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PubMed1991

[Uric acid and arterial hypertension. I. Relation between serum uric acid level and its renal excretion in primary arterial hypertension].

In forty patients with mild to moderate essential hypertension and in twenty healthy subjects serum uric acid was measured and parameters of renal excretion of urate were evaluated. Serum uric acid concentration and prevalence of hyperuricemia were significantly higher in hypertensive patients. Patients with essential hypertension and concomitant hyperuricemia showed significantly decreased clearance and fractional excretion of uric acid in comparison with normotensive subjects. Adverse correlation between serum uric acid and clearance as well as fractional excretion of urate found in hypertensive patients indicates that high prevalence of hyperuricemia in essential hypertension is caused by impaired renal excretion of uric acid.

Adult↗
PubMed1987

Renal disease from excess uric acid.

Excess uric acid or urate deposition is a common element in three different forms of renal disease: acute uric acid nephropathy, chronic urate nephropathy, and uric acid nephrolithiasis. Clinical features vary with each form. Therapy is directed at decreasing production of uric acid, increasing its solubility, or both. When possible, preventive measures are taken.

Chronic Disease↗
PubMed1999

Uricase-catalyzed oxidation of uric acid using an artificial electron acceptor and fabrication of amperometric uric acid sensors with use of a redox ladder polymer.

Electrochemical oxidation of uric acid catalyzed by uricase (uric acid oxidase, UOx; EC 1.7.3.3) was studied using several redox compounds including 5-methylphenazinium (MP) and 1-methoxy-5-methylphenazinium (MMP) as electron acceptors for UOx, which does not contain any redox cofactor. It was found that MP and MMP were useful to mediate electrons from UOx to an electrode in the enzymatic oxidation of uric acid. A novel redox polymer, poly(N-methyl-o-phenylenediamine)(poly-MPD), containing the MP units was also found to possess the mediation ability for UOx, and poly-MPD was immobilized together with UOx onto an electrode substrate covered with a self-assembled monolayer of 2-aminoethanethiolate with use of glutaraldehyde as a binding agent. The resulting electrode (poly-MPD/UOx/Au) exhibited amperometric responses to uric acid with very fast response of approximately 30 s, allowing reagentless amperometric determination in a concentration range covering that in the blood of a healthy human being. Kinetic parameters of the apparent Michaelis constant and the maximum current response obtained at the poly-MPD/UOx/Au suggested that electrochemical oxidation of uric acid was controlled by diffusion of uric acid into the enzyme film and that the redox polymer worked well in mediating between active sites of UOx molecules and the electrode substrate.

Candida↗
PubMed1990

Acute uric acid nephropathy.

Uric acid, as the end-product of purine metabolism in humans, presents a clinical problem because of its relative insolubility, particularly in the acid environment of the distal nephron of the kidney. As a result, states of enhanced purine catabolism increase the urate load on the kidney, leading to intrarenal precipitation. Major causes of increased purine metabolism are malignancies with rapid cell turnover, such as leukemias and lymphomas, and the added acceleration of cell lysis that occurs with chemotherapy and radiation. Serum urate levels rise rapidly, and acute renal failure occurs as a consequence of tubular deposition of urate and uric acid. The keys to the diagnosis of acute uric acid nephropathy are the appropriate clinical setting of increased cell lysis, oliguria, marked hyperuricemia, and hyperuricosuria. A urinary uric acid-to-creatinine ratio greater than 1 helps to distinguish acute uric acid nephropathy from other catabolic forms of acute renal failure in which serum urate is elevated. Preventive treatment involves pharmacologic xanthine oxidase inhibition with allopurinol and alkaline diuresis. Occasionally, acute renal failure occurs despite allopurinol because of the tubular precipitation of the precursor metabolites, such as xanthine, which accumulate with xanthine oxidase inhibition. Dialysis therapy may be required both to correct azotemia and to reduce the body burden of urate. Hemodialysis is preferred because it can achieve greater clearance than other dialysis modes.

Acute Disease↗
PubMed1982

Influence of dietary purines on pool size, turnover, and excretion of uric acid during balance conditions. Isotope studies using 15N-uric acid.

Pool size, turnover, and excretion of uric acid were investigated in three normal subjects both during purine-free, isoenergetic liquid formula diet and during additional purine administration by use of isotope dilution techniques. The fractional turnover of the uric acid pool was increased during dietary purine administration suggesting an increased total body uric acid clearance as a result of the increase in renal clearance. Fractional turnover increased more in the female subject than in males, while pool size was increased less. It can be calculated from the results obtained that endogenous uric acid synthesis is not inhibited by dietary purines.

Adenosine Monophosphate↗
PubMed2006

Simultaneous voltammetric measurement of ascorbic acid, epinephrine and uric acid at a glassy carbon electrode modified with caffeic acid.

A stable electroactive thin film of poly(caffeic acid) has been deposited on the surface of a glassy carbon electrode by potentiostatic technique in an aqueous solution containing caffeic acid. Poly(caffeic acid) was used as a modified electrode for the detection of ascorbic acid (AA), epinephrine (EP), uric acid (UA) and their mixture by cyclic voltammetry. This modified electrode exhibits potent and persistent electron-mediating behavior followed by well-separated oxidation peaks towards AA, EP and UA with activation overpotential. For the ternary mixture containing AA, EP and UA, the three compounds can well separate from each other at the scan rate of 20 mVs(-1) with a potential difference of 156, 132 and 288 mV between AA and EP, EP and UA and AA and UA, respectively, which was large enough to determine AA, EP and UA individually and simultaneously. The catalytic peak current obtained, was linearly dependent on the AA, EP and UA concentrations in the range of 2.0 x 10(-5) to 1.0 x 10(-3) mol l(-1), 2.0 x 10(-6) to 8.0 x 10(-5) mol l(-1) and 5.0 x 10(-6) to 3.0 x 10(-4) mol l(-1), and the detection limits for AA, EP and UA were 7.0 x 10(-6), 2.0 x 10(-7) and 6.0 x 10(-7) mol l(-1), respectively. The modified electrode shows good sensitivity, selectivity and stability, and has been applied to the determination of EP in practical injection samples and that of EP, UA and AA simultaneously with satisfactory results.

Ascorbic Acid↗
PubMed2000

Reaction of uric acid with peroxynitrite and implications for the mechanism of neuroprotection by uric acid.

Peroxynitrite, a biological oxidant formed from the reaction of nitric oxide with the superoxide radical, is associated with many pathologies, including neurodegenerative diseases, such as multiple sclerosis (MS). Gout (hyperuricemic) and MS are almost mutually exclusive, and uric acid has therapeutic effects in mice with experimental allergic encephalomyelitis, an animal disease that models MS. This evidence suggests that uric acid may scavenge peroxynitrite and/or peroxynitrite-derived reactive species. Therefore, we studied the kinetics of the reactions of peroxynitrite with uric acid from pH 6.9 to 8.0. The data indicate that peroxynitrous acid (HOONO) reacts with the uric acid monoanion with k = 155 M(-1) s(-1) (T = 37 degrees C, pH 7.4) giving a pseudo-first-order rate constant in blood plasma k(U(rate))(/plasma) = 0.05 s(-1) (T = 37 degrees C, pH 7.4; assuming [uric acid](plasma) = 0.3 mM). Among the biological molecules in human plasma whose rates of reaction with peroxynitrite have been reported, CO(2) is one of the fastest with a pseudo-first-order rate constant k(CO(2))(/plasma) = 46 s(-1) (T = 37 degrees C, pH 7.4; assuming [CO(2)](plasma) = 1 mM). Thus peroxynitrite reacts with CO(2) in human blood plasma nearly 920 times faster than with uric acid. Therefore, uric acid does not directly scavenge peroxynitrite because uric acid can not compete for peroxynitrite with CO(2). The therapeutic effects of uric acid may be related to the scavenging of the radicals CO(*-)(3) and NO(*)(2) that are formed from the reaction of peroxynitrite with CO(2). We suggest that trapping secondary radicals that result from the fast reaction of peroxynitrite with CO(2) may represent a new and viable approach for ameliorating the adverse effects associated with peroxynitrite in many diseases.

Bicarbonates↗
PubMed1991

[Uric acid and arterial hypertension. III. Effect of nifedipine on serum uric acid level and its renal excretion in primary arterial hypertension].

In sixteen patients with moderate essential hypertension the effects of 10-day nifedipine treatment on serum uric acid and renal excretion of uric acid were evaluated. Neither serum uric acid nor clearance and fractional excretion of uric acid changed significantly during treatment with nifedipine. Positive correlation between fall in systolic arterial pressure and decrease of serum uric acid in hypertensive patients treated with nifedipine was found.

Adult↗
PubMed1984

Postmortem changes of uric acid in various rat tissues: determination of uric acid by reversed-phase high-performance liquid chromatography with electrochemical detection.

As a function of time after decapitation, postmortem changes of uric acid in various rat tissues have been studied by reversed-phase high-performance liquid chromatography with electrochemical detection. The chromatographic examination revealed that uric acid in rat tissues such as brain, liver, musculus rectus abdominis, and femoral muscle tends to increase after decapitation as a function of time between the sacrifice and homogenization in a 2.0% metaphosphoric acid solution.

Animals↗
PubMed1976

A case of uric acid renal stone with hypouricemia caused by tubular reabsorptive defect of uric acid.

A 60-year-old man had a uric acid stone in the kidney and laboratory findings of hypouricemia (1.1 mg. per 100 ml.) and increased uric acid clearance (43 ml. per minute per 1.73 m.2). Clearance of uric acid exceeded the endogenous creatinine clearance after administration of pyrazinamide, an inhibitor of renal tubular secretion of uric acid. It was suggested that our patient had a complete defective mechanism for uric acid reabsorption, resulting in hyperuricuria and the formation of the uric acid stone.

Creatinine↗
PubMed1995

Uric acid and coronary heart disease risk: evidence for a role of uric acid in the obesity-insulin resistance syndrome. The Normative Aging Study.

Various epidemiologic studies have linked an increase in serum uric acid level to an increased risk of coronary heart disease. The reasons for this finding are unclear. The authors examined the influence of a number of cardiovascular disease risk factors on serum uric acid level in 886 middle-aged and older men participating in the Normative Aging Study. The men were examined between 1987 and 1991. In a multivariate regression model predicting serum uric acid level, uric acid was positively associated with body mass index (weight (kg)/height (m)2 beta = 0.041 mg/dl per kg/m2, p = 0.003), abdomen: hip circumference ratio (beta = 1.88 mg/dl per cm/cm, p = 0.048), log alcohol intake (beta = 0.150 mg/dl per g/week, p = 0.0001), and log postcarbohydrate insulin level (beta = 0.157 mg/dl per log(microIU/ml), p = 0.005). Serum uric acid level was negatively associated with age (beta = -0.012 mg/dl per year of age, p = 0.017) and log physical activity (beta = -0.152 mg/dl per kcal/week, p = 0.0001). The data suggest that serum uric acid may be involved in the obesity-insulin resistance syndrome, which in turn may explain the relation of serum uric acid to coronary atherosclerosis.

Adult↗