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PubMed1966

The treatment of gout and disorders of uric acid metabolism with allopurinol.

Allopurinol (4-hydroxypyrazolo (3,4-d)-pyrimidine) is a potent xanthine oxidase inhibitor which inhibits the oxidation of naturally occurring oxypurines, thus decreasing uric acid formation. The clinical and metabolic effects of this agent were studied in 80 subjects with primary and secondary gout and other disorders of uric acid metabolism. Allopurinol has been universally successful in lowering the serum uric acid concentration and uric acid excretion to normal levels, while not significantly affecting the clearance of urate or other aspects of renal function. Oxypurine excretion increased concomitantly with the fall in urine uric acid. The agent is particularly valuable in the management of problems of gout with azotemia, acute uric acid nephropathy and uric acid urolithiasis. The minor side effects, clinical indications and theoretical complications are discussed.

Aged↗
PubMed1991

Theophylline-induced increase in plasma uric acid--purine catabolism increased by theophylline.

The effect of theophylline on the concentration of uric acid in plasma was investigated. Theophylline increased the plasma concentrations of purine bases (uric acid, hypoxanthine and xanthine) without a decreased urinary excretion of these purine bases in normal subjects. 1-methyl uric acid, a metabolite of theophylline, was not converted to uric acid in a detectable level by the hepatoma-derived cell line HuH-7 cells. Although theophylline affected neither the concentration of nucleotides nor the activities of the enzymes related to purine metabolism (hypoxanthine-guanine phosphoribosyl transferase, 5'-nucleotidase, adenosine deaminase and purine nucleoside phosphorylase) in erythrocytes, these results suggested that theophylline-induced purine degradation seems to be a cause of the increased concentration of uric acid in plasma.

Administration, Oral↗
PubMed2002

AT1 blockers and uric acid metabolism: are there relevant differences?

BACKGROUND: Serum urate is commonly elevated in essential hypertension (26-33%). Some studies have claimed that losartan increases urinary uric acid excretion and diminishes serum urate levels. However, a detailed, controlled study on the influence of losartan on uric acid metabolism in hypertensive patients has not been performed and the existent results are conflicting. Two small studies claimed that losartan reduced serum urate levels but only one showed a simultaneous increased uric acid excretion rate. The development of several AT1 receptor blockers raises the question whether these antihypertensive drugs influence uric acid metabolism. STUDY: In a randomized, prospective (4 weeks), double blind, parallel study we have compared the influence of losartan (50 mg/day) versus eprosartan (600 mg/day) on uric acid metabolism in 58 patients with mild to moderate essential hypertension. The mean uric acid to creatinine ratio change from baseline at 4 weeks was +0.11 for losartan and -0.04 for eprosartan (P < 0.01). The mean increase in 24-h urinary uric acid excretion with losartan was +0.7 mmol/24 h (25% increase from baseline). The change in serum urate levels versus baseline was similar after 4 weeks with losartan (-23.4 mumol/l) and eprosartan (-19.5 mumol/l). Patients with hyperuricemia in both treatment groups showed similar modifications of uric acid metabolism compared with non-hyperuricemic subjects. Blood pressure control was achieved in 22 patients (73%) with eprosartan and in 16 (53%) with losartan. CONCLUSIONS: Losartan increased uric acid excretion in hypertensive patients but eprosartan did not. Neither AT1 receptor antagonist substantially modified serum urate concentrations.

Acrylates↗
PubMed1982

Pathogenesis and clinical course of mixed calcium oxalate and uric acid nephrolithiasis.

By direct measurement, urine from patients who form calcium oxalate stones was supersaturated abnormally with respect to calcium oxalate monohydrate but not supersaturated with respect to undissociated uric acid. Urine from patients who form uric acid stones was supersaturated excessively with undissociated uric acid but not calcium oxalate. Patients who form both calcium oxalate and uric acid stones, however, produce urine that is supersaturated with respect to both solid phases. Low urine pH was the primary factor that increased supersaturation with respect to undissociated uric acid. The formation of both calcium oxalate and uric acid stones appears to be explained by a dual abnormality of urine supersaturation.

Calcium Oxalate↗
PubMed1993

Physiologic levels of uric acid inhibit xanthine oxidase in human plasma.

Xanthine oxidase, a key source of reactive oxygen species, and purine substrates are detected in the circulation after ischemia-reperfusion. High levels of uric acid, produced by a xanthine oxidase-catalyzed reaction, are found in human plasma. We studied whether uric acid could alter xanthine oxidase activity in plasma obtained from eight adults and eight neonates. Known amounts of uric acid were added to xanthine and xanthine oxidase-supplemented buffer and plasma, and the production of uric acid and superoxide was determined. Uric acid, 150 and 300 microM, decreased the oxidation of xanthine to uric acid in adult plasma by 37.5 +/- 5.6 and 48.9 +/- 6.1% and formation of superoxide by 23.2 +/- 1.9 and 32.0 +/- 2.3%, respectively, compared with plasma without uric acid. In newborn plasma, a similar pattern and extent of inhibition was observed. Superoxide formation, however, was inhibited to a greater extent than in adult plasma. Endogenous xanthine oxidase was detected in newborn plasma in nine additional neonates using HPLC. These results indicate that uric acid is an effective inhibitor of the formation of superoxide and hydrogen peroxide by xanthine oxidase at the levels found in human plasma. Plasma uric acid may play an important role in attenuating the oxidant-mediated tissue damage caused by xanthine oxidase released into the circulation during ischemia-reperfusion.

Adult↗
PubMed1996

Evidence in hyponatremia related to inappropriate secretion of ADH that V1 receptor stimulation contributes to the increase in renal uric acid clearance.

In hyponatremia related to syndrome of inappropriate antidiuretic hormone (SIADH), hypouricemia is explained primarily by the high uric acid clearance rate that results from the decrease in tubular uric acid reabsorption. This modification of tubular handling of uric acid is considered to be induced by the increase in the "effective vascular volume". This study was designed to determine if V1-receptor stimulation participates in the development of a high uric acid clearance rate as in SIADH, in which the antidiuretic hormone acts on V1 and V2 receptors. Therefore, the urate clearance rate was measured in seven volunteers with 1-desamino-8-D-arginine vasopressin (dDAVP)-induced hyponatremia, with dDVAP stimulating exclusively the V2 receptors (Group I), and in six patients with SIADH (Group II) during both normo- and hyponatremia. As expected, in both groups, the serum uric acid concentration decreased during hyponatremia, but did so to a larger extent in the patients with SIADH (-53% versus -29%, P < 0.02). Despite similar levels of hyponatremia (126 +/- 5 mmol/L and 125 +/- 5.5 mmol/L), of hypoproteinemia (64 +/- 5 g/L and 63 +/- 5 g/L) and of salt excretion (FENa, 0.66 +/- 0.28% and 0.73 +/- 0.25%), the urate clearance (8.3 +/- 3.3 mL/min) and the fractional excretion of filtered uric acid (5.7 +/- 2%) in Group I were not significantly different during hyponatremia than during normonatremia (6.4 +/- 1.5 mL/min and 5.4 +/- 0.9%). On the other hand, in Group II, both parameters were increased (17.8 +/- 2.9 mL/min and 19.6 +/- 5.3%; P < 0.001) and both values were higher than in the dDAVP-induced hyponatremia (P < 0.01). Additionally, the administration of a potent V1-receptor agonist (triglycyl-lysine-vasopressin) in a patient with central diabetes insipidus with preexisting dDAVP-induced hyponatremia produced a rapid increase of urate clearance. Because dDAVP acts only on the V2 receptors, these data suggest that the higher urate clearance observed during hyponatremia related to SIADH is not only the consequence of an increased "effective vascular volume," but that V1-receptor stimulation also contributes to it, by a mechanism that remains to be determined.

Adult↗
PubMedDate not supplied

Effect of valsartan on renal handling of uric acid in healthy subjects.

OBJECTIVE: To evaluate the effect of valsartan on renal handling of uric acid in healthy subjects. METHODS: A randomized, single-blind, placebo-controlled clinical trial was performed in twelve healthy volunteers. Six received a morning dose of valsartan 80 mg orally during 14 to 21 days and the other six received placebo. Before and after valsartan or placebo, clearance, fractional excretion and excretion uric acid rates were calculated. Presecretory reabsorption, tubular secretion and postsecretory reabsorption of uric acid were assessed by pharmacological tests using pyrazinamide or probenecid. RESULTS: There were no differences in clearance, fractional excretion and excretion uric acid rates with valsartan and placebo. Valsartan did not affect presecretory reabsorption (p = 0.92), tubular secretion (p = 0.62) or postsecretory reabsorption (p = 0.52) of uric acid. CONCLUSION: Valsartan did not significantly affect renal handling of uric acid in healthy subjects.

Adult↗
PubMed1996

Simultaneous determination of uric acid and creatinine in biological fluids by column-switching liquid chromatography with ultraviolet detection.

A column-switching liquid chromatographic method for the simultaneous determination of uric acid and creatinine in human serum and urine was developed. Creatinine and uric acid were separated by size-exclusion chromatography on a hydrophilic gel column (C1) and creatinine eluted from C1 was separated from proteins by filtration through a longer hydrophilic gel column (C2). The creatinine fraction eluted from C2 was transferred to a weakly acidic cation-exchange column (C3) and then to a strongly acidic cation-exchange column (C4). Uric acid eluted from C1 after creatinine was transferred to an anion-exchange column (C5) and then to a hydrophilic gel column (C6). The mobile phase was a mixed buffer of pH 5.1 (propionic acid-succinic acid-NaOH, 60:15:60 mmol/l in water). Diluted serum and urine could be injected onto C1, and C1 was backflushed after the transfer of uric acid from C1 to C5. Creatinine and uric acid in the eluate were determined by measuring their ultraviolet absorption at 234 and 290 nm, respectively. The recovery of uric acid and creatinine added to diluted serum (20-fold dilution, concentration 20 and 5 mumol/l, respectively) was 98.9 +/- 0.56% and 100.9 +/- 1.29%, respectively. The recovery of uric acid and creatinine added to diluted urine (100-fold dilution, concentration 50 and 100 mumol/l, respectively) was 99.4 +/- 0.72% and 98.7 +/- 1.45%, respectively (mean +/- R.S.D., n = 6).

Chromatography, Gel↗
PubMed2005

Association between serum uric acid, metabolic syndrome, and carotid atherosclerosis in Japanese individuals.

OBJECTIVE: There are few data available on possible independent association between uric acid and carotid atherosclerosis. Here we first sought to investigate association between uric acid levels and metabolic syndrome in Japanese; second, we assessed whether there is an independent association of uric acid with prevalence of carotid atherosclerosis in individuals subdivided according to gender and metabolic syndrome status. METHODS AND RESULTS: Cross-sectional data from 8144 individuals who underwent general health screening were analyzed. After adjusting for age, total cholesterol, and smoking status, the odds ratios (95% CI) of sex-specific quartiles of serum uric acid for metabolic syndrome were 1.0, 1.06 (0.60 to 1.87), 2.18 (1.30 to 3.64), and 4.17 (2.56 to 6.79) in women, and 1.0, 0.92 (0.74 to 1.14), 1.52 (1.25 to 1.65), and 1.97 (1.61 to 2.40) in men. After adjusting for age, serum levels, total cholesterol, and smoking status, prevalence of carotid plaque was higher in subjects in the second, third, and fourth quartiles of uric acid level with odds ratios (95% CI) of 1.24 (1.01 to 1.52), 1.37 (1.11 to 1.68), and 1.31 (1.05 to 1.63), respectively, in men without metabolic syndrome but not in men with metabolic syndrome or in women with or without metabolic syndrome. CONCLUSIONS: The prevalence of metabolic syndrome showed a graded increase according to serum uric acid values in both genders. In men who did not have metabolic syndrome, uric acid was found to be an independent risk factor for incidence of carotid plaque.

Adult↗
PubMed2000

Haemodynamic correlates and prognostic significance of serum uric acid in adult patients with Eisenmenger syndrome.

OBJECTIVE: To assess haemodynamic correlates and prognostic significance of serum uric acid in adult patients with Eisenmenger syndrome. DESIGN: Retrospective observational study. SETTING: Tertiary referral centre. PATIENTS: 94 adult patients with Eisenmenger syndrome who were diagnosed between September 1982 and July 1998. MAIN OUTCOME MEASURES: Serum uric acid was measured in all patients, together with clinical and haemodynamic variables related to mortality. RESULTS: Serum uric acid was raised in patients with Eisenmenger syndrome compared with age and sex matched control subjects (7.0 v 4.7 mg/dl, p < 0.0001) and increased in proportion to the severity of New York Heart Association functional class. Serum uric acid was positively correlated with mean pulmonary arterial pressure (r = 0.30, p = 0.0052) and total pulmonary resistance index (r = 0.55, p < 0.0001), and negatively correlated with cardiac index (r = -0.50, p < 0.0001). During a mean follow up period of 97 months, 38 patients died of cardiopulmonary causes. Among various clinical, echocardiographic, and laboratory variables, serum uric acid remained predictive in multivariate analysis. Kaplan-Meier survival curves based on median serum uric acid showed that patients with high values had a significantly worse survival rate than those with low values (log-lank test: p = 0.0014 in male patients, p = 0.0034 in female patients). CONCLUSIONS: Serum uric acid increases in proportion to haemodynamic severity in adult patients with Eisenmenger syndrome and is independently associated with long term mortality.

Adolescent↗
PubMed2006

The relationship between uric acid and its oxidative product allantoin: a potential indicator for the evaluation of oxidative stress in birds.

Uric acid is the main nitrogenous waste product in birds but it is also known to be a potent antioxidant. Hominoid primates and birds lack the enzyme urate oxidase, which oxidizes uric acid to allantoin. Consequently, the presence of allantoin in their plasma results from non-enzymatic oxidation. In humans, the allantoin to uric acid ratio in plasma increases during oxidative stress, thus this ratio has been suggested to be an in vivo marker for oxidative stress in humans. We measured the concentrations of uric acid and allantoin in the plasma and ureteral urine of white-crowned sparrows (Zonotrichia leucophrys gambelii) at rest, immediately after 30 min of exercise in a hop/hover wheel, and after 1 h of recovery. The plasma allantoin concentration and the allantoin to uric acid ratio did not increase during exercise but we found a positive relationship between the concentrations of uric acid and allantoin in the plasma and in the ureteral urine in the three activity phases. In the plasma, the slope of the regression describing the above positive relationships was significantly higher immediately after activity. We suggest that the slope indicates the rate of uric acid oxidation and that during activity this rate increases as a result of higher production of free radicals. The present study demonstrates that allantoin is present in the plasma and in the ureteral urine of white-crowned sparrows and therefore might be useful as an indicator of oxidative stress in birds.

Allantoin↗
PubMed1978

The effects of fasting in Ramadan. 1. Serum uric acid and lipid concentrations.

1. The changes in serum levels of uric acid and lipids during 1 month of starvation-refeeding were measured in sixteen male volunteers. 2. Uric acid levels increased linearly with the duration of the experiment. The increase was positively correlated with the increase in serum triglycerides but not with cholesterol or phospholipids. 3. Triglycerides increased at a faster rate than uric acid implying that the increase in uric acid was secondary to that of the lipid. 4. It was concluded that the purine and lipid synthetic pathways are linked through a common small-molecular-weight effector rather than through the sharing of a common enzyme.

Adult↗
PubMed2002

Pathophysiology of uric acid nephrolithiasis.

Humans although a predominantly ureotylic organism, has preserved the ability to excrete nitrogen as uric acid and ammonia. An imbalance between these two secondary modes of nitrogen excretion has resulted in uric acid precipitation in human urine. Uric acid nephrolithiasis can arise from diverse etiologies all with distinct underlying defects converging to one or more of three defects of hyperuricosuria, acidic urine pH, and low urinary volume, originating from secondary, genetic or heretofore undefined (idiopathic) causes. A subset of idiopathic uric acid nephrolithiasis (gouty diathesis) may be the "tip of the icebergp" of a broader systemic illness characterized by insulin resistance. A novel renal manifestation of insulin resistance is a mild defect in ammonium excretion, which is not severe enough to disturb acid-base homeostasis, but is sufficient to set up the chemical milieu for uric acid nephrolithiasis.

Humans↗
PubMed1989

On-line electrochemistry/thermospray/tandem mass spectrometry as a new approach to the study of redox reactions: the oxidation of uric acid.

The electrochemical oxidation pathway of uric acid was determined by on-line electrochemistry/thermospray/tandem mass spectrometry. Intermediates and products formed as a result of electrooxidation were monitored as the electrode potential was varied. Several reaction intermediates have been identified and characterized by tandem mass spectrometry. The tandem mass spectrometric results provide convincing evidence that the primary intermediate produced during the electrooxidation of uric acid has a quinonoid diimine structure. The results indicate that once formed via electrooxidation, the primary intermediate can follow three distinct reaction pathways to produce the identified final products. The final electrochemical oxidation products observed in these studies were urea, CO2, alloxan, alloxan monohydrate, allantoin, 5-hydroxyhydantoin-5-carboxamide, and parabanic acid. The solution reactions that follow the initial electron transfer at the electrode are affected by the vaporizer tip temperature of the thermospray probe. In particular, it was found that at different tip temperatures either hydrolysis or ammonolysis reactions of the initial electrochemical oxidation products can occur. Most importantly, the results show that the on-line combination of electrochemistry with thermospray/tandem mass spectrometry provides otherwise difficult to obtain information about redox and associated chemical reactions of biological molecules such as the structure of reaction intermediates and products, as well as providing insight into reaction pathways.

Chemical Phenomena↗
PubMed1994

[In situ dissolution of uric acid obstructive calculi].

The dissolution of uric acid calculi can be obtained by per os or parenteral alkalinization, but this method cannot be used in case of obstructive calculi. With 3 patients, whose urinary tract was obstructed by a radio-transparent calculi at the pyelo-ureteral junction, the ureteral probe setting by endoscopic way permitted to realize the in situ alkalinization. After 5 to 11 days of treatment, the calculi have been completely dissolved. A patient also presented a slightly radio-opaque lithiasis, but it remained still. The in situ alkalinization is an effective and non invasive treatment in case of obstructive uric acid calculi, and completes the release of the urinary tract logically by ureteral probe setting.

Adult↗
PubMed1979

[Uric-acid reduction with high allopurinol dosages (author's transl)].

At the high dosage of 600 mg daily, the uric-acid reducing effect of allopurinol depends on the initial level of uric-acid concentration in the same manner as at the usual dosage of 300 mg daily, but is more marked at the entire hyperuricaemic concentration range of 65--71 mumol/l (11--12 mg/l). After eight days at the same dosage of 600 mg daily allopurinol there is a highly significant correlation between the two variables, corresponding to the equation of uric acid effect of allopurinol = 0.893 x serum uric-acid concentration--29.27. At an uric-acid concentration of 476 mumol/l (80 mg/l); at a uric-acid level of about 595 mumol/l (100 mg/l) the average concentration reduction will be around 357 mumol/l (60 mg/l).

Aged↗