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PubMed2001

Is serum uric acid level associated with all-cause mortality in high-functioning older persons: MacArthur studies of successful aging?

OBJECTIVES: To explore the effect of serum uric acid level on subsequent all-cause mortality in high-functioning community-dwelling older persons. It is controversial whether high serum uric acid level is a true independent risk factor for cardiovascular and total mortality or the association is due to other confounding variables. Furthermore, it remains unclear whether the predictive value of uric acid level on mortality observed in younger cohorts can be extended to older people. DESIGN: Prospective cohort study. SETTING: A sample of community-dwelling older people. PARTICIPANTS: A cohort of 870 participants from the MacArthur Studies of Successful Aging. MEASUREMENTS: Baseline information was obtained for serum uric acid level, C-reactive protein (CRP), interleukin-6 (IL-6), prevalent medical conditions, and health behaviors. Crude and multivariate logistic regression analyses were used to examine the association between serum uric acid levels and 7-year all-cause mortality, while adjusting for potential confounders. RESULTS: In men, the multiply adjusted risk ratios for 7-year total mortality were 1.07 (95% CI=0.61-1.88) for the mid tertile of uric acid level and 1.24 (95% CI=0.70-2.20) for the top tertile. In women, the multiply adjusted risk ratios were 0.58 (95% CI=0.29-1.18) and 0.47 (95% CI=0.22-0.99), for the mid and top tertiles respectively. CRP and IL-6 were important confounders in the relationship between serum uric acid and overall mortality. CONCLUSIONS: High serum uric acid level is not independently associated with increased total mortality in high-functioning older men and women. When evaluating the association between serum uric acid and mortality, the potential confounding effect of underlying inflammation and other risk factors must be considered.

Aged↗
PubMed1977

Transport of uric acid and hypoxanthine across the isolated guinea pig placenta.

Transport of uric acid and hypoxanthine across the isolated guinea pig placenta is investigated quantitatively. The clearances measured are independent of concentration. It is shown that the uric acid transport is not greatly influenced by variations in flow, so it is concluded that the uric acid transport is membrane limited. The clearance of hypoxanthine is even less than the uric acid clearance, so hypoxanthine transport is also membrane limited. Xanthine oxidase is shown to be present in the uterine tissues, and an apparent Km and a maximum velocity have been determined.

Animals↗
PubMed1993

Accumulation of allantoin and uric acid in plasma of exercising trotters.

Plasma concentrations of hypoxanthine, uric acid, and allantoin, which are breakdown products of adenine nucleotides, were measured in Standardbred and Finnhorse trotters during and after an exercise test on a high-speed treadmill, after an incremental exercise test performed on a racetrack, and after a racing competition. Fiber-type composition of the middle gluteal muscle and the muscle concentrations of adenine nucleotides and inosine monophosphate were measured after the racetrack test. Changes in the concentration of hypoxanthine were not observed in any of the tests. Peak concentration of uric acid was measured between 5 and 30 minutes after exercise, and it was three- to tenfold higher than the value at rest. The variability can be explained by intensity of the exercise test and variation among horses. The concentration of allantoin after exercise was 2 to 3 times as high as that at rest, depending on the intensity of the exercise, although the absolute increase was about 10 times as high as the increase in the concentration of uric acid. Peak values of allantoin for the treadmill and the racetrack tests were obtained 4 to 6 minutes after exercise and < 30 minutes after the races. Peak concentration of allantoin correlated positively with the percentage of type-II (IIA+IIB) fibers in the middle gluteal muscle. Significant correlations were not observed between plasma concentration of uric acid or allantoin and muscle concentrations of adenosine triphosphate (ATP) or inosine monophosphate. It can be concluded that in horses, breakdown of ATP during and after exercise continues until allantoin is produced.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMedDate not supplied

A micromethod for plasma uric acid determinations in companion birds.

A simple inexpensive method is described for determining plasma uric acid levels in companion birds. Plasma uric acid concentrations in 33 healthy parakeets were determined by a modification of the uricase spectrophotometric procedure utilizing 50 microliters of plasma. The mean uric acid level in parakeets was 5.60 mg/dl blood plasma, with no significant difference between males and females. In White Leghorn chickens, however, the mean level of uric acid in plasma was 7.19 mg/dl in males and 3.05 mg/dl in females. This method may be useful for the diagnosis and study of gout in small birds.

Animals↗
PubMed2000

The effects of the addition of losartan on uric acid metabolism in patients receiving indapamide.

OBJECTIVE: A number of adverse metabolic effects are associated with indapamide administration, including an increase in serum uric acid levels. It has been reported that losartan can significantly decrease serum uric acid levels. However, there are no data on the effects of combination therapy of losartan with indapamide on uric acid metabolism. METHODS: We studied 20 hypertensive patients in whom serum metabolic parameters, including uric acid levels in serum and urine, were studied before and after eight weeks of indapamide administration (2.5 mg once daily) as well as eight weeks after combination treatment with indapamide (2.5 mg once daily)and losartan (50 mg/day). RESULTS: Indapamide evoked a significant decrease in systolic and diastolic blood pressure from a mean value of 157 +/- 12 mmHg/96 +/- 10 mmHg to a mean value of 139 +/- 14 mmHg/92 +/- 5 mmHg (p<0.01 for both comparisons). However, a significant increase in serum uric acid levels was noticed after indapamide administration (from a mean value of 4.9 +/- 1.6 mg/dl to a mean value of 5.9 +/- 1.2 mg/dl, p<0.01), associated with a decrease in the fractional excretion of uric acid(from a mean value of 9 +/- 5% to a mean value of 7 +/- 5.5%, p<0.05). The addition of losartan caused a further decrease in blood pressure from a mean value of 139 +/- 14 mmHg/92 +/- 5 mmHg to a mean value of 120 +/- 15 mmHg/84 +/- 4 mmHg (p<0.01 for both comparisons). This was followed by a significant decrease in serum uric acid levels to 5 +/- 1.1 mg/dl(p<0.01) due to a substantial increase in fractional urate excretion (from 7 +/- 5.5 to 8.7 +/- 6%, p<0.05). CONCLUSION: The addition of losartan could offset the hyperuricaemic effect of indapamide administration.

Adult↗
PubMed1981

Caecal decomposition of uric acid in captive and free ranging willow ptarmigan (Lagopus lagopus lagopus).

Urine entering the caeca of birds contains significant amounts of uric acid. The discovery of great numbers of bacteria utilizing uric acid in the caeca has encouraged the discussion about nitrogen recycling in birds. In this work caecal decomposition of uric acid in wild and captive willow ptarmigan has been investigated using radioactively labelled uric acid injected directly into one of the caeca. The appearance of radioactive CO2 in the expired air was taken as an indication of uric acid breakdown. The decomposition occurred at a rate corresponding to a half-life of 26 min (11-36 min). The results are in accordance with the previously reported observations of huge numbers of uric acid utilizing bacteria in the caeca of a variety of birds, and also with the nitrogen recycling theory. However, no conclusion concerning the nitrogen recycling can be drawn.

Amoeba↗
PubMed1966

Uric acid dihydrate: crystallography and identification.

Unit-cell dimensions and optical data for uric acid and uric acid dihydrate show that there are structural resemblances, but that either can be readily distinguished by x-ray methods or by optical techniques. Density separation may be unsatisfactory because the dihydrate can lose water rather easily. Powder diffraction data are given.

Crystallography↗
PubMedDate not supplied

Stored wheat insect infestation related to uric acid as determined by liquid chromatography.

Liquid chromatography is used to measure the uric acid content of wheat internally infested by various growth stages of granary weevil (Sitophilus granarius), rice weevil (Sitophilus oryzae), and lesser grain borer (Ryzopertha dominica). Good correlation exists between numbers of insects and uric acid content of grain infested by a given stage of an internally infesting stored product insect, with correlation coefficients ranging from 0.970 to 0.998. Uric acid content of infested grain increases as the insect life cycle progresses, with granary weevil producing the greatest quantities of uric acid followed in order by rice weevil and lesser grain borer. A detection limit for the analytical procedure of less than 1.0 ppm uric acid allows detection of infestation levels as low as one kernel per 100 g grain for late instar granary weevil larvae. This limit is sufficiently sensitive to detect levels of infestation that may be commonly encountered in commerce.

Animals↗
PubMed1991

Female gout. Clinical spectrum and uric acid metabolism.

We reviewed the clinical features and uric acid metabolism in 37 female patients with gout. In 32 female patients (86%), gout was diagnosed after menopause. Among the five premenopausal patients, four had renal insufficiency and one had superactivity of phosphoribosylpyrophosphate synthetase. More than 50% of the female patients had osteoarthritis, hypertension, or renal insufficiency or were treated with diuretics. Comparison with 220 male patients with gout showed that female patients developed gout significantly later, more frequently had associated diseases, and more often were receiving diuretics, whereas significantly more male than female patients had alcoholism. The articular features of gout were similar in both groups. However, the prevalence of tophi was higher and its localization different in female than in male patients. Female patients with gout had a higher mean serum urate concentration and a lower mean urinary uric acid excretion than did male patients with gout. These differences were significant and independent of the effects of age, renal insufficiency, alcoholism, or previous diuretic intake. Renal underexcretion of uric acid appears to be more severe in female than in male patients with gout.

Adult↗
PubMed2000

Serum uric acid, diuretic treatment and risk of cardiovascular events in the Systolic Hypertension in the Elderly Program (SHEP).

OBJECTIVE: To assess longitudinally the association of serum uric acid and its change due to diuretic treatment with cardiovascular events in hypertensive patients. DESIGN: Cohort study in a randomized trial. SETTING: Cohort of hypertensive patients. PARTICIPANTS: A total of 4327 men and women, aged > or = 60 years, with isolated systolic hypertension, randomized to placebo or chlorthalidone, with the addition of atenolol or reserpine if needed, were observed for 5 years. MAIN OUTCOME MEASURES: Major cardiovascular events, coronary events, stroke and all-cause mortality. RESULTS: Cardiovascular event rates for quartiles of baseline serum uric acid were: I, 32.7 per 1000 person-years; II, 34.5 per 1000 person-years; III, 38.1 per 1000 person-years; and IV, 41.4 per 1000 person-years (P for trend = 0.02). The adjusted hazard ratio (HR), of cardiovascular events for the highest quartile of serum uric acid versus the lowest quartile was 1.32 (95% CI, 1.03-1.69). The benefit of active treatment was not affected by baseline serum uric acid. After randomization, an increase of serum uric acid < 0.06 mmol/l (median change) in the active treatment group was associated with a HR of 0.58 (0.37-0.92) for coronary events compared with those with a serum uric acid increase > or = 0.06 mmol/l. This difference was not explained by blood pressure effects. Those with a serum uric acid increase > or = 0.06 mmol/l in the active treatment group had a similar risk of coronary events as the placebo group. CONCLUSIONS: Serum uric acid independently predicts cardiovascular events in older persons with isolated systolic hypertension. Monitoring serum uric acid change during diuretic treatment may help to identify patients who will most benefit from treatment.

Adrenergic beta-Antagonists↗
PubMed1977

Uptake of uric acid by separated renal tubules of the rabbit. I. Characteristics of transport.

A rapid filtration procedure was used to determine rates of uric acid uptake by a preparation of separated renal cortical tubules of the rabbit. The rate of uric acid uptake was temperature dependent and showed saturation kinetics with a K of 3.2 mM. The uptake was 50% lower when measured under nitrogen as compared with uptake under oxygen. The uptake rate increased with increasing sodium concentration and decreased with increasing potassium concentration. Uptake was stimulated by citrate, succinate and pyruvate, and inhibited by alpha-ketoglutarate. Parathyroid hormone and 10(-4) M adenosine 3':5'-monophosphate increased the uric acid uptake rate when preincubated with the tubules for 130 minutes before the addition of uric acid. Uric acid uptake in this preparation appears to occur by some form of carrier-mediated active transport.

Animals↗
PubMed2002

Prognostic significance of uric acid serum concentration in patients with acute ischemic stroke.

BACKGROUND AND PURPOSE: We sought to assess in 881 consecutive patients with acute ischemic stroke the clinical relevance in regard to functional outcome of the natural antioxidant uric acid measured at hospital admission. METHODS: Patients had serum uric acid (mg/dL) measured by standard procedures 18.2+/-15.5 hours from clinical onset. At hospital discharge (11.0+/-6.0 days), neurological impairment was classified as moderate/severe (Mathew score < or =75; n=304) or mild/absent (Mathew score >75; n=577). Demographics, atherosclerotic risk factors, history of organ disease, baseline neurological score, stroke subtype, infarction size, renal function, aspirin use before stroke, stroke therapy, diuretic use, and laboratory markers, including erythrocyte sedimentation rate, were analyzed in both outcome groups with the use of backward logistic regression. RESULTS: Increased uric acid values were found in men, hypertensives, alcohol drinkers, and patients with coronary, pulmonary, or renal diseases. Diabetic patients had lower uric acid levels on admission. Uric acid was directly associated with hematocrit (P=0.001), sodium (P=0.001), creatinine (P=0.001), and triglycerides (P=0.001) and inversely related with nonfasting glucose (P=0.001) levels. Neurological impairment on admission (P=0.001) and final infarction size on CT/MRI (P=0.01) were also inversely associated with uric acid. A logistic regression adjusted for confounders confirmed the following independent (odds ratio, 95% CI) good outcome predictors: age (0.97, 0.96 to 0.99), Mathew score on admission (1.14, 1.12 to 1.17), erythrocyte sedimentation rate (0.98, 0.97 to 0.99), infarction volume (0.98, 0.98 to 0.99), and uric acid (1.12, 1.00 to 1.25). CONCLUSIONS: In patients with acute ischemic stroke, there is a 12% increase in the odds of good clinical outcome for each milligram per deciliter increase of serum uric acid. This finding reinforces the relevance of oxidative damage in ischemic stroke.

Acute Disease↗
PubMed2003

Uric acid stimulates monocyte chemoattractant protein-1 production in vascular smooth muscle cells via mitogen-activated protein kinase and cyclooxygenase-2.

Previous studies have reported that uric acid stimulates vascular smooth muscle cell (VSMC) proliferation in vitro. We hypothesized that uric acid may also have direct proinflammatory effects on VSMCs. Crystal- and endotoxin-free uric acid was found to increase VSMC monocyte chemoattractant protein-1 (MCP-1) expression in a time- and dose-dependent manner, peaking at 24 hours. Increased mRNA and protein expression occurred as early as 3 hours after uric acid incubation and was partially dependent on posttranscriptional modification of MCP-1 mRNA. In addition, uric acid activated the transcription factors nuclear factor-kappaB and activator protein-1, as well as the MAPK signaling molecules ERK p44/42 and p38, and increased cyclooxygenase-2 (COX-2) mRNA expression. Inhibition of p38 (with SB 203580), ERK 44/42 (with UO126 or PD 98059), or COX-2 (with NS398) each significantly suppressed uric acid-induced MCP-1 expression at 24 hours, implicating these pathways in the response to uric acid. The ability of both n-acetyl-cysteine and diphenyleneionium (antioxidants) to inhibit uric acid-induced MCP-1 production suggested involvement of intracellular redox pathways. Uric acid regulates critical proinflammatory pathways in VSMCs, suggesting it may have a role in the vascular changes associated with hypertension and vascular disease.

Animals↗
PubMed1990

Cyclosporine inhibits renal uric acid transport in renal transplants not in children treated for nephrotic syndrome.

Children with various grades of renal insufficiency (CON group) maintained uric acid excretion over a range of glomerular filtration rate (GFR) from 27 to 160 ml/min*1.73m2 despite a decreased filtered load which was paralleled by glomerular filtration of uric acid. This was achieved by a compensatory decrease of net uric acid reabsorption (TUA) and an increasing fractional excretion of uric acid (FEUA) with decreasing GFR. Although there was a decreased GFR in the group of children after transplantation (NTx group) there was no difference in TUA and FEUA between the NTx group and the CON group. Uric acid transport was not affected in children treated with Cyclosporine (CyA) for nephrotic syndrome (NEPH group) compared to the CON group. Decreased fractional phosphate reabsorption in the NTx group suggests proximal tubule damage associated with disturbed uric acid handling. Under conditions of water diuresis hyperuricemia seen in NTx may result from an indirect effect of renal ischemic damage due to the transplantation procedure causing disturbance of proximal tubular uric acid (active) secretion/reabsorption.

Adolescent↗
PubMed1990

Effects of uric acid and caffeine on A1 adenosine receptor binding in developing rat brain.

Previous studies have demonstrated that elevated levels of serum uric acid or caffeine are associated with increased locomotor activity in rats and humans. Since uric acid and caffeine are structurally similar, it was hypothesized that these compounds alter locomotor activity through a common neural mechanism, specifically by acting as receptor antagonists at adenosine A1 binding sites. In vitro competition of caffeine and uric acid against the A1 agonist, [3H] cyclohexyladenosine ([3H]CHA), was conducted using homogenates of adult rat forebrain. Caffeine effectively competed for the A1 binding site as previously reported (IC50 = 107 microM), but uric acid failed to compete with [3H]CHA binding at concentrations within a relevant physiological range. Nevertheless, in vivo experiments indicated that chronic elevation of uric acid following allantoxanamide treatment of male rats on days 4-27 of life significantly decreased A1 receptor binding in the striatum, a region traditionally implicated in mammalian locomotion. In contrast, chronic caffeine treatment on days 4-27 of life caused an increase in A1 receptor binding in the cortex similar to increases reported previously in whole brain. These changes in A1 receptor binding following chronic elevation of uric acid or caffeine did not persist in rats that had been withdrawn from allantoxanamide or caffeine treatment for 14 days. Results from in vitro and in vivo experiments indicate that despite a similar molecular structure uric acid does not act by the same mechanism as caffeine to increase locomotor activity in rats.

Adenosine↗
PubMed2005

Epitaxial deposition of calcium oxalate on uric acid rich stone matrix is induced by a 29 kDa protein.

BACKGROUND: Association of macromolecules particularly the role of proteins in urolithiasis has been studied for last few centuries, but still a complete profile of stone matrix proteins that mediate co-precipitation of uric acid and calcium oxalate has not been characterized. We isolated and characterize proteins from uric acid rich stone matrix, which have oxalate binding activity. METHODS: Matrix proteins were isolated from uric acid rich stone matrix using EDTA as a demineralizing agent. The radiolabelled solubilized proteins were fractionated with increasing ionic concentration by DEAE cellulose column chromatography to identify the oxalate binding protein. It was purified using Sephadex G-200 column chromatography. Amino acid composition was determined and monoclonal antibody was produced against the oxalate binding uric acid rich stone matrix protein. Urinary uric acid binding proteins were isolated from stone formers urine, their oxalate binding activity assayed and cross reactivity with the produced monoclonal antibody were checked using ELISA and Western blotting. RESULTS: Matrix on DEAE column chromatography elution yielded 3 protein peaks and they were named as fraction I, II and III among which fraction I had higher oxalate binding activity which was further purified with Sephadex G-200 column which yielded 2 protein peaks designated as Ia and Ib. Fraction Ib with molecular weight 29 kDa exhibited the maximum oxalate binding activity. Forty percent of this 29 kDa protein is comprised of basic amino acids. Monoclonal antibody (IgG1) was produced against the 29 kDa stone matrix protein. Urinary uric acid binding proteins were isolated from stone formers, 4 protein peaks were obtained named as fraction I to IV. Among them, fraction IV having molecular weight of approximately 29 kDa cross reacted up to 85.6% with 29 kDa stone matrix protein. Moreover, urinary 29 kDa protein exhibited oxalate binding activity of 94.16 +/- 6.08 pmol/mg protein at pH 5.5. CONCLUSION: The 29 kDa protein isolated from uric acid rich stone matrix and urine are one and the same, thereby insinuating that 29 kDa protein might play a major role in epitaxial deposition of calcium oxalate over uric acid core, consequently favoring the lithogenic events like uric acid and calcium oxalate nucleation, aggregation and retention.

Animals↗
PubMed2002

Uric acid concentration in subjects at risk of type 2 diabetes mellitus: relationship to components of the metabolic syndrome.

High uric acid concentration is a common finding in subjects with risk factors for cardiovascular disease (CVD), including some characteristics of the metabolic syndrome. However, its exact role in this setting and in the progression to type 2 diabetes mellitus (DM) is not well understood and could be affected by confounding factors such as hypertriglyceridemia. Our study aimed to establish the relationship between uric acid (avoiding the interference of high triglyceride levels), insulin sensitivity, and components of the metabolic syndrome in a group of subjects at high risk of developing DM. Among 201 subjects included in the study, 111 (55.2%) showed an abnormal oral glucose tolerance and uric acid levels higher than those measured in subjects with normal glucose tolerance. Body mass index (BMI), triglycerides, diastolic blood pressure (DBP), and 2-hour glycemia in the oral glucose tolerance test (OGTT) contributed independently to uric acid concentration (R2 =.59). However, uric acid did not affect either insulin sensitivity or glucose tolerance. The recovery tests revealed that a triglyceride concentration > or = 3 mmol/L interfered with the measurement of uric acid level when a colorimetric method was used, but not when a dry-chemistry method was used. In conclusion, uric acid concentration is higher in subjects at high risk of DM with abnormal glucose tolerance and is independently determined by various components of the metabolic syndrome.

Adult↗
PubMed1989

[A recommended method for determination of uric acid in serum].

SFBC work group on uric acid propose a method for evaluation in blood serum which is modeled on the one defined by American Association for Clinical Chemistry. Serum is deproteinized by trichoracetic acid and the supernatant, buffered to pH 8.5, is submitted to uricase action. The disappearing of the strong band of uric acid in UV is measured by derivative spectrophotometry; this procedure vanished the effect of trouble which remains in the supernatant. This spectrophotometric technic permit to reach, in multiple sites, a variation coefficient near of 1 p. cent.

Analysis of Variance↗