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PubMed2006

Uric acid, the metabolic syndrome, and renal disease.

Metabolic syndrome, characterized by truncal obesity, hypertriglyceridemia, elevated BP, and insulin resistance, is recognized increasingly as a major risk factor for kidney disease and also is a common feature of patients who are on dialysis. One feature that is common to patients with metabolic syndrome is an elevated uric acid. Although often considered to be secondary to hyperinsulinemia, recent evidence supports a primary role for uric acid in mediating this syndrome. Specifically, fructose, which rapidly can cause metabolic syndrome in rats, also raises uric acid, and lowering uric acid in fructose-fed rats prevents features of the metabolic syndrome. Uric acid also can accelerate renal disease in experimental animals and epidemiologically is associated with progressive renal disease in humans. It is proposed that fructose- and purine-rich foods that have in common the raising of uric acid may have a role in the epidemic of metabolic syndrome and renal disease that is occurring throughout the world.

Animals↗
PubMed2001

Serum uric acid for short-term prediction of cardiovascular disease incidence in the Gubbio population Study.

OBJECTIVE: The Gubbio Study is an Italian population study measuring risk factors for and incidence of major cardiovascular diseases. This analysis investigates the association of serum uric acid with the incidence of coronary and cardiovascular events. METHODS: A population sample of 2469 men and women aged 35-74 years, free from major cardiovascular diseases and in whom serum uric acid was measured in 1983 along with other standard risk factors, were followed up for 6 years and the incidence of coronary heart disease (CHD) and all cardiovascular atherosclerotic (CVD) events, both fatal and non-fatal, was computed. Proportional hazards models were used for the prediction of these events. RESULTS: In six years 61 CHD hard criteria, 109 CHD any criterion and 149 CVD events were recorded. Age-adjusted rates per 1000 of the 3 event categories were computed in sex-specific quintiles (Q) of serum uric acid with 428 +/- 76 (Q5) and 198 +/- 42 (Q1) micromol/l, respectively. Although higher rates were seen in Q5 as compared to Q1 for all three first event categories considered (relative risks 6.2, 3.6 and 3.7, respectively), a statistically significant trend was seen only for CVD all criteria (t = 3.63, p < 0.036). These trends were borderline significant for CHD any criterion (t = 2.92, p < 0.06) and not significant for CHD hard criteria (t = 2.23, p < 0.11). In multivariate models, adjusted for 8 other risk factors, serum uric acid showed a statistically significant contribution to predict CVD incidence [relative risk (RR) for 92 micromol/l difference of 1.24 with 95% confidence intervals (CI) 1.05-1.45], whereas the statistical contribution to predict CHD any criterion (RR = 1.19 with CI 0.98-1.45) and CHD hard criteria (RR = 1.20 with CI 0.93-1.55) was not significant. Diuretic treatment and blood urea, as further confounders, were positively and significantly related to event incidence (RR ranging from 1.21 to 2.00) but serum uric acid maintained its independent and statistically significant role in the prediction of CVD events (RR = 1.18 with CI 1.00-1.39). Presence of specific treatments to lower serum uric acid levels (in 1.13% of the population), tested as final confounders, was not statistically contributory. CONCLUSIONS: Increased serum uric acid levels are independently and significantly associated with risk of CVD events in the 6-year follow-up of the Gubbio Study. Longer follow-up is needed before the contributory role of serum uric acid can be properly assessed to explain CHD incidence.

Adult↗
PubMed1977

The effect of weight loss on plasma and urinary uric acid and lipid levels.

Plasma uric acid levels in 35 obese gouty and non-gouty subjects showed a highly significant mean fall of 0.6 mg/100 ml after weight reduction on a low-calorie diet. Urinary urate also fell by a mean value of 87 mg/100 ml. Serum cholesterol and triglyceride levels have been studied in 20 of the subjects. Both have shown some overall fall with weight loss. So far the degree of change of plasma urate has shown a correlation with that of cholesterol but not that of triglyceride, but further data are needed on these inter-relationships.

Body Weight↗
PubMed1995

[Retinopathy and serum uric acid in diabetics].

Low serum uric acid (UA) levels have been reported in diabetics. In a group followed for 15 years it was reported that low UA levels preceded the onset of diabetic retinopathy. We studied 95 consecutive diabetic clinic patients between July and September 1992. There was no significant difference in UA levels between those with or without retinopathy: 5.0 +/- 1.2 (SD) mg--vs. 5.3 +/- 1.3, respectively. Multiple regression analysis showed that higher UA levels were related independently to high body mass index (overweight, obesity), and male gender, but not to age, duration of diabetes, glycosylated hemoglobin, diabetic treatment or retinopathy.

Body Mass Index↗
PubMed1996

Ultrasonic velocities of concentric laminated uric acid stones.

In concentric laminated uric acid samples two different sound velocities are observed with very different values, the one in the organic matrix varies from 670 to 1170 m s(-1), the other in the crystalline layers between 3200 and 5300 m s(-1). This large difference illustrates the importance of the internal stone structure on the fracture behaviour of urinary stones and reveals the weakness of the actual disintegration models, attributing the destructive effect of shock waves on the differences in acoustical impedance at the water/stone interface and not on the differences in acoustical impedance at the matrix/crystalline interfaces inside the urinary calculus.

Acoustics↗
PubMed1999

A biomimetic phospholipid/alkanethiolate bilayer immobilizing uricase and an electron mediator on an Au electrode for amperometric determination of uric acid.

A biomimetic bilayer membrane immobilizing uricase (urate oxidase; EC 1.7.3.3) (UOx) and a redox agent of 1-methoxy-5-methylphenazinium (MMP) was fabricated on an Au electrode substrate with use of the Au substrate coated with a self-assembled monolayer of n-octanethiolate (OT/Au) and L-alpha-phosphatidylcholine beta-oleoyl-gamma-palmitoyl (PCOP). The preparation was carried out by successively immersing an Au electrode substrate in an ethanol solution of OT, an MMP aqueous solution, and a suspension of proteoliposome formed by PCOP containing UOx and MMP. The prepared electrode exhibited such fast steady amperometric responses to uric acid as to allow its determination within 20 s after injecting uric acid, indicating that UOx-catalyzed electrochemical oxidation of uric acid was accomplished with assistance of electron mediation by MMP between UOx and the Au substrate. An increase in the response currents with increasing concentration of uric acid was obtained in a concentration range of uric acid found in healthy human blood. Any interference in the current response that is caused by direct anodic oxidation of uric acid or ascorbic acid was not observed at the prepared sensor electrode because the densely packed bilayer effectively blocked the diffusion of these substrates toward the Au surface, making it possible to determine amperometrically uric acid at the electrode with high precision.

Electrochemistry↗
PubMed1982

The Clinical Lipid Research Clinic Family Study: familial determinants of plasma uric acid.

Commingling analysis of plasma uric acid levels in a random sample of 160 nuclear families supports the hypothesis that there is a mixture of three distributions. Assuming one, two, and three components in the underlying distribution, we obtained the corresponding p-values (for power transformation) as 0.059, 1.040, and 1.643, respectively. Path analysis with p = 0.059, 1.040, and 1.643 respectively. Path analysis with p = 0.059 gives genetic (h2) and cultural (c2) heritabilities as 0.256 and 0.199, without much support for intergenerational differences, assortative mating, or maternal effects. Complex segregation analysis with p = 0.059 supports multifactorial inheritance, consistent with the findings of Gulbrandsen et al. (1979) and Morton (1979) in other populations. This study also fails to support a major locus hypothesis, contrary to earlier reports.

Adolescent↗
PubMed1990

Evidence of enhanced uric acid clearance in macrohematuric patients with IgA nephropathy: prognostic significance of macrohematuria.

Renal handling of uric acid and clinical prognosis following episodes of macroscopic hematuria (EMH) were examined in 113 patients with IgA nephropathy (IgAN). EMH was observed in 34 out of 113 patients (30.1%). The levels of blood urea nitrogen, proteinuria, serum uric acid, beta 2-microglobulin in sera and the degrees of glomerular sclerosis in renal tissues in macrohematuric patients were significantly decreased than those in patients without EMH. The levels of uric acid clearance (Cua) and fractional excretion of uric acid (FEua) was significantly enhanced in macrohematuric patients (p less than 0.01, p less than 0.05, respectively). There was a significant correlation between the tubular atrophy and the levels of Cua in macrohematuric patients (p less than 0.005). The levels of serum creatinine in macrohematuric patients before and after three years were significantly decreased when compared with microhematuric patients (p less than 0.005). It is concluded that enhanced Cua was related to renal tubular atrophy, and EMH did not clinically influence the glomerular deterioration in patients with IgAN.

Adult↗
PubMedDate not supplied

[The relationship between serum uric acid and the prognosis of children admitted to pediatric intensive care unit].

To investigate the relationship between hyperuricemia and the prognosis of acute ill children, we evaluated the usefulness of serum uric acid (SUa) and urinary uric acid concentration on admission as prognostic indices in 94 consecutive children admitted to a pediatric intensive care unit. Patients with hyperuricemia (13.1 +/- 5.6 mg/dl) had a higher mortality (13/26, 50% vs 7/68, 10%, P < 0.001), lower blood pH (7.20 +/- 0.18 vs 7.37 +/- 0.10, p < 0.05), lower systolic blood pressure (85 +/- 24 vs 102 +/- 28 mmHg, p < 0.05) and lower body temperature (36.6 +/- 0.8 vs 37.4 +/- 1.0 degrees C, p < 0.05) than did patients with normouricemia (5.0 +/- 1.5 mg/dl). There are no significant difference in uric acid and sodium excretion between hyperuricemic and normouricemic patients. We concluded that elevated serum uric acid on admission is associated with a higher mortality in pediatric ICU patients, therefore it may be used as an important prognostic index to evaluate patients' outcome in acute ill children. Hyperuricemia should also alert physicians to the possibility of profound cell injury caused by various etiology.

Child↗
PubMed1963

The effects of oral salicylate on serum uric acid levels.

Thirteen males and six females were given 40 grains of oral salicylate daily for six days. The serum uric acid of 16 of the 19 subjects fell, the mean post-treatment level being 1.1 mg. % less than the control mean. In five males and five females, administration of 20 grains of oral salicylate daily for six days resulted in a uniform rise of serum uric acid, the post-treatment mean being 1.4 mg. % above the pretreatment mean. Salicylate therapy in common dosage may therefore falsely elevate or depress serum uric acid levels. An accurate evaluation of a serum uric acid level can be made only if the patient is not under the influence of salicylates.

Aspirin↗
PubMed2000

Segregation analysis of serum uric acid in the NHLBI Family Heart Study.

Segregation analysis was performed on the serum uric acid measurements from 523 randomly ascertained Caucasian families from the NHLBI Family Heart Study. Gender-specific standardized residuals were used as the phenotypic variable in both familial correlation and segregation analysis. Uric acid residuals were adjusted for age, age2, age3, body mass index (kg/m2), creatinine level, aspirin use (yes/no), total drinks (per week), HOMA insulin resistance index [(glucose * insulin)/22.5], diuretic use (yes/no), and triglyceride level. Sibling correlations (r=0.193) and parent-offspring correlations (r=0.217) were significantly different from zero, but these two familial correlations were not significantly different from one another. After adjustment for covariates, the heritability estimate for serum uric acid was 0.399. Segregation analysis rejected the "no major gene" model but was unable to discriminate between an "environmental" and a "Mendelian major gene" model. These results support the hypothesis that uric acid is a multifactorial trait possibly influenced by more than one major gene, modifying genes, and environmental factors.

Arteriosclerosis↗
PubMed2001

Serum uric acid and the risk for hypertension and Type 2 diabetes in Japanese men: The Osaka Health Survey.

OBJECTIVE: To investigate the association of serum uric acid level with the risk for hypertension and Type 2 diabetes. DESIGN: Prospective cohort study. SETTING: Work site in Osaka, Japan. PARTICIPANTS: A total of 6,356 Japanese men, aged 35-60 years with systolic blood pressure < 140 mmHg and diastolic blood pressure < 90 mmHg, normal glucose intolerance, and no history of hypertension or diabetes at baseline. MAIN OUTCOME MEASURES: Blood pressure was measured by standard techniques, using 160/95 mmHg for diagnosis of hypertension. Type 2 diabetes was defined as a fasting plasma glucose level > or = 126 mg/dl or a 2 h post-loaded plasma glucose level > or = 200 mg/dl. RESULTS: During the 61,716 person-years follow-up period, we confirmed 639 cases of hypertension and 454 cases of Type 2 diabetes. Serum uric acid level was associated with an increased risk for hypertension but not for Type 2 diabetes. After adjustment for known risk factors, including daily alcohol consumption, the serum uric acid level was associated with an increased risk for hypertension; the relative risks for hypertension were 1.00 for quintile 1 of the serum uric acid level, 1.24 [95% confidence interval (CI), 0.94-1.65] for quintile 2, 1.34 (CI, 1.03-1.76) for quintile 3, 1.76 (CI, 1.35-2.29) for quintile 4, and 2.01 (CI, 1.56-2.60) for quintile 5 (P for trend < 0.001). Even among both non-drinkers and lean subjects, serum uric acid level was associated with an increased risk for hypertension. CONCLUSIONS: Serum uric acid level was associated with an increased risk for hypertension but not for Type 2 diabetes.

Adult↗
PubMedDate not supplied

Urinary uric acid excretion in patients with carcinoma of the cervix undergoing intracavitary radium therapy.

An attempt is made here to determine the pattern of urinary uric acid excretion in patients with carcinoma of the cervix undergoing intracavitary radium therapy. Eight patients from the Philippine General Hospital were studied using 24-hour urine collection method to study the uric acid level. Result showed a proportionate increased in uric acid excretion with increasing dose of radiation up to 4,800-5,400 rads, after which, uric acid excretion produced an unexpected downtrend even with continued radiation. Maximum uric acid excretion ranged from 680-1,500 mg% with a mean of 1,005 +/- 100 mg%.

Adult↗
PubMed1980

Uric acid saturation in calcium nephrolithiasis.

Hyperuricosuria appears to cause calcium oxalate nephrolithiasis by promoting the formation of monosodium urate or uric acid crystals, which either act as seed crystals for calcium oxalate or adsorb normally occurring macromolecular inhibitors of calcium oxalate crystallization. Both mechanisms require that hyperuricosuria cause excessive supersaturation of the urine, but this has not yet been studied under conditions of normal lifestyle. We have measured the saturation with respect to sodium hydrogen urate and the concentration of undissociated uric acid in the urine samples of 67 patients with calcium nephrolithiasis, who had idiopathic hypercalciuria, hyperuricosuria, both, or neither disorder. Patients with hyperuricosuria excreted urine that was supersaturated with respect to monosodium urate or undissociated uric acid more frequently than did other stone formers or normal subjects, and are therefore at a greater risk of forming a solid phase of monosodium urate or uric acid. Treatment measures that lowered uric acid excretion also lowered urine saturation, and this may be the reason that such treatment tends to prevent calcium stone recurrence.

Adolescent↗
PubMed2006

Gender-related association of serum uric acid and left ventricular hypertrophy in hypertension.

BACKGROUND: The aim of the present study was to determine whether sex differences contribute to the association of serum uric acid and left ventricular hypertrophy in individuals with hypertension. METHODS AND RESULTS: Seventy participants with essential hypertension (34 men, 36 women; 54.4 +/- 1.6 years old) were enrolled to undergo echocardiography to calculate the left ventricular mass index (LVMI). Twenty-four-hour ambulatory blood pressure monitoring was done to assess blood pressure level precisely. The LVMI was significantly correlated with serum uric acid (r = 0.295, p = 0.013) in all participants. After controlling for factors such as age, sex, mean 24-h systolic blood pressure, creatinine clearance, and duration of hypertension, serum uric acid was still found to be significantly and independently associated with LVMI. Because serum uric acid was significantly higher in men than in women (6.8 +/- 0.3 and 5.1 +/- 0.2 mg/dl, respectively), subsequent analysis was performed by gender. Multiple regression analysis revealed that the LVMI was significantly and independently associated with serum uric acid in women, but not in men. CONCLUSIONS: The potential effect of uric acid on LV hypertrophy is more pronounced in female than in males with essential hypertension.

Age Factors↗
PubMed1985

[Decreased renal excretory capacity of uric acid in rats fed a low sodium diet under consecutive administration of thiazide diuretics].

The effect of consecutive treatments with thiazide diuretics on renal handling of uric acid was investigated with clearance experiments using rats. Two weeks of oral administration of trichlormethiazide (2 mg/kg, twice a day) in rats fed an ordinary diet caused no change in the uric acid excretory capacity. However, a week of oral administration of trichlormethiazide (0.1, 0.5 and 2 mg/kg, twice a day) in rats maintained on a purified diet containing low sodium amounts decreased the fractional excretion of uric acid. At 2 mg/kg, the decrease of inulin clearance developed clearly. Similar treatments with hydrochlorothiazide (10 mg/kg) and cyclopenthiazide (0.5 mg/kg) also decreased the inulin clearance and the fractional excretion of uric acid. Administration of the above diuretics during sodium deprivation resulted in a marked rise of the hematocrit and hypokalemia. Purified diet containing low sodium amounts alone did not change the uric acid excretory capacity as compared to the ordinary diet. Trichlormethiazide treatment and continued sodium deprivation caused marked losses of body weight and food intake and promotions of urine output and water intake. Histologically, hyperplasia of the cells and tubular dilatation at macula densa were slightly developed during sodium deprivation. With these severe changes, dilatation of the proximal tubules with flattened and regenerated epithelium was shown by the trichlormethiazide treatment (0.5 mg/kg). From these results, the characteristics of chronic treatment with thiazide diuretics acting on renal uric acid retention could be understood in the rat under sodium deprivation.

Animals↗
PubMed1977

[Evidence of an excretion of uric acid by a caecal pouch in the rabbit (author's transl)].

Uric acid was estimated in the blood plasma, the caecal content, and in the lumen of a caecal pouch in operated rabbits. It was also histochemically detected in the caecal wall. A non negligible excretion of uric acid through the perfused caecal pouch was demonstrated. There was also an accumulation of amorphous uric acid in the enterocytes, probably due to the absence of intestinal transit, and of microorganism's uricase.

Animals↗
PubMed1980

Use of 3,5-dichloro-2-hydroxybenzenesulfonic acid/4-aminophenazone chromogenic system in direct enzymic assay of uric acid in serum and urine.

A new direct colorimetric procedure for uric acid assay in serum or urine is described, utilizing a 3,5-dichloro-2-hydroxybenzene sulfonic acid/4-aminophenazone chromogenic system in the presence of horseradish peroxidase and uricase from Aspergillus flavus. This chromogen system has a high absorptivity, affording useful results with sample/reagent volume ratios as low as 0.025. The procedure is applicable to serum, plasma, or diluted urine. A single working reagent is used; the reaction is complete in less than 15 min at room temperature. The red dye formed is measured at 520 nm; a blank sample measurement is not needed. The standard curve for the method is linear for uric acid concentrations up to 1500 mumol/L. Average analytical recovery of uric acid in human sera and urine exceeded 99%; within-run and between-run precision studies showed CV's of less than or equal to 1.2 and less than or equal to 2.2%, respectively. The new procedure correlated well with the uricase/catalase and uricase/ultraviolet methods. The method is suitable for automation.

Aminopyrine↗