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PubMed1987

The antisickling role of uric acid in sickle cell disease.

Based on the antisickling properties of structurally similar compounds, uric acid (urate) was investigated and found to possess antisickling activity on sickle cell erythrocytes, in particular at higher urate concentrations. Serum urate levels were subsequently determined for 60 sickle cell patients of both sexes within the age limit of 1-27 years. The mean serum urate values were computed at discrete age groups, and the values obtained were compared with the mean serum urate concentration for 15 normal subjects of both sexes and similar age range. Although a definite age-dependent trend did exist in the mean serum urate concentration in sickle cell disease (SCD), this elevation could not be truly referred to as "hyperuricaemia'. Hence, any possible contribution by elevated serum urate to a gouty trait and SCD bone crisis remains unclear. However, these observed serum urate values corresponded well with those concentrations which inhibited the sickling of sickle cell erythrocytes in vitro, permitting the speculation that the elevated serum urate might well be beneficial to sickle cell patients in a compensatory way.

Adolescent↗
PubMed1987

[Influence of acute administration of ramipril on the excretion of uric acid].

The influence of a new ACEI, Ramipril (R) on renal handling of UA was investigated. 13 hypertensives with normal renal function received either R (10 mg p.o.) or placebo (P). Arterial pressure (AP), GFR (Inulin clearance), Renal Plasma Flow (RPF, PAH clearance), UA urinary excretion (UAV) and fractional clearance (FeAU: UA clearance/GFR) were studied for seven hours after drug administration. GFR remained stable in all cases. R had no effect on sodium excretion rate. Compared to P, R significantly increased UAV by 25 p. 100, FeAU by 32 p. 100, RPF by 26.5 p. 100 and decreased mean arterial pressure (MAP) by 10 p. 100. ACE activity was maximally suppressed at 2 hours. More than 80 p. 100 of the maximal changes in UAU and FeAU were observed within the first two hours, while a progressive increase in RPF up to the fifth hour, and a progressive fall in MAP up to the fourth hour was evident. Except for PAM, all these changes were still present at the end of the study (seventh hour). In conclusion, Ramipril increases the fractional excretion of uric acid. This effect is observed independently of any change in sodium balance and preceeds by two to three hours the changes in renal hemodynamics. The simultaneous changes in FeAU and in ACE activity indicate that the effect on uric acid excretion is presumably due to the fall in angiotensin concentration.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Plasma uric acid level and risk for incident hypertension among men.

Several studies have found that uric acid (UA) level is associated with an increased risk for hypertension, but the association could be confounded by metabolic factors that were not included in these previous studies. UA level and risk for incident hypertension was examined prospectively among men who participated in the Health Professionals' Follow-up Study. From among men without hypertension at the time blood was collected, 750 participants who developed hypertension during the subsequent 8 yr and 750 age-matched controls were selected. In addition to adjustment for standard hypertension risk factors and renal function, adjustments controlled for fasting insulin, triglyceride, and cholesterol levels. The mean age of participants was 61 yr, and mean plasma UA level was 6.0 mg/dl (SD 1.25 mg/dl). The multivariable relative risk (RR) for a 1-SD increase in UA was 1.02 (95% confidence interval [CI]0.87 to 1.18); the RR comparing the highest with lowest quartile of UA was 1.08 (95% CI 0.71 to 1.63). The multivariable RR associated with a 1-SD increase in UA was 1.38 (95% CI 1.05 to 1.81) for men aged <60 yr and 0.90 (95% CI 0.74 to 1.10) for men >or=60 yr (P = 0.04 for interaction). However, further adjustment for fasting insulin, triglyceride, and cholesterol levels attenuated the results (RR for men <60 yr 1.24; 95% CI 0.93 to 1.66). In conclusion, no independent association between UA level and risk for incident hypertension was found among older men.

Age Factors↗
PubMed1999

Serum uric acid levels correlate with the severity and the mortality of primary pulmonary hypertension.

Serum uric acid (UA), the final product of purine degradation, has been proposed to be a marker for impaired oxidative metabolism and a possible predictor of mortality in patients with chronic heart failure. To elucidate whether serum UA correlates with the severity and the mortality of primary pulmonary hypertension (PPH), serum UA was assessed in 90 patients with PPH together with other clinical variables. Right heart catheterization was performed in all patients. Serum UA was significantly elevated in patients with PPH compared with age-matched control subjects (7.5 +/- 2.5 versus 4.9 +/- 1.2 mg/ml, p < 0.001). Serum UA negatively correlated with cardiac output (r = -0.52, p < 0.001) and positively correlated with total pulmonary resistance (r = 0.57, p < 0.001). Serum UA significantly decreased from 7.1 +/- 1.9 to 5.9 +/- 1.6 mg/dl with vasodilator therapy, associated with a reduction in total pulmonary resistance from 22 +/- 6 to 17 +/- 7 Wood units. During a mean follow-up period of 31 mo, 53 patients died of cardiopulmonary causes. Among noninvasive variables, serum UA was independently related to mortality by a multivariate Cox proportional-hazards analysis. The Kaplan-Meier survival curves according to the median value of serum UA demonstrated that patients with high serum UA had a significantly higher mortality rate than did those with low serum UA (log-rank test, p < 0.01). These results suggest that serum UA increases in proportion to the clinical severity of PPH and has independent association with long-term mortality of patients with PPH.

Adult↗
PubMed2000

Effect of uric acid on liver injury during hemorrhagic shock.

BACKGROUND: It remains unproven whether nitric oxide (NO) exerts a toxic effect on hepatocytes directly or through the formation of a more toxic compound during hemorrhagic shock (HS). NO reacts at a very high rate constant with superoxide to give peroxynitrite, a potentially toxic molecule. In this study, we investigated whether or not peroxynitrite contributed to tissue injury in the liver during HS. METHODS: Male Sprague-Dawley rats were subjected to decompensated HS followed by resuscitation. In addition to the time course of tissue injury and inducible NO synthase (iNOS) messenger RNA (mRNA) expression in the liver during HS, we investigated the effect of N6-(iminoethyl)-L-lysine(LNIL) (a specific inhibitor of iNOS) and also that of uric acid (a natural scavenger of peroxynitrite) on tissue injury and nitrotyrosine formation (a footprint of peroxynitrite) in the liver. RESULTS: The liver injury, evaluated by plasma aminotransferase levels and histology, became evident at the end of the shock period and had significantly increased 1 hour after the start of resuscitation (Shock-1 h). There was no iNOS mRNA expression in the liver at baseline, and it had clearly increased by Shock-1 h. Treatment with LNIL or uric acid significantly attenuated the tissue injury with a prominent reduction in nitrotyrosine formation in the liver. CONCLUSIONS: These lines of evidence suggest that one of the mechanisms by which NO production causes liver injury during HS may be its reaction with superoxide to form peroxynitrite.

Animals↗
PubMedDate not supplied

Effects of acute administration of nifedipine on glomerular filtration rate and urinary excretion of sodium and uric acid in patients with mild-moderate essential hypertension.

A prospective study was conducted in 25 patients with essential hypertension to study the effects of sublingual administration of nifedipine on some renal functions. Glomerular filtration rate was estimated by radioisotope clearance techniques using Tc-99m diethylene triamine pentaacetic acid (DTPA). The change in urinary excretion of sodium and uric acid were also monitored. A basal estimation of these parameters was followed by repeat studies after lowering the blood pressure to normotensive levels by sublingual administration of nifedipine. It was observed that acute administration of nifedipine does not produce a significant change in the glomerular filtration rate, but causes marked and significant natriuresis and uricosuria.

Administration, Sublingual↗
PubMed2002

Association of GYS1 and beta(3)-AR gene with postprandial hyperglycemia and serum uric acid in type 2 diabetes mellitus.

OBJECTIVE: To determine the relationships of Met416Val and XbaI polymorphism of muscle glycogen synthase (GYS1) gene and Trg64Arg variant of the beta(3)-adrenergic-receptor (beta(3)-AR) gene with type 2 diabetes mellitus (DM) and its intermediate phenotypes in the Chinese population. METHODS: Polymerase chain reaction-oligonucleotide ligation assay and restriction fragment length polymorphism assay were used to evaluate the GYS1 and beta(3)-AR gene polymorphisms in 102 pairs of case-control Chinese spouses. RESULTS: Subjects with Met416Val variant had a significantly higher 2-hour post-glucose level than subjects without this variant had in diabetic group (P = 0.032). The Met416Val polymorphism of GYS1 gene was not significantly associated with the risk of type 2 DM (adjusted OR = 1.67; 95% CI: 0.73 - 3.81, P = 0.223). Subjects with Trp64Arg variant had a significantly higher serum uric acid level than subjects without this variant had in diabetic group (P = 0.034). The combination of BMI and Arg64 allele carrier of the beta(3)-AR gene increased the diabetic risk over four-fold (adjusted OR = 4.00; 95% CI: 1.53 - 10.45, P = 0.005). CONCLUSIONS: In the Chinese population, Met416Val polymorphism is identified in a subgroup of diabetic subjects with high 2-hour post-glucose. It will explain why some diabetic patients appear to be genetically predisposed to developing high postpradial glucose level. The presence of the Arg64 allele in the beta(3)-AR gene may predispose patients to higher serum uric acid level.

Adult↗
PubMed1994

Purification and properties of uricase from Candida sp. and its application in uric acid analysis in serum.

The purification of uricase from Candida sp. was carried out by precipitation with ammonium sulfate then further proceeded with Sephadex G200, and DEAE-cellulose DE52 chromatographies. The specific activity of the enzyme was enhanced from 0.05-12 (U/mg protein). The purity of the enzyme was judged to be homogeneous by SDS-PAGE. Some of the general properties of enzyme were investigated. The optimum reaction pH and temperature were 8.5 and 30 degrees C, respectively. The enzyme was stable at a pH range from 8.5-9.5 and at temperatures lower than 35 degrees C. The apparent Km value of the enzyme was calculated to be about 5.26 x 10(-6) mol/L. The molecular weight was determined to be 70,000-76,000 by the gel filtration and SDS-PAGE techniques. The isoelectric point was determined to be pH 5.6. The effects of some metallic ions on enzyme activity and stability were discussed. The partial purified uricase was used in serum uric acid determination. The within-batch imprecision percentage ranged from 2.16-2.63 and the between-batch imprecision percentage ranged from 2.4-3.6. The recovery ratio were from 96-101%. The correlation among this method and Boehringer, Roche, or Biotrol enzymatic kits were Y = 1.086x-0.50 (r = 0.981), Ya = 0.959x-0.29 (r = 0.97), and Yb = 1.110x-0.45 (r = 0.956), respectively. A linear calibration curve was obtained at 2.5-15 mg/dL uric acid. The stability of reagents and the effects of some substances in serum were also surveyed.

Candida↗
PubMedDate not supplied

Relation between the tumor necrosis factor-alpha (TNF-alpha) gene and protein expression, and clinical, biochemical, and genetic markers: age, body mass index and uric acid are independent predictors for an elevated TNF-alpha plasma level in a complex risk model.

BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) has been implicated in the pathogenesis of numerous complex diseases. The plasma level of this pro-inflammatory cytokine is associated with a variety of different risk factors, but little is known about the genetic background and the complex interactions. METHODS: in this clinical study, correlations were studied between plasma levels of circulating TNF-alpha protein (ELISA), its mRNA expression in monocytes (RT-PCR) and genetic variants of TNF-alpha gene (SSCP), with several diseases, including obesity, atherosclerosis, diabetes mellitus, hypertension, as well as risk factors such as age, gender, inflammatory markers, the coagulation\fibrinolysis balance, and lipid metabolism. One hundred and ninety four clinically and biochemically well-characterized patients were enrolled. RESULTS: At the transcriptional level, measured in monocytes, no association with any clinical or biochemical parameter investigated was found, including TNF-alpha protein level. Investigating the influence of genetic variants of the TNF-alpha gene on mRNA and protein levels, only one promoter polymorphism, namely c.-238G > A, was shown to be associated with transcriptional but not with translational expression. However, at the translational level, significant positive, but weak associations were determined for obesity (P -/+ 0.037), age (P -/+ 0.038), uric acid (P < 0.001), body mass index (P -/+ 0.01), plasminogen (P -/+ 0.013), and fibrinogen (P -/+ 0.002) in bivariate regression analyses, whereas HDL-cholesterol (P -/+ 0.005) was shown to be negatively correlated. However, investigating confounding effects in stepwise multivariate regression analysis, body mass index (P -/+ 0.009), uric acid (P -/+ 0.026) and age (P -/+ 0.037) turned out to be significantly associated with plasma levels of circulating TNF-alpha (adjusted R(2) -/+ 0.117; SE: 0.688).

Adult↗
PubMed2002

High urinary excretion of uric acid combined with high excretion of calcium links kidney stone disease to familial hypertension.

BACKGROUND: Past studies identified an association between kidney stone disease (KSD) and hypertension. We recently reported a high occurrence of hypertension in families of patients with hyperuricosuric KSD. As hypercalciura frequently coexists with hyperuricosuria and high urinary excretion of calcium is found in patients with hypertension, we hypothesized that hyperuricosuria that is accompanied by hypercalciuria better describes the familial association between KSD and hypertension. METHODS: Four hundred and eighty-six KSD patients, aged 18-50 years, attending a lithotripsy unit collected a 24-h urine sample for metabolic analysis and provided information on family history of hypertension. The familial occurrence of hypertension was compared among four groups of patients: those who had combined elevation of both urinary calcium and uric acid excretions ("combined" abnormality, n=56), those who had hyperuricosuria without concomitant hypercalciuria ("pure" hyperuricosuria, n=67), those who had hypercalciuria without concomitant hyperuricosuira ("pure" hypercalciuria, n=52), and a control KSD patient group ("other" abnormality, n=311). The prevalence of treated hypertension in patients from the four groups was 16%, 12%, 2%, 10%, respectively. RESULTS: Thirty-four per cent of the patients with the "combined" abnormality had a positive family history of hypertension, defined as two or more first-degree relatives with treated hypertension, that was significantly higher than in patients with either "pure" hyperuricosuira (15%, P<0.02), "pure" hypercalciuria (8%, P<0.001), or patients with "other" abnormality (10%, P<0.001). The adjusted OR for positive family history of hypertension in the "combined" abnormality group compared to the control KSD patient group was 5.6 (2.39-13.30). The prevalence of hypertension in siblings of patients with the "combined" abnormality (13%) was significantly higher than in siblings of patients with either "pure" hyperuricosuria (3%, P<0.001), "pure" hypercalciuria (1%, P<0.001), or siblings of control patients with "other" abnormality (4%, P<0.001). The adjusted OR for hypertension in siblings of a patient with "combined" abnormality compared to a control KSD patient was 3.4 (1.97-5.91). Patients in the "combined" abnormality group were also characterized by significantly elevated urinary sodium, phosphorus, citrate and potassium excretions. CONCLUSIONS: Our data suggest that there is a strong, independent association between familial occurrence of hypertension and the phenotype characterized by combined elevation of both urinary uric acid and calcium excretions. The association is not present in those with "pure" hyperuricosuria or "pure" hypercalciuria. Ascertainment of patients based on this phenotype may identify more homogeneous populations for genetic analysis of hypertension.

Adult↗
PubMed2006

Uric acid determination in the presence of ascorbic acid using self-assembled submonolayer of dimercaptothiadiazole-modified gold electrodes.

This article reports the determination of uric acid (UA) in the presence of ascorbic acid (AA) using a self-assembled submonolayer of heteroaromatic dithiol, 2,5-dimercapto-1,3,4-thiadiazole (DMcT), on gold (Au) electrode. Submonolayer to multilayers of DMcT can be prepared on Au electrode by varying the soaking time of Au electrode in 1mM aqueous solution of DMcT. The formation of submonolayer, monolayer, and multilayers of DMcT on Au electrode was confirmed from its reductive desorption measurements and electrochemical blocking behavior toward ferricyanide. Interestingly, submonolayer of DMcT separates the voltammetric signal of UA from AA by 210 mV, whereas monolayer and multilayers of DMcT fail to separate them. The voltammetric signals of AA and UA are highly stable and reproducible at submonolayer of DMcT. Fast electron transfer, weak hydrogen bonding interactions with AA and UA, and prevention of fouling effect caused by oxidized product of AA can be achieved at submonolayer of DMcT, and thus it successfully separates the voltammetric signals of AA and UA. The practical application of the current system is demonstrated by measuring the concentration of UA in human urine samples without any treatment.

Acetylcysteine↗
PubMed1987

[Uric acid levels of the serum of healthy persons and patients with various rheumatic diseases].

Serum uric acid levels were investigated in a series of 1715 subjects. Of them 596 were patients with inflammatory rheumatic disorders, 162 gout patients, 236 with osteoarthrosis, 79 with systemic lupus erythematosus or diffuse scleroderma and 642 healthy subjects. On analyzing the results, very high uricemia values were found in the gout patients. Increased uricemia values were observed is patients with psoriatic arthritis and diffuse connective tissue disorders (systemic lupus erythematosus and diffuse scleroderma). Hyperuricemia was found in psoriatic arthritis, rheumatoid arthritis and in nosological entities classified under diffuse connective tissue disorders in 5.6 to 10.1% of patients. In the healthy examinees hyperuricemia was recorded in 3.8% of the cases.

Adolescent↗
PubMed1987

[Level of uric acid in the blood of healthy subjects and ischemic heart disease patients].

The level of uric acid (UA) was studied in the blood of healthy persons and CHD patients. A total of 428 males aged 40 to 59 were examined. The level of blood UA in CHD patients was much higher than in healthy persons of the same age. The frequency of hyperuricemia among CHD patients was 31%, in the control groups 10-15%. There was a direct correlation of UA levels with concentrations of triglycerides and total blood cholesterol. In CHD patients with atherogenic dyslipoproteinemia the UA concentration was higher than in patients without lipid metabolic derangements. The importance of a raised UA level in CHD development was discussed.

Adult↗
PubMed1982

The relationship of serum uric acid to hypertension and ischemic heart disease in Hisayama population, Japan.

The association of serum uric acid (SUA) with hypertension, ischemic ECG change, diabetes mellitus, and drinking and smoking habits was studied by multivariate analysis among 1871 residents aged 40 and over in Hisayama, Japan. Blood pressure level and history of hypertension did not correlate with an increased level of SUA when other factors such as serum creatinine, obesity, beta-lipoprotein and leucineaminopeptidase were taken into account. Antihypertensive medication was a significant factor influencing SUA. The association of SUA with Minnesota code 4.1-3 (S-T depression) was insignificant in men and significant in women when other factors influencing SUA were taken into account. Glycosuria was negatively correlated with SUA, while alcohol ingestion has positive correlation. There was no correlation between the amount of tobacco smoked and the level of SUA.

Alcohol Drinking↗
PubMed1988

Uric acid levels: a useful index of the severity of preeclampsia and perinatal prognosis.

Maximum serum uric acid (SUA) levels during the third trimester of pregnancy were selected in 215 hypertensive pregnant women: 100 with mild preeclampsia (PE), 25 with severe PE, 70 with essential hypertension (EH) and 20 with EH with superimposed PE (EH + PE). The increase in SUA levels was statistically significant in women with severe PE (6.22 mg% +/- 1.30 mg%) and with EH + PE (6.09 mg% +/- 1.53 mg%) when compared with values in mild PE and EH women (4.85 mg% +/- 1.34 mg% and 4.95 mg% +/- 1.22 mg%, respectively). A significant decrease in average gestational age at delivery and a greater percentage of small-for-gestational age newborns were observed in women with severe PE and EH + PE, compared with patients with mild PE and EH. No correlation within the groups was found between SUA levels and fetal weight. To conclude, the determination of SUA concentration for the clinical screening of a pregnancy complicated by hypertension is an easy and inexpensive method for the prediction of perinatal results associated with severe PE.

Birth Weight↗