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PubMed2004

Childhood uric acid predicts adult blood pressure: the Bogalusa Heart Study.

Uric acid has been proposed as an important risk factor in the development of primary hypertension in humans. However, limited information is available linking childhood uric acid levels and blood pressure levels in adulthood. This study examined 334 whites and 243 blacks enrolled in the Bogalusa Heart Study as children aged 5 to 17 years and as adults aged 18 to 35 years. The average follow-up period was 12 years. Childhood uric acid was significantly correlated with childhood and adult blood pressure, both systolic and diastolic. In a multivariate regression analysis, adjusting for age, sex, race, childhood body mass index, childhood uric acid levels, and change in levels of uric acid were significant predictors of adult diastolic blood pressure, whereas change in uric acid was a significant predictor of adult systolic blood pressures. In conclusion, elevated childhood serum uric acid levels are associated with increased blood pressure beginning in childhood and higher blood pressure levels that persist into adulthood, in males and females, whites and blacks, suggesting that early elevations in serum uric acid levels may play a key role in the development of human hypertension.

Adolescent↗
PubMed1998

Aqueous humor uric acid and ascorbic acid concentrations and outcome of trabeculectomy.

OBJECTIVE: To determine if there is an association between the surgical outcome of trabeculectomy and uric acid and ascorbic acid concentrations in the aqueous humor at the time of the procedure. PATIENTS, MATERIALS, AND METHODS: Aqueous humor samples were collected from the eyes of 169 of 249 adult patients who underwent trabeculectomy alone for any type of glaucoma between April 1989 and July 1995. Postoperatively, all medical records were reviewed and outcomes were classified as successful, unsuccessful, or indeterminate. The ascorbic acid and uric acid concentrations were determined in masked fashion by high-pressure liquid chromatography. Factors associated with surgical outcome were determined. RESULTS: Uric acid concentration was higher in unsuccessful eyes (mean+/-SD, 0.21+/-0.08 mmol/L, n=26) than in successful eyes (0.15+/-0.09 mmol/L, n=91, 95% confidence interval for difference, 0.02-0.10 mmol/L). Ascorbic acid levels were not significantly different in the eyes with unsuccessful (1129.9+/-601.9 micromol/L) and successful (1334.3+/-511.0 micromol/L) surgery (95% confidence interval for difference, -475.2 to 66.4 micromol/L, P=.13) surgery. Other factors associated with failure were previous surgery and surgery performed at the inferior limbus. A multiple polytomous logistic regression analysis was performed, after excluding the small number of operations performed at the inferior limbus. The odds ratio for failure increased by a factor of 1.68 for every 1-mmol/L increase in uric acid (95% confidence interval, 1.16-2.43, P=.006). CONCLUSIONS: Uric acid levels were higher at the time of surgery in eyes that had unsuccessful outcomes than in those with successful outcomes. No significant difference in ascorbic acid levels was detectable. A higher uric acid level in the aqueous humor is a risk factor for trabeculectomy failure and might be tested as a prognostic indicator [corrected].

Aged↗
PubMed2005

Uric acid, a nucleic acid degradation product, down-regulates dsRNA-triggered arthritis.

Uric acid, the naturally occurring degradation product of purine metabolism, is a danger signal, driving maturation of dendritic cells. It is well known that uric acid crystals display potent proinflammatory properties--the cause of gout--whereas the biological properties of soluble uric acid are less well documented. We have demonstrated previously that nucleic acids of endogenous and exogenous origin display proinflammatory properties. The aim of the present study was to assess the impact of soluble uric acid on in vivo inflammatory responses. Mice were administered with uric acid suspension in saline or saline alone prior to induction of neutrophil-mediated inflammation, delayed-type hypersensitivity, histamin-induced edema (measure of vasodilation capacity), as well as double-stranded (ds)RNA-triggered arthritis. Frequency and severity of arthritis were decreased significantly in mice exposed to dsRNA and simultaneously treated with uric acid as compared with saline-treated controls. Also, granulocyte-mediated inflammatory response and vasodilation capacity were reduced significantly in mice treated with uric acid as compared with their control group. The data suggest that down-regulation of inflammation was mediated by skewing the inflammatory response from the peripheral sites to the peritoneal cavity and down-regulating vasodilatatory capacity and thereby affecting leukocyte migration. In contrast, the T cell-mediated delayed-type hypersensitivity reaction was not affected significantly in mice exposed to uric acid. These findings demonstrate that uric acid displays a potent, distant anti-inflammatory effect in vivo. This property seems to be mediated by down-regulation of neutrophil influx to the site of inflammatory insult.

Animals↗
PubMed2006

[Relationships between arterial hypertension, metabolic disturbances and uric acid nephropathy].

AIM: To study effects of uric acid disbolism in combination with other metabolic disturbances on prevalence and clinical symptoms of arterial hypertension; contribution of uric acid nephropathy to its development. MATERIAL AND METHODS: A cohort of 243 representatives from a general population (107 males, 136 females, age 19-59 years) was studied in 1986 and 15 years later. At the beginning and end of the trial the participants were examined for arterial hypertension, microalbuminuria, uric acid nephropathy, blood biochemical tests were made. RESULTS: For 15-year follow-up prevalence of arterial hypertension doubled, incidence of hyperuricemia and hyperuricosuria, hypertriglyceridemia increased considerably. The number of hypertensive subjects was maximal in the group with the greatest number of signs of uric acid nephropathy. CONCLUSION: The population studied exhibited increasing frequency of some risk factors, especially of uric acid metabolism, contributing to formation of arterial hypertension.

Adult↗
PubMed1991

Serum and urinary uric acid levels in healthy subjects and in patients with urolithiasis.

Serum uric acid and 24-hour urine uric acid levels were determined in 47 patients with urolithiasis and in 177 healthy volunteers. The normal volunteers had serum and urinary uric acid levels of 6.0-6.4 mg/dl, 619.4-683.7 mg/day for males and 4.6-4.8 mg/dl, 531.5-589.6 mg/day for females. Uric acid levels in both serum and urine were higher in male volunteers than in female volunteers (p less than 0.05), whereas, among patients the ranges of serum and urinary uric acid levels were not significantly different between males and females (p greater than 0.05). However, the normal distribution of the determined small experimental data, was statistically different and is obviously reliable. Patients with urolithiasis showed significantly higher levels of serum uric acid (8.0 +/- 0.3 mg/dl) than healthy volunteers (5.5 +/- 0.1 mg/dl) (p less than 0.05), but showed no difference in urinary uric acid levels compared with healthy volunteers (p greater than 0.05). The highest number of urolithiasis in both male and female patients fell within the same age range of 41-50 years. The 24-hour urine pH of healthy volunteers showed a range of 5.1-7.0 while the patients with urolithiasis had a pH range of 4.6-7.0. It was also found that 33 per cent of patients had urine pH less than 5.0.

Adult↗
PubMed2005

Associations among lead dose biomarkers, uric acid, and renal function in Korean lead workers.

Recent research suggests that both uric acid and lead may be nephrotoxic at lower levels than previously recognized. We analyzed data from 803 current and former lead workers to determine whether lead biomarkers were associated with uric acid and whether previously reported associations between lead dose and renal outcomes were altered after adjustment for uric acid. Outcomes included uric acid, blood urea nitrogen, serum creatinine, measured and calculated creatinine clearances, and urinary N-acetyl-ss-d-glucosaminidase (NAG) and retinol-binding protein. Mean (+/- SD) uric acid, tibia lead, and blood lead levels were 4.8 +/- 1.2 mg/dL, 37.2 +/- 40.4 microg/g bone mineral, and 32.0 +/- 15.0 microg/dL, respectively. None of the lead measures (tibia, blood, and dimercaptosuccinic-acid-chelatable lead) was associated with uric acid, after adjustment for age, sex, body mass index, and alcohol use. However, when we examined effect modification by age on these relations, both blood and tibia lead were significantly associated (ss = 0.0111, p < 0.01 and ss = 0.0036, p = 0.04, respectively) in participants in the oldest age tertile. These associations decreased after adjustment for blood pressure and renal function, although blood lead remained significantly associated with uric acid (ss = 0.0156, p = 0.01) when the population was restricted to the oldest tertile of workers with serum creatinine greater than the median (0.86 mg/dL). Next, in models of renal function in all workers, uric acid was significantly (p < 0.05) associated with all renal outcomes except NAG. Finally, in the oldest tertile of workers, associations between lead dose and NAG were unchanged, but fewer associations between the lead biomarkers and the clinical renal outcomes remained significant (p less than or equal to 0.05) after adjustment for uric acid. In conclusion, our data suggest that older workers comprise a susceptible population for increased uric acid due to lead. Uric acid may be one, but not the only, mechanism for lead-related nephrotoxicity.

Adolescent↗
PubMed1975

Serum uric acid in hypertensive patients.

Both the average serum uric acid and annual increment were determined in 250 treated patients attending a hypertension clinic. The average serum uric acid was greater in men compared with women, in patients receiving a thiazide diuretic and in patients with a high average plasma urea. The mean annual increment in uric acid was close to zero (0.0017 mmol/litre per year) and was not related to sex, age, blood pressure control, diuretic therapy, or plasma urea. There was an unexplained positive association between annual increment and methyldopa therapy though this drug was not associated with a significantly high average serum uric acid. A table is presented giving the theoretical upper limits for average serum uric acid according to sex, plasma urea concentration, and whether or not a thiazide diuretic has been prescribed. It is hoped that this table will be of assistance in assessing the normality or otherwise of a high serum uric acid found in a hypertensive patient.

Adult↗
PubMed1991

Uric acid as an inhibitor of biochemical changes induced by cyclophosphamide in mice.

The biochemical changes induced by uric acid, cyclophosphamide and uric acid plus cyclophosphamide were evaluated in Swiss albino male mice. Uric acid dissolved in water was administered orally in different doses for 7 days. Some mice from each group were injected intraperitoneally with cyclophosphamide (25 mg/kg) and sacrificed after 30 h. The blood of all animals was analyzed for uric acid levels. Uric acid was found not to affect the biosynthesis of nucleic acids and proteins in liver, testes and brain at 10-100 mg/kg/d. Pretreatment with uric acid provided significant protection against cyclophosphamide-induced impairment of DNA, RNA and protein biosynthesis.

Animals↗
PubMed2002

Purine nucleotide catabolism in rat liver: labelling of uric acid and allantoin after administration of various labelled precursors.

Uric acid and allantoin are the key compounds of purine nucleotide catabolism formed in liver and many other organs of the rat. We observed that, after administration of 14C-formate, incorporation of radioactivity into uric acid and allantoin is not similar, as one would expect. The phenomenon was demonstrated to be specific to liver and perfused liver, and not to other organs such as heart, jejunal mucosa, lung, spleen, and kidney. To interpret these results, the specific radioactivity of uric acid and allantoin in rat liver were analysed comparatively, after administration of the following labelled precursors: 14C-glycine, 14C-formate, 14C-hypoxanthine, 14C-uric acid and 14C-adenine. After administration of 14C-formate the specific radioactivity of allantoin was higher than that of uric acid and the same behavior was observed after 14C-uric acid and 14C-hypoxanthine, but not after 14C-glycine and 14C-adenine administration. The results indicate that the rate of their incorporation into uric acid and allantoin, and the subsequent export of these compounds into serum, can only partially explain the observed phenomenon, while the presence of different pools of uric acid and allantoin may give a complete explanation.

Adenine↗
PubMed2000

Microfabricated electrophoresis chips for simultaneous bioassays of glucose, uric acid, ascorbic acid, and acetaminophen.

A micromachined capillary electrophoresis chip is described for simultaneous measurements of glucose, ascorbic acid, acetaminophen, and uric acid. Fluid control is used to mix the sample and enzyme glucose oxidase (GOx). The enzymatic reaction, a catalyzed aerobic oxidation of glucose to gluconic acid and hydrogen peroxide, occurs along the separation channel. The enzymatically liberated neutral peroxide species is separated electrophoretically from the anionic uric and ascorbic acids in the separation/reaction channel. The three oxidizable species are detected at the downstream gold-coated thick-film amperometric detector at different migration times. Glucose can be detected within less than 100 s, and detection of all electroactive constituents is carried out within 4 min. Measurements of glucose in the presence of acetaminophen, a neutral compound, are accomplished by comparing the responses in the presence and absence of GOx in the running buffer. The reproducibility of the on-chip glucose measurements is improved greatly by using uric acid as an internal standard. Factors influencing the performance, including the GOx concentration, field strength, and detection potential, are optimized. Such coupling of enzymatic assays with electrophoretic separations on a microchip platform holds great promise for rapid testing of metabolites (such as glucose or lactate), as well as for the introduction of high-speed clinical microanalyzers based on multichannel chips.

Acetaminophen↗
PubMed1986

The transport of uric acid across mouse small intestine in vitro.

The in vitro recirculation technique was used to study the uptake and transport of uric acid by the jejunum of mouse small intestine. Three components of the serosal secretions appeared to be endogenously derived nucleic acid derivatives; two of these were identified as uric acid and uracil. There was no detectable metabolism of uric acid by the intestine. Uric acid transported from the lumen appeared in the serosal fluid at a concentration higher than that in the lumen. The final serosal/luminal concentration ratio of about 1.18 for exogenous uric acid was found to be constant over the concentration range studied (0.01-0.1 mM). The presence of exogenous uric acid in the lumen did not affect the production of endogenous uric acid by the intestine and its release into the serosal secretions. Mucosal concentration of exogenous uric acid was below, but the total mucosal concentration (exogenous+endogenous) was above, that in the lumen. There was no evidence for the secretion of endogenous uric acid into the lumen. Oxypurinol significantly decreased the rate of serosal appearance of exogenous uric acid. Allopurinol did not affect the transport of exogenous uric acid from the lumen and there was negligible metabolism of allopurinol to oxypurinol by the tissue. Uracil did not affect the transport of exogenous uric acid from the lumen, or the serosal appearance of endogenous uric acid. Likewise uracil transport was unaffected by luminal uric acid.

Allopurinol↗
PubMed1998

Emerging concepts in cardiovascular disease: should elevated serum uric acid be considered a risk factor?

Uric acid is the final breakdown product of purine metabolism in man. There is a growing body of evidence that indicates that elevated uric acid levels increase the probability of developing hypertension and cardiovascular disease. The frequency of hyperuricaemia in untreated hypertensive individuals ranges from 25 - 50%. Furthermore, elevated serum uric acid has been reported to increase the probability of developing hypertension by 87% and to increase the mortality rate from ischaemic heart disease. Several studies have reported that changes in serum cholesterol parallel changes in serum uric acid in both order and magnitude. Most recently, hyperuricaemia has been added to the constellation of abnormalities that comprise Syndrome X. The pathophysiology of hyperuricaemia and the link between hyperuricaemia, hypertension and cardiovascular disease are poorly understood. It is entirely possible that hyperuricaemia is part of a pathologic process that underlies fundamental alterations in renal function, as well as other metabolic pathophysiologies that ultimately lead to hypertension and cardiovascular disease.

Journal Article↗
PubMed1973

Evidence for a postsecretory reabsorptive site for uric acid in man.

The effects of administration of drug combinations on uric acid excretion were studied in order to test the hypothesis that a portion of renal tubular reabsorption of uric acid occurs distal to the uric acid secretory site. Oral administration of pyrazinamide (3 g) during probenecid uricosuria (probenecid 500 mg every 6 h) decreased urate excretion from 463 mug/min following probenecid medication alone to 135 mug/min following probenecid plus pyrazinamide (P < 0.01). When a greater uricosuric effect was induced with a 2 g oral dose of probenecid, the decrement in urate excretion which followed pyrazinamide administration (3 g) was more pronounced (2,528 mug/min following probenecid alone, 574 mug/min following probenecid plus pyrazinamide). Results were similar when an 800 mg oral dose of sulfinpyrazone was given in place of probenecid (1,885 mug/min following sulfinpyrazone alone, 475 mug/min following sulfinpyrazone plus pyrazinamide). Thus, apparent urate secretion (measured as the decrease in excretion of urinary uric acid resulting from pyrazinamide administration) appeared to vary, depending upon the degree of inhibition of reabsorption produced by probenecid or sulfinpyrazone. When small doses of aspirin were administered in place of pyrazinamide to produce secretory inhibition, the results were similar. Neither probenecid nor pyrazinamide significantly altered urate excretion when administered to patients with serum salicylate levels above 14 mg/100 ml. These results are interpreted as suggesting that renal tubular reabsorption of uric acid occurs at least in part at a postsecretory site and that a portion of secreted urate is reabsorbed. During maximum probenecid- or sulfinpyrazone-induced uricosuria, inhibition of urate secretion with either pyrazinamide or low doses of aspirin resulted in a decrease in uric acid excretion which exceeded total urinary uric acid during control periods by two- to fourfold. This suggests that renal tubular secretion of urate may greatly exceed uric acid excretion and that a large fraction of secreted urate is reabsorbed. The pyrazinamide suppression test underestimates urate secretion. Uricosuria induced by some drugs, including probenecid, sulfinpyrazone, and iodinated radioopaque dyes, appears to represent, at least in part, inhibition of postsecretory urate reabsorption.

Absorption↗
PubMed1984

Ethanol induced alterations of uric acid metabolism.

Our observations have shown that chronic oral ethanol administration was associated with increased serum urate, urine uric acid excretion, urine uric acid clearance and oxypurine excretion. The daily rate of uric acid turnover was significantly increased. Intravenous ethanol administration was associated with increased uric acid excretion, increased uric acid clearance and significantly increased oxypurine excretion. Excretion of radioactivity derived from intravenously administered adenine increased significantly. We conclude that hyperuricemia related to ethanol consumption at lower blood ethanol levels (less than 150 mg/dl) results from increased production of uric acid probably secondary to accelerated degradation of adenine nucleotides.

Alcohol Drinking↗
PubMed2001

[Uric acid as a prognostic marker in critically ill patients].

BACKGROUND: Elevated uric acid concentrations reflect adenosine triphosphate degradation and suggest poor prognosis since they indicate a cellular bioenergetic crisis. OBJECTIVE: To study uric acid concentrations as a prognostic marker of disease severity in critically ill children. PATIENTS AND METHODS: Seventy-eight patients admitted to our pediatric intensive care unit with different diseases were prospectively studied. Thirty-five patients with meningococcal infection were retrospectively studied. Data on uric acid concentrations, diagnosis, length of stay, age, weight, the therapeutic intervention scoring system (TISS) and the pediatric risk of mortality score (PRISM) were collected. In patients with meningococcal infection severity was evaluated by studying evolution (death and the presence of sequelae or otherwise). RESULTS: Uric acid concentrations on admission were significantly correlated with TISS on the first day (r 0.260; p 0.023) and with PRISM during the first 24 hours (r 0.277; p 0.015). In patients without craniocerebral trauma, correlations between uric acid concentrations and PRISM during the first 24 hours (r 0.524; p < 0.001) and correlations between uric acid concentrations with TISS on day 1 (r 0.483; p < 0.001) and day 2 (r 0.373; p 0.014) improved. In patients with craniocerebral trauma no significant correlations were found between uric acid and any of the other variables. In patients with meningococcal infection, uric acid concentrations on admission were closely related to evolution (uric acid concentrations were 13.20 8.2 mg/dl in patients who died, 8.01 1.77 mg/dl in those with sequelae and 4.72 1.84 mg/dl in in those without sequelae; p < 0.003). CONCLUSIONS: Serum uric acid concentrations can be considered as a marker of severity in critically ill patients without craniocerebral trauma and especially in patients with meningococcal infection.

Child, Preschool↗
PubMed1997

Decreased first trimester uric acid production in future preeclamptic patients.

The relationship between first trimester uric acid production and later development of pregnancy induced hypertensive disorders (PIHD) was investigated. An anti-oxidant role for uric acid has been mentioned. Since uric acid and fibronectin (PF) are both markers of preeclampsia, the relationship between these two substances was also studied. Controls (n = 72) and patients with PIHD (n = 120) were selected. Uric acid was measured in serum and 24-hours urine samples (uric acid excretion) and PF in blood plasma in 270 nulliparous women at 13 +/- 2 weeks of gestation. Uric acid excretion was significantly lower in the first trimester in a group of patients who later develop PIHD as compared to patients who remain normotensive (p < 0.05), especially when corrected for body weight (p < 0.01). Patients with elevated PF levels in the first trimester showed a significantly lower uric acid excretion than patients with normal PF levels (p < 0.05). The data show diminished uric acid production in patients who will likely develop preeclampsia suggesting an impaired anti-oxidant production in the first trimester. This observation fits well with the hypothesis that an imbalance between anti-oxidant and oxidants plays an important role in the pathogenesis of preeclampsia.

Acids↗
PubMed1982

Screening procedure for uric acid as indicator of infestation in spices.

Uric acid levels in selected spice products were determined by using a glucose analyzer, modified and calibrated for uric acid. In the method, uricase is used to decompose the uric acid; the reaction is monitored with an oxygen-sensitive electrode. Uric acid levels correlated with infestation as determined by AOAC methods.

Condiments↗
PubMed1994

Dietary aspects of uric acid stone disease.

Kidney stones composed of uric acid present a treatment challenge, particularly in terms of successful prevention of recurrence over the long term. Between 5-12% of all stone patients form calculi composed partially or completely of uric acid. These stones have traditionally been treated with a combination of pharmacological and surgical techniques. The role of diet and fluids in the pathogenesis and management is gradually being recognized and there is potential for dietary intervention to become a major treatment modality for this type of stone. This paper discusses the stone formation process, the metabolism or uric acid and its physical and chemical properties. Specific risk factors for uric acid calculi formation are covered. Dietary protein is reviewed in detail. A comprehensive strategy for the dietary management of uric acid renal calculi disease is suggested.

Journal Article↗