Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “URIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed1984

Decreased renal excretion of uric acid following diuretic administration in rats.

In order to evaluate the cause of diuretic-induced hyperuricemia which has been well documented in clinical studies, clearance experiments were performed in rats using furosemide and trichlormethiazide . The net flux in the tubular transport of uric acid was reabsorptive, and the fractional excretion of uric acid responded sensitively to the transtubular transport inhibitors, sodium probenecid and pyrazinoic acid. When the hemoconcentration was induced by highly potent doses of test diuretics, the inulin clearance and the fractional excretion of uric acid clearly decreased. The contraction of body fluid produced by intraperitoneal administration of polyethylene glycol resulted in marked decrease of inulin clearance and fractional excretion of uric acid. The decrease of uric acid excretory capacity under the treatment with trichlormethiazide was completely corrected by saline loading. Moreover, no significant change was found in the pyrazinoic acid-suppressible fractional excretion of uric acid between the diuretic-treated rats and the control animals. These studies suggest that furosemide- and trichlormethiazide -induced changes in the renal handling of uric acid are mediated by the fluid volume contraction and that the decrease in fractional excretion of uric acid by test diuretics is the result of reabsorptive enhancement of uric acid.

Animals↗
PubMed2005

The serum uric acid and related cardiovascular risk factors in south Taiwan.

Hyperuricemia has been shown to be related to cardiovascular morbidity and mortality. Uric acid is a metabolic product synthesized from nucleic acids, amino acids and the Krebs cycle, reflecting a multiple metabolic associations in humans. The relation between uric acid and various cardiovascular metabolic parameters in Asians has rarely been reported on. In this study, we report the relationship between uric acid and various cardiovascular risk factors in 1,027 healthy Taiwanese adults living in Alien, an agricultural town in subtropical South Taiwan. Serum uric acid levels increased in proportion to age in women, but not in men. There were age and gender-specific correlations between uric acid and various cardiovascular metabolic parameters. Triglycerides and creatinine levels were two independent factors predicting serum uric acid levels in men, while only creatinine predicted uric acid levels in women of all age groups. Processes that influence the metabolism of uric acid and its association with other metabolic parameters differs by gender and age.

Adult↗
PubMed1996

Effect of insulin on renal sodium and uric acid handling in essential hypertension.

In normal subjects, insulin decreases the urinary excretion of sodium, potassium, and uric acid. We tested whether these renal effects of insulin are altered in insulin resistant hypertension. In 37 patients with essential hypertension, we measured the changes in urinary excretion of sodium, potassium, and uric acid in response to physiological euglycemic hyperinsulinemia (by using the insulin clamp technique at an insulin infusion rate of 6 pmol/min/kg). Glucose disposal rate averaged 26.6 +/- 1.5 mumol/min/kg, i.e., 20% lower than in normotensive controls (33.1 +/- 2.1 mumol/min/kg, P = .015) In the basal state, fasting plasma uric acid concentrations were higher in men than women (P < .001), were positively related to body mass index (r = 0.38, P = .02), waist/hip ratio (r = 0.35, P < .05), and serum triglyceride levels (r = 0.59, P = .0001), and negatively related to HDL cholesterol concentrations (r = -0.59, P = .0001) and glucose disposal rate (r = 0.42, P < .01). Uric acid clearance, on the other hand, was inversely related to body mass index (r = 0.41, P = .01), plasma uric acid (r = 0.65, P < .0001) and triglyceride concentrations (r = 0.39, P < .02), and directly related to HDL cholesterol levels (r = 0.52, P < .001). During insulin infusion, blood pressure, plasma uric acid and sodium concentration, and creatinine clearance did not change. In contrast, hyperinsulinemia caused a significant decrease in the urinary excretion of uric acid (2.67 +/- 0.12 to 1.86 +/- .14 mumol/min/1.73 m2, P = .0001), sodium (184 +/- 12 to 137 +/- 14 mumol/min/1.73 m2, P = .0001), and potassium (81 +/- 7 to 48 +/- 4 mumol/ min/1.73 m2, P = .0001). Both in absolute terms (clearance and fractional excretion rates) and percentagewise, these changes were similar to those found in normotensive subjects. Insulin-induced changes in urate excretion were coupled (r = 0.55, P < .0001) to the respective changes in sodium excretion. In hypertensive patients, higher uric acid levels and lower renal urate clearance rates cluster with insulin resistance and dyslipidemia. Despite insulin resistance of glucose metabolism, acute physiological hyperinsulinemia causes normal antinatriuresis, antikaliuresis, and antiuricosuria in these patients.

Adult↗
PubMed2005

Uric acid, microalbuminuria and cardiovascular events in high-risk patients.

BACKGROUND: Elevated levels of serum uric acid and albuminuria are associated with cardiovascular disease, but the relationships have not consistently been demonstrated to be independent of hypertension, other risk factors, or each other. The purpose of this study was to evaluate people at high risk for cardiovascular disease for the influence of uric acid and microalbuminuria on cardiovascular events. METHODS: Consecutive consenting patients undergoing elective angiography (n = 316) had coronary artery disease, risk factors, renal function and diuretic use assessed at baseline. Cardiovascular mortality and major clinical events (myocardial infarction, stroke, amputation, and kidney failure) were ascertained over 5 years. RESULTS: Cardiovascular events occurred in 10% of the patients. Significant correlates (p < 0.05) of cardiovascular events with baseline measures included uric acid > or =5.2 mg/dl, total cholesterol > or =200 mg/dl, severe angiographic coronary artery disease, loop diuretic therapy, and diagnosis of hypertension. A stepwise Cox modeling procedure identified uric acid (p = 0.040), the interaction of hypertension and uric acid (p = 0.029), the interaction of total cholesterol and severe coronary artery disease (p = 0.001) and loop diuretic therapy (p = 0.009) as significant independent predictors of events. Although microalbuminuria was not retained in the final multivariate model, it was associated with poorer cardiovascular disease outcomes. The mean event-free survival for albumin-to-creatinine >30 mg/g was 51 months and for albumin-to-creatinine <30 mg/g the mean was 57 months (p = 0.021). CONCLUSIONS: Uric acid > or =5.2 mg/dl independently imparted a 3.5-fold increased risk (OR 3.5, 95% CI 1.0-11.9) for cardiovascular death and major clinical events over a 5-year period. Uric acid may be a contributing factor to the progression of atherosclerosis and its complications.

Albuminuria↗
PubMed1994

Behavioural and biological correlates of serum uric acid: a study of self-defence officials in Japan.

BACKGROUND: In Japan epidemiological data on correlates of serum uric acid are sparse. METHODS: Behavioural and biological correlates of serum uric acid were investigated in 2487 men who received a retirement health examination at the Self-Defence Forces Fukuoka Hospital from October 1986 through 1990, excluding those under medication for hyperuricaemia, hypertension or hyperlipidaemia. RESULTS: Multiple regression analysis demonstrated that serum creatinine was the strongest correlate followed by serum triglycerides, body mass index and diastolic blood pressure; these four variables accounted for 16% of the overall variation in serum uric acid. Serum total cholesterol, alcohol intake and past smoking were positively associated with serum uric acid levels while diabetes mellitus and serum high density lipoprotein (HDL) cholesterol were negatively related to serum uric acid; these five variables additionally explained 2% of the variation. Although an independent impact was minimal, beer consumption was significantly associated with an elevated level of serum uric acid after allowing for the previously mentioned correlates. CONCLUSIONS: Serum creatinine and triglycerides are major correlates of serum uric acid in Japanese men. Our data add to the body of evidence suggesting that weight control, avoiding excessive drinking and adequate control of hypertension are beneficial in the prevention of hyperuricaemia.

Aged↗
PubMed1999

The presentation of serum lipids and uric acid in cerebral ischemia.

In this study, we examine the relationship between serum lipids and uric acid in nonembolic cerebral ischemia (NECI) patients. The serum level of total cholesterol (TC) and uric acid increased significantly in male, while TC and triglyceride in female patients. The increase of TC was more significance in female patients. There was no correlation between serum lipids and uric acid in NECI patients or controls, but a significant correlation between triglyceride and uric acid was present in diabetic patient. These findings suggest that lipids and uric acid are essential risk factors for cerebral ischemia in our population. Although there is no association of their metabolism, their parallellic abnormality in diabetic NECI individuals indicates that some possible factors changing in diabetics can influence the metabolic pathway of both lipid and uric acid, which may promote each other for atherogenesis in diabetics.

Aged↗
PubMed2004

Uric acid: role in cardiovascular disease and effects of losartan.

A substantial body of epidemiological and experimental evidence suggests that serum uric acid is an important, independent risk factor for cardiovascular and renal disease especially in patients with hypertension, heart failure, or diabetes. Elevated serum uric acid is highly predictive of mortality in patients with heart failure or coronary artery disease and of cardiovascular events in patients with diabetes. Further, patients with hypertension and hyperuricemia have a 3- to 5-fold increased risk of experiencing coronary artery disease or cerebrovascular disease compared with patients with normal uric acid levels. Although the mechanisms by which uric acid may play a pathogenetic role in cardiovascular disease is unclear, hyperuricemia is associated with deleterious effects on endothelial dysfunction, oxidative metabolism, platelet adhesiveness, hemorheology, and aggregation. Xanthine oxidase inhibitors (e.g., allopurinol) or a variety of uricosuric agents (e.g., probenecid, sulfinpyrazone, benzbromarone, and benziodarone) can lower elevated uric acid levels but it is unknown whether these agents reversibly impact cardiovascular outcomes. However, the findings of the recent LIFE study in patients with hypertension and left ventricular hypertrophy suggest the possibility that a treatment-induced decrease in serum uric acid may indeed attenuate cardiovascular risk. LIFE showed that approximately 29% (14% to 107%, p = 0.004) of the treatment benefit of a losartan-based versus atenolol-based therapy on the primary composite endpoint (death, myocardial infarction, or stroke) may be ascribed to differences in achieved serum uric acid levels. Overall, serum uric acid may be a powerful tool to help stratify risk for cardiovascular disease. At the very least, it should be carefully considered when evaluating overall cardiovascular risk.

Angiotensin Receptor Antagonists↗
PubMed2005

Intake of purine-rich foods, protein, and dairy products and relationship to serum levels of uric acid: the Third National Health and Nutrition Examination Survey.

OBJECTIVE: Various commonly consumed foods have long been suspected of affecting the serum uric acid level, but few data are available to support or refute this impression. Our objective was to evaluate the relationship between dietary factors and serum uric acid levels in a nationally representative sample of men and women in the US. METHODS: Using data from 14,809 participants (6,932 men and 7,877 women) ages 20 years and older in the Third National Health and Nutrition Examination Survey (for the years 1988-1994), we examined the relationship between the intake of purine-rich foods, protein, and dairy products and serum levels of uric acid. Diet was assessed with a food-frequency questionnaire. We used multivariate linear regression to adjust for age, sex, total energy intake, body mass index, use of diuretics, beta-blockers, allopurinol, and uricosuric agents, self-reported hypertension and gout, serum creatinine level, and intake of alcohol. RESULTS: The serum uric acid level increased with increasing total meat or seafood intake and decreased with increasing dairy intake. After adjusting for age, the differences in uric acid levels between the extreme quintiles of intake were 0.48 mg/dl for total meat (95% confidence interval [95% CI] 0.34, 0.61; P < 0.001 for trend), 0.16 mg/dl for seafood (95% CI 0.06, 0.27; P = 0.005 for trend), and -0.21 mg/dl for total dairy intake (95% CI -0.37, -0.04; P = 0.02 for trend). After adjusting for other covariates, the differences between the extreme quintiles were attenuated but remained significant (P < 0.05 for all comparisons). The total protein intake was not associated with the serum uric acid level in multivariate analyses (P = 0.74 for trend). Those who consumed milk 1 or more times per day had a lower serum uric acid level than did those who did not drink milk (multivariate difference -0.25 [95% CI -0.40, -0.09]; P < 0.001 for trend). Similarly, those who consumed yogurt at least once every other day had a lower serum uric acid level than did those who did not consume yogurt (multivariate difference -0.26 [95% CI -0.41, -0.12]; P < 0.001 for trend). CONCLUSION: These findings from a nationally representative sample of adults in the US suggest that higher levels of meat and seafood consumption are associated with higher serum levels of uric acid but that total protein intake is not. Dairy consumption was inversely associated with the serum uric acid level.

Adult↗
PubMed1998

Holmium:YAG lithotripsy: photothermal mechanism converts uric acid calculi to cyanide.

PURPOSE: Holmium:YAG lithotripsy fragments stones through a photothermal mechanism. Uric acid when heated is known to be converted into cyanide. We test the hypothesis that holmium: YAG lithotripsy of uric acid calculi produces cyanide. MATERIALS AND METHODS: Human calculi of known uric acid composition were irradiated with holmium:YAG energy in water. Stones received a total holmium:YAG energy of 0 (control), 0.1, 0.25, 0.5, 0.75, 1.0 or 1.25 kJ. The water in which lithotripsy was performed was analyzed for cyanide concentration. A graph was constructed to relate holmium:YAG energy to cyanide production. RESULTS: Holmium:YAG lithotripsy of uric acid calculi in vitro produced cyanide consistently. Cyanide production correlated with total holmium:YAG energy (p <0.001). CONCLUSIONS: Holmium:YAG lithotripsy of uric acid calculi risks production of cyanide. This study raises significant safety issues.

Aluminum Silicates↗
PubMed1996

[Uric acid level in human aqueous and vitreous humor].

Uric acid--a potent endogenous antioxidant--may play a certain role in some eye diseases. However, its content in intraocular humors has not been examined so far. Samples of aqueous and vitreous humor were collected from 32 dead persons for examination. Uric acid was marked by indirect method with uricase. Uric acid level in aqueous humor ranges from 166.67 to 446.4 mumol/l (mean 309.34), whereas in vitreous humor from 77.38 to 452.00 mumol/l (mean 220.80).

Aqueous Humor↗
PubMed2005

Correlation of uric acid and urinary albumin excretion rate in patients with type 2 diabetes mellitus in Taiwan.

BACKGROUND: Uric acid is detrimental to the kidneys in animal models. However, its role in human diabetic nephropathy has not been extensively studied. This study evaluated the association between serum uric acid and urinary albumin-to-creatinine ratio (ACR) among patients with type 2 diabetes mellitus in Taiwan. METHODS: A total of 343 patients (144 men and 199 women), aged 62.8 +/- 10.8 years and not using uric acid-lowering agents, diuretics, or alcohol, were recruited. Serum uric acid and urinary ACR were determined. Normoalbuminuria, microalbuminuria, and macroalbuminuria were defined as ACR <30.0, 30.0 to 299.9, and > or =300.0 microg/mg, respectively. RESULTS: The respective uric acid levels for normoalbuminuria (N= 166), microalbuminuria (N= 130), and macroalbuminuria (N= 47) were 5.2 +/- 1.6 mg/dL, 5.6 +/- 1.9 mg/dL, and 6.7 +/- 2.1 mg/dL (P < 0.001). The mean +/- SD (minimum-maximum) values of uric acid for the first to the fourth quartile were 3.4 +/- 0.6 (1.7-4.2), 4.9 +/- 0.4 (4.3-5.4), 6.0 +/- 0.3 (5.5-6.5), and 8.1 +/- 1.2 (6.6-12.2), respectively. Prevalence of abnormal albuminuria (microalbuminuria plus macroalbuminuria) for the respective quartiles were 38.4%, 51.2%, 50.6%, and 66.3% (P trend <0.01). In men, uric acid correlated positively with triglycerides and natural logarithmic [ln (ACR)] (gamma= 0.168, P < 0.05). In women, uric acid correlated positively with triglycerides, ln (ACR) (gamma= 0.277, P < 0.01) and body mass index (borderline significant P < 0.1), but negatively with calculated creatinine clearance. The standardized regression coefficient for ln (ACR) and the odds ratio for abnormal albuminuria for every 1 mg/dL increment of uric acid after adjusting for calculated creatinine clearance and other confounders were 0.138 (P < 0.05) and 1.183 (1.025-1.364), respectively. The results after excluding 127 cases with a history of hypertension were similar. CONCLUSION: Serum uric acid is an independent correlate of urinary ACR in Taiwanese patients with type 2 diabetes mellitus.

Aged↗
PubMed1998

Uric acid protects neurons against excitotoxic and metabolic insults in cell culture, and against focal ischemic brain injury in vivo.

Uric acid is a well-known natural antioxidant present in fluids and tissues throughout the body. Oxyradical production and cellular calcium overload are believed to contribute to the damage and death of neurons that occurs following cerebral ischemia in victims of stroke. We now report that uric acid protects cultured rat hippocampal neurons against cell death induced by insults relevant to the pathogenesis of cerebral ischemia, including exposure to the excitatory amino acid glutamate and the metabolic poison cyanide. Confocal laser scanning microscope analyses showed that uric acid suppresses the accumulation of reactive oxygen species (hydrogen peroxide and peroxynitrite), and lipid peroxidation, associated with each insult. Mitochondrial function was compromised by the excitotoxic and metabolic insults, and was preserved in neurons treated with uric acid. Delayed elevations of intracellular free calcium levels induced by glutamate and cyanide were significantly attenuated in neurons treated with uric acid. These data demonstrate a neuroprotective action of uric acid that involves suppression of oxyradical accumulation, stabilization of calcium homeostasis, and preservation of mitochondrial function. Administration of uric acid to adult rats either 24 hr prior to middle cerebral artery occlusion (62.5 mg uric acid/kg, intraperitoneally) or 1 hr following reperfusion (16 mg uric acid/kg, intravenously) resulted in a highly significant reduction in ischemic damage to cerebral cortex and striatum, and improved behavioral outcome. These findings support a central role for oxyradicals in excitotoxic and ischemic neuronal injury, and suggest a potential therapeutic use for uric acid in ischemic stroke and related neurodegenerative conditions.

Animals↗
PubMed2002

The role of serum uric acid as a prognostic indicator of the severity of maternal and fetal complications in hypertensive pregnancies.

OBJECTIVE: To examine whether an elevated serum uric acid level in hypertensive pregnant women is a useful prognostic indicator of severe hypertension; hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome; and small for gestational age (SGA) infants. METHODS: A total of 459 women newly diagnosed with hypertension in pregnancy were categorized into "gestational hypertension" and "hypertension with proteinuria (preeclampsia)" groups. Their serum uric acid levels were correlated with the development of HELLP syndrome, severity of hypertension, and incidence of SGA newborns (< 10th percentile birth weight). HELLP syndrome was divided into 3 classes depending on the severity of the thrombocytopenia. Prior to this study, serum uric acid levels had been measured in a group of normotensive women. Mean and standard deviation of serum uric acid levels for each group were compared using analysis of variance and student t-tests, where necessary. RESULTS: Significant elevation in serum uric acid levels over normotensive pregnant women (285 +/- 72 micromol/L) was observed in both the gestational hypertensive group (341 +/- 83 micromol/L) and the preeclamptic group (384 +/- 93 micromol/L) of women (p < 0.001 and p < 0.05 respectively). Serum uric acid levels were also significantly elevated (p < 0.001) in women with gestational hypertension with HELLP syndrome (382 +/- 78 micromol/L) compared to those without HELLP syndrome (330 +/- 80 micromol/L). Preeclamptic women with HELLP syndrome (412 +/- 99 micromol/L) also demonstrated elevated uric acid levels (p < 0.05) over those without HELLP syndrome (374 +/- 87 micromol/L). However, the level of uric acid did not predict the severity of HELLP syndrome. The presence of SGA infants in the gestational hypertensive group was not associated with increased uric acid levels. CONCLUSION: Uric acid levels, although significantly elevated in women with gestational hypertension and preeclampsia as compared to normotensive pregnant women, are not good prognostic indicators of the severity of the maternal or fetal complications.

Biomarkers↗
PubMed2004

BSE and vCJD cause disturbance to uric acid levels.

Bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) are two new members of the family of neurodegenerative conditions termed prion diseases. Oxidative damage has been shown to occur in prion diseases and is potentially responsible for the rapid neurodegeneration that is central to the pathogenesis of these diseases. An important nonenzymatic antioxidant in the brain is uric acid. Analysis of uric acid in the brain and cerebrospinal fluid (CSF) of cases of BSE and CJD showed a specific reduction in CSF levels for both BSE and variant CJD, but not sporadic CJD. Further studies based on cell culture experiments suggested that uric acid in the brain was produced by microglia. Uric acid was also shown to inhibit neurotoxicity of a prion protein peptide, production of the abnormal prion protein isoform (PrP(Sc)) by infected cells, and polymerization of recombinant prion protein. These findings suggest that changes in uric acid may aid differential diagnosis of vCJD. Uric acid could be used to inhibit cell death or PrP(Sc) formation in prion disease.

Animals↗
PubMed1978

Enhancement of renal excretion of uric acid during long-term thiazide therapy.

The effect of thiazide (hydrochlorothiazide 100 mg per day orally in two divided doses for up to 3 years) on uric acid metabolism was examined in 21 patients with renal stones suffering from renal hypercalciuria or absorptive hypercalciuria. Serum concentration of uric acid increased during thiazide therapy in every patient. In 12 of 21 patients, there was a transient or persistent rise in urinary uric acid of more than 50 mg per day during treatment. The mean urinary uric acid produced by thiazide was positively correlated with the change in the renal clearance of uric acid. Thus, an increase in urinary uric acid was often associated with a rise in uric acid clearance. The results suggest that thiazide may either increase the production of uric acid or decrease the extrarenal disposal of uric acid, in some patients.

Administration, Oral↗
PubMed2001

Biochemical profile of idiopathic uric acid nephrolithiasis.

BACKGROUND: The objective of this study was to elucidate a biochemical profile of patients with idiopathic uric acid nephrolithiasis, without secondary causes (such as dehydration or diarrhea). Study subjects comprised 56 patients with idiopathic uric acid nephrolithiasis (UA stone group) who underwent a full outpatient evaluation. The control group was composed of 54 with absorptive hypercalciuria and 2 normal subjects, matched with the UA stone group according to age, body mass index, and gender. METHODS: Urinary pH and ammonium and serum and urinary uric acid were measured. The fractional excretion of urate was calculated. RESULTS: Compared with the control group, the UA stone group had a significantly higher serum uric acid and significantly lower urinary uric acid, pH (5.34 +/- 0.23 vs. 6.17 +/- 0.36, P < 0.001), and fractional excretion of urate (0.052 +/- 0.028 vs. 0.080 +/- 0.029, P < 0.001), but individual values overlapped considerably between the two groups. Discriminant analysis of the relationship between urinary pH and fractional excretion of urate yielded a "discriminant score," which provided a much better separation between the two groups, with a correct classification in 95.5% of subjects. In contrast, urinary ammonium, citrate, sulfate, and potassium did not differ between two groups. CONCLUSIONS: In idiopathic uric acid nephrolithiasis, urinary pH and fractional excretion of urate are significantly lower than in control subjects, suggestive of defects in urinary acidification and urate excretion. Since these impairments are believed to be associated with primary gout, the underlying disturbance in idiopathic uric acid nephrolithiasis may be primary gout.

Adult↗
PubMed1996

[Abnormal serum uric acid level in endocrine disorders].

Among the factors, which may influence on the uric acid metabolism, the excess or deficiency of some hormones apparently induces the abnormal serum uric acid level. We described hyperuricemia and hypouricemia associated with endocrine disorders. Hyperuricemia due to the increased production of uric acid is observed in myopathy associated with hypothyroidism, hyperthyroidism or hypoparathyroidism. Hyperuricemia due to the decreased renal uric acid clearance is associated with hypopituitarism, hypothyroidism, hyperparathyroidism, central diabetes insipidus, nephrogenic diabetes insipidus, Bartter syndrome, and diabetic ketoacidosis. Hypouricemia due to the increased renal uric acid clearance is associated with hypoparathyroidism, primary aldosteronism and inappropriate secretion of antidiuretic hormone (SIADH).

Adrenal Glands↗