal handling of uric acid at doses which showed major effects similar to those of other diuretics. The results should aid the understanding of the utility of S-8666 as a new diuretic antihypertensive which does not cause hyperuricemia during therapy.

Animals↗
PubMed1975

Field dependence, blood uric acid and cholesterol.

A preliminary report of the correlation of field dependence, blood uric acid, and cholesterol is presented here for 65 recently admitted patients to the psychiatric services of the University of Minnesota. The values for all three variables were taken once within 24 to 48 hr. after admission and prior to drug treatment whenever possible. Results are suggestive that the initial hypothesis; high blood uric acid, low-cholesterol individuals are more field-independent and high-cholesterol, low blood-uric acid individuals are more field-dependent holds, although this difference is mostly influenced by the values of cholesterol. Probably because of the small number of subjects tested no relationship could be observed with blood types used as genetic markers. Further controlled studies are suggested and are currently being carried out.

Adolescent↗
PubMed1987

L-dihydroxyphenylalanine-induced asymmetric changes in striatal uric acid peak: determination by in vivo electrochemical detection in rats with unilateral nigrostriatal lesions.

Rats were unilaterally lesioned with 6-hydroxydopamine to destroy the nigrostriatal pathway. Following injection with 25 mg/kg L-dopa, circling behavior away from the lesioned side was monitored. Concurrently, in vivo electrochemical detection was used to compare changes in striatal extracellular levels of ascorbic acid (Peak 1) and uric acid (Peak 2) on the lesioned and unlesioned sides. Peak 1 changes did not differ, but Peak 2 changed asymmetrically on the two sides. The difference in the changes in Peak 2 was highly correlated with the circling behavior, with the greater increase on the lesioned side.

Animals↗
PubMed1987

Determination of uric acid by an anion-exchange column chromatography.

A column chromatography using a conventional anion-exchange resin for the separation of uric acid from other purine metabolites is described. It uses a HCl gradient, and the amount of uric acid is quantified directly by monitoring the absorbance of the effluent at 285 nm. The linear range of response is 0.5 to 100 nmol. The method was applied to the analysis of uric acid in urine and serum. Urine was injected directly into the system, while serum required removal of an interfering substance which absorbs the light and coelutes with uric acid. However, this substance was simply removed by heat coagulation of serum by heating in a boiling water bath for 2 min.

Anion Exchange Resins↗
PubMed1981

Quantitation of urinary uric acid by reversed-phase liquid chromatography.

The proposed isocratic liquid-chromatographic method for uric acid has good performance characteristics. Results by this procedure and by an enzymic method for uric acid correlated well (r = 0.986). Our method is inexpensive, rapid, and considerably simpler than other techniques for determining uric acid in urine.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

Biochemical analysis of human seminal plasma. II. Protein, non-protein nitrogen, urea, uric acid and creatine.

Seminal levels of protein, non-protein nitrogen (NPN), urea, uric acid and creatine were determined in human males divided as normal (Group I), azoospermia (Group II), infertile (Groups III, IV and V) with different sperm numbers and vasectomized (Group VI) cases. The geometrical mean level of seminal protein of Gr. I and Gr. V were significantly greater than that of Gr. IV. No significant difference in the levels of NPN and urea between any of the groups revealed. The seminal creatine level of Gr. I was significantly higher than that of Gr. III which in its turn was greater than that of Gr. VI, which recorded a value lowest of all the groups. Mean levels of uric acid of Gr. I was significantly greater than those of other five groups, taken individually. A direct correlation between uric acid level and sperm counts is an important observation that has emerged from this study.

Creatine↗
PubMed1998

Uric acid in chronic heart failure: a marker of chronic inflammation.

BACKGROUND: Chronic heart failure is associated with hyperuricaemia and elevations in circulating markers of inflammation. Activation of xanthine oxidase, through free radical release, causes leukocyte and endothelial cell activation. Associations could therefore be expected between serum uric acid level, as a marker of increased xanthine oxidase activity, and markers of inflammation. We have explored these associations in patients with chronic heart failure, taking into account the hyperuricaemic effects of diuretic therapy and insulin resistance. METHODS AND RESULTS: Circulating uric acid and markers of inflammation were measured in 39 male patients with chronic heart failure and 16 healthy controls. All patients underwent a metabolic assessment, which provided a measure of insulin sensitivity (intravenous glucose tolerance tests and minimal modelling analysis). Compared to controls, patients with chronic heart failure had significantly higher levels of circulating uric acid, interleukin-6, soluble tumour necrosis factor receptor (sTNFR)-1, soluble intercellular adhesion molecule-1 (ICAM-1, all P<0.001), E-selectin and sTNFR2 (both P<0.05). In patients with chronic heart failure, serum uric acid concentrations correlated with circulating levels of sTNFR1 (r=0.74), interleukin-6 (r=0.66), sTNFR2 (r=0.63), TNFa (r=0.60) (all P<0.001), and ICAM-1 (r=0.41, P<0.01). In stepwise regression analyses, serum uric acid emerged as the strongest predictor of ICAM-1, interleukin-6, TNF, sTNFR1 and sTNFR2, independent of diuretic dose, age, body mass index, alcohol intake, serum creatinine, plasma insulin and glucose, and insulin sensitivity. CONCLUSIONS: Serum uric acid is strongly related to circulating markers of inflammation in patients with chronic heart failure. This is consistent with a role for increased xanthine oxidase activity in the inflammatory response in patients with chronic heart failure.

Cardiomyopathy, Dilated↗
PubMed1970

A method for deriving normal ranges from laboratory specimens applied to uric acid in males.

Plasma specimens from male blood donors gave a normal range for uric acid concentration of 3.3 to 7.5 mg/100 ml. Specimens from male outpatients, which were received in the laboratory for the analysis of urea but not of uric acid and proved to have normal concentrations of urea, showed a positively skewed distribution of values for uric acid from which a ;normal range' of 3.2 to 7.6 mg/100 ml was derived. We suggest that specimens from outpatients selected in the way described here may prove to be a convenient source of data for determining the normal range of other substances.

Blood Donors↗
PubMed2004

Serum uric acid levels show a 'J-shaped' association with all-cause mortality in haemodialysis patients.

BACKGROUND: Although elevated serum levels of uric acid are common in patients with kidney disease or in those receiving maintenance dialysis therapy, the clinical impact of uric acid on mortality in haemodialysis (HD) patients remains unclear. This work was designed to explore the predictive value of serum uric acid levels on all-cause mortality of HD patients. METHODS: We retrospectively analysed mortality rates in 146 chronic HD patients that were treated with HD three times per week at our HD unit for a period of one full year. The analysed parameters included demographic characteristics, aetiology of end-stage renal disease, co-morbid conditions, duration (at least 1 year) and delivered dose of HD, normalized protein catabolic rate, serum albumin concentration, haematocrit, serum uric acid (UA) levels and other laboratory parameters. A multivariate Cox proportional hazards model, which included adjustment for the above factors, was applied to identify the predictive value of UA levels on patient mortality. RESULTS: A Cox proportional hazards model revealed that decreased serum albumin, underlying diabetic nephropathy (DMN) and UA groups (< or =20th, 20-80th and > or =80th percentiles; P = 0.016) were all significant, independent predictors of all-cause mortality in HD patients. The hazard ratios of death were: serum albumin (per 0.5 g/dl decrease), 3.10 [95% confidence interval (95% CI), 1.80-5.34, P < 0.001]; DMN (vs non-DMN), 3.47 (95% CI, 1.25-9.59, P = 0.017); and UA groups (vs 20th to 80th percentile): < or =20th percentile, 2.98 (95% CI, 0.82-10.90, P = 0.099); > or = 80th percentile, 5.67 (95% CI, 1.71-18.78, P = 0.004). CONCLUSIONS: These preliminary observations suggest that HD patients in the lowest and highest quintiles of UA levels would face higher risk of mortality. Further studies with larger sample sizes will be needed to confirm these findings.

Adult↗
PubMed1977

A precise semi-automated uricase method for determining uric acid in serum or urine.

1. A semi-automated uricase method is described for measuring uric acid in serum or urine directly at 292 nm at reduced cost. 2. The coefficient of variation within and between batch assays, is estimated to be 2.5% and 4.3% respectively, which is less than the estimated daily intrapersonal variation in uric acid levels. 3. Recovery of uric acid added to samples ranges from 98.5% to 101.2% with a mean of 99.6%. 4. The cost of reagents per sample determination is estimated at $0.05, and in batch analyses the mean time required per sample determination is 2-3 minutes.

Analysis of Variance↗
PubMed1992

[Comparison of measurements of cholesterol, glucose and uric acid taken at 5-year intervals in children and adolescents].

BACKGROUND: There are several reports on cardiovascular disease risk factors but, except for lipids and lipoproteins, there have been few studies tracking blood uric acid and glucose in healthy school children. MATERIAL AND METHODS: Blood specimens were collected from 4,299 children and adolescents for determination of cholesterol, uric acid and glucose. The first samples were collected between 1977 and 1979 from subjects aged 4 to 17 years. The second samples were collected 5 years later. RESULTS: The blood glucose concentrations increased before the age of 10 years; those of uric acid increased during the second decade and those of cholesterol decreased during puberty, to a greater degree in boys. Hypercholesterolemia (cholesterol > 5.9 mmol/l) was found in about 6% of boys and 10% of girls. Eight boys and 3 girls had blood glucose concentrations higher than 6.7 mmol/l at the first collection. 5 years later, the correlation coefficients by sex and by cross section of age were greater than 0.5 for cholesterol and uric acid and were about 0.3 for glucose. CONCLUSIONS: Successive blood values of glucose and uric acid are highly correlated; those of cholesterol are more highly correlated. However, the probability of remaining in the same percentile distribution remains below 50% for subjects whose initial values were above the 80th percentile.

Adolescent↗