The transport of uric acid in serum.
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Humans↗
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Comparison of the Archibald-Kern and Stransky colorimetric procedure and the Praetorius enzymatic procedure for the determination of uric acid.
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Colorimetry↗
A simplified procedure for the routine determination of uric acid.
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Humans↗
Serum uric acid: correlation with biological, clinical and behavioral factors in Japanese men.
Cross-sectional associations between biological, clinical and behavioral factors and serum uric acid (SUA) levels were examined in 2,438 Japanese male office workers aged 20 to 59 years in Osaka, Japan. Stepwise regression analysis for SUA was carried out for all persons and repeated excluding those under medication for hypertension, hyperuricemia or diabetes mellitus. The results were essentially the same without change in the sequence of the seven most important variables. When 150 men under medication were excluded, independent correlates with SUA levels were, in order of relative importance, history of gout, log triglyceride, creatinine, hemoglobin A1c (negative association), body mass index, total protein, alcohol intake, age (negative association), and total cholesterol. 32.7 percent of total variation in SUA was accounted for by these variables combined. Our data suggest that weight and serum lipids control and avoiding excessive drinking may be beneficial in the prevention of hyperuricemia.
Adult↗
The relation of postmenopausal hormone therapy to serum uric acid and the risk of coronary heart disease events: the Heart and Estrogen-Progestin Replacement Study (HERS).
PURPOSE: To determine whether baseline serum uric acid (UA) levels and estrogen-progestin (E+P)-associated change in serum UA in postmenopausal women with coronary disease are associated with recurrent coronary heart disease (CHD) events. METHODS: 2763 postmenopausal women enrolled in the Heart and Estrogen-Progestin Replacement Study (HERS) were randomly assigned to take conjugated E+P or placebo in a secondary CHD prevention study. The primary outcome for these analyses was nonfatal myocardial infarction or CHD death during a mean follow up of 4.1 years. RESULTS: The baseline serum UA for the cohort was 5.4 mg/dl and, compared with placebo, E+P on average lowered serum UA levels slightly (0.2 mg/dl) at one year of follow up (p<0.0001). Baseline serum UA levels were associated in simple proportional hazards models with CHD events; each standard deviation increase (1.3 mg/dl) was associated with a 22% increased risk of primary CHD events (p=.0001). This association, however, was no longer statistically significant after multivariable adjustment (p=0.36). There was no association between on-study change in serum UA level and any CHD outcome. CONCLUSION: Treatment with E+P lowered serum UA levels slightly, but neither baseline UA nor change in UA affected CHD risk.
Aged↗
Differences in postmortem urea nitrogen, creatinine and uric acid levels between blood and pericardial fluid in acute death.
Previous studies showed significant differences in postmortem urea nitrogen (UN), creatinine (Cr) and uric acid (UA) levels in heart blood depending on the causes of death, including acute death. In addition, the levels in pericardial fluid approximated the clinical serum reference ranges, and their elevations may be assessed based on clinical criteria. The present study investigated difference between blood and pericardial levels of these markers. Medicolegal autopsy cases (n=556, within 48h postmortem) of the following causes of death were examined: injury (n=136), asphyxiation (n=50), drowning (n=39), fire fatalities (n=99), hyperthermia (n=11), hypothermia (n=8), poisoning (n=26), delayed traumatic death (n=44) and natural diseases (n=143). When serum UN, Cr and UA levels were compared with the pericardial levels, there was an equivalency for delayed traumatic death and chronic renal failure, although each level was markedly elevated. Parallel increases in serum and pericardial UA and/or Cr levels were also observed for hypothermia and gastrointestinal bleeding. However, in drowning cases, the left cardiac and pericardial UN levels were lower than the right cardiac and peripheral levels, suggesting the influence of water aspiration. Significant elevations in serum and pericardial Cr and UA levels with a higher serum/pericardial UA ratio for fatal methamphetamine intoxication suggest progressive skeletal muscle damage due to advanced hypoxia/acidosis. Similar findings were often observed for other acute and subacute deaths. These findings suggest that a comparison between blood and pericardial nitrogenous compounds would be useful for investigating the cause and process of death.
Adolescent↗
Separation of urea, uric acid, creatine, and creatinine by micellar electrokinetic capillary chromatography with sodium cholate.
The capillary electrophoretic separation of the four nonprotein nitrogenous compounds (NPNs; urea, uric acid, creatine, and creatinine) typically employed in clinical and medical settings for the monitoring of renal function is described. Successful resolution of these compounds is achieved with the use of a bile salt micelle system composed of sodium cholate at phosphate buffer pH 7.4. The elution patterns of four NPNs are obtained within 30 min with a voltage of 30 kV. The effect of varying the applied voltage, temperature, and the mole ratio of phosphate buffer with bile salt surfactant on the migration behavior is also examined.
Chromatography, Micellar Electrokinetic Capillary↗
Comparative accumulation of uric acid and hypoxanthine by slices of avian renal cortex.
The purpose of the study was to compare the concentrative uptake processes of the 14C-labeled purines uric acid (UA) and hypoxanthine (HX) by slices of chicken renal cortex. It was found that both purines were accumulated by the slices and that, while UA was unaltered metabolically, HX was partially oxidized to UA during the incubation. Inhibition of the oxidation of HX to UA by use of the enzyme inhibitor allopurinol did not alter accumulation indicating that metabolism of HX did not drive accumulation. UA accumulation was eliminated by the presence of low concentrations of the organic anion transport inhibitors probenecid and 4-acetamido-4'-isothiocyano-stilbene-2,2'-disulfonic acid. However, HX accumulation was unaffected by probenecid and significantly decreased by 4-acetamido-4'-isothiocyano-stilbene-2,2'-disulfonic acid only at concentrations considerably in excess of those needed to eliminate UA accumulation. The lack of effect of probenecid is in contrast to its reported inhibitory action on HX excretion by the chicken in vivo, a difference which may reflect lack of luminal transport by in vitro slices. Neither was HX accumulation sensitive to the presence of high concentrations of the organic cations quinine and tetraethylammonium. Despite the insensitivity of the HX accumulation process to organic anions or cations, the process was blocked by cyanide and an N2 atmosphere indicating energy dependence. The results suggest that both UA and HX are accumulated by separable transport processes indicating that the renal tubules possess more than one system capable of contributing to purine excretion.
4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
Uric acid, monosodium urate and ammonium urate urinary relative saturations in normo-uricuric calcium oxalate stone formers.
Monosodium urate (NaU), ammonium urate (NH4U) and uric acid (UA) urinary relative saturations were studied in 15 normo-uricuric calcium oxalate (CaOx) recurrent stone formers whose CaOx relative saturation was identical to age- and sex-matched controls. NaU and NH4U relative saturations were constantly below 1 and not higher in stone formers than in controls, suggesting that heterogeneous nucleation is an unlikely mechanism of CaOx stone formation in vivo. Such values of NaU relative saturation would also tend to rule out any change in the CaOx formation product or urinary inhibitory activity. However, at a given urinary flow rate, NaU relative saturation was suggestively higher in stone formers than in controls. Some disturbance in the equilibrium between NaU and urinary inhibitors might then exist even in normo-uricuric CaOx stone formers.
Animals↗
Acute obstructive uric acid nephropathy after treatment of neoplastic adenopathy.
Patients with lymphoma and leukemia are at increased risk of therapy-related sudden increase in the serum uric acid level, with resultant precipitation and obstruction in the more acidic and concentrated distal nephron. Appropriate pretreatment measures can prevent intrarenal crystal formation. The acute obstruction responds well to treatment, and aggressive measures are indicated.
Acute Disease↗
Uric acid, phosphate and oxalate stones: treatment and prophylaxis.
Medical treatment for the most commonly encountered types of renal stones is described. Nowadays treatment for uric acid stones is well-defined: alkalinizing urine is easy with drugs that are sufficiently active and well enough managed. Relapse is avoided in a high percentage of patients. Medical treatment of phosphate or calcium stones is a more open question as results are far from satisfactory compared with intra- and extra-corporeal approaches which are often minimally invasive and well accepted by both patient and urologist. Relapses are not easy to control because prophylactic measures such as changes in lifestyle and diet are never activated or because they are adopted for a brief period of time. Water therapy is examined, with the choice of water depending on the type of stone, together with drug therapy. Drugs such as citrate, with or without magnesium, and thiazides are considered excellent for curing renal stones and relapses. Although medical therapy has a limited role in many types of stones, its use is decisive in some others.
Calcium Oxalate↗
Quantification of uric acid, xanthine and hypoxanthine in human serum by HPLC for pharmacodynamic studies.
A simple HPLC method was developed and validated for the determination of uric acid (UA), xanthine (X) and hypoxanthine (HX) concentrations in human serum to support pharmacodynamic (PD) studies of a novel xanthine oxidase inhibitor during its clinical development. Serum proteins were removed by ultrafiltration. The hydrophilic analytes and the I.S. were eluted by 100% aqueous phosphate buffer mobile phase. The hydrophobic matrix components (late peaks) were eluted with a step gradient of a higher organic mobile phase. Validation on linearity, sensitivity, precision, accuracy, stability, and robustness of the method for PD biomarkers (UA, X, and HX) was carried out in a similar manner to that for pharmacokinetic (PK) data where applicable. Issues of selectivity for endogenous biomarker analytes and individual concentration variations were addressed during method validation. Standards were prepared in analyte-free phosphate buffer. Quality control samples were prepared in control serum from individuals not dosed with the xanthine oxidase inhibitor. The method was simple and robust with good accuracy and precision for the measurement of serum UA, X, and HX concentrations.
Chromatography, High Pressure Liquid↗
Is there a role for uric acid in an animal model of calcium phosphate nephrocalcinosis and calcium phosphate crystallization in urine of patients with idiopathic calcium urolithiasis? An orientational study.
Uric acid (UA), a waste product of purine metabolism, may be involved in calcium phosphate crystallization and deposition. Rats, which develop nephrocalcinosis on high-fat or magnesium-deficient diets, and patients with idiopathic calcium urolithiasis have hyperproteinuria, especially of nonalbumin protein, and a shift toward elevated serum UA. In rats, an increase in UA precursors and renal UA suggests hypoxemia, which stimulates xanthine oxidase. In patients, a primary increase in renal xanthine oxidase would explain the low urine UA in the presence of an elevated serum concentration. For calcium phosphate deposition (rats) or incorporation into stones (humans) to occur, a crucial factor may be xanthine oxidase-mediated overproduction of free radical species and subsequent tissue damage. Another factor may be whether sufficient UA is synthesized to neutralize these free radicals. Allopurinol use, which inhibits xanthine oxidase and has long been favored for the treatment of idiopathic calcium urolithiasis, may not prevent stones, because it also diminishes the availability of UA. An investigation of the factors that control serum UA homeostasis may be rewarding in research into the etiology of idiopathic calcium urolithiasis.
Animals↗
[Continuous flow determination of plasma uric acid by an enzyme method using a sequential autoanalyzer. Combination with glucose determination in the presence of glucose oxidase].
The simultaneous assays of glucose and uric acid in blood plasma use first a specific oxidase, then a peroxidase and the same chromogenic system. The coupling of the two methods on Autoanalyser SMA 12/60 use five reagents, three of which are identical in the two methods.
Autoanalysis↗
The peroxynitrite scavenger uric acid prevents inflammatory cell invasion into the central nervous system in experimental allergic encephalomyelitis through maintenance of blood-central nervous system barrier integrity.
Uric acid (UA), a product of purine metabolism, is a known scavenger of peroxynitrite (ONOO(-)), which has been implicated in the pathogenesis of multiple sclerosis and experimental allergic encephalomyelitis (EAE). To determine whether the known therapeutic action of UA in EAE is mediated through its capacity to inactivate ONOO(-) or some other immunoregulatory phenomenon, the effects of UA on Ag presentation, T cell reactivity, Ab production, and evidence of CNS inflammation were assessed. The inclusion of physiological levels of UA in culture effectively inhibited ONOO(-)-mediated oxidation as well as tyrosine nitration, which has been associated with damage in EAE and multiple sclerosis, but had no inhibitory effect on the T cell-proliferative response to myelin basic protein (MBP) or on APC function. In addition, UA treatment was found to have no notable effect on the development of the immune response to MBP in vivo, as measured by the production of MBP-specific Ab and the induction of MBP-specific T cells. The appearance of cells expressing mRNA for inducible NO synthase in the circulation of MBP-immunized mice was also unaffected by UA treatment. However, in UA-treated animals, the blood-CNS barrier breakdown normally associated with EAE did not occur, and inducible NO synthase-positive cells most often failed to reach CNS tissue. These findings are consistent with the notion that UA is therapeutic in EAE by inactivating ONOO(-), or a related molecule, which is produced by activated monocytes and contributes to both enhanced blood-CNS barrier permeability as well as CNS tissue pathology.
Animals↗
Relationship of uric acid concentrations and severe intraventricular hemorrhage/leukomalacia in the premature infant.
The purine metabolite hypoxanthine accumulates with hypoxia ischemia and with reperfusion is converted to uric acid (UA). We hypothesized that elevated UA concentration is a marker of previous hypoxia ischemia and would identify infants at greatest risk for having subsequent intraventricular hemorrhage (IVH)/periventricular leukomalacia (PVL). We determined the relationship between UA concentrations in the first postnatal day and the development of severe IVH, PVL, or both in 58 infants of birth weight 865 +/- 177 gm and gestational age 27 +/- 2 weeks. Severe IVH developed in 10 (17%) infants and PVL in 3 (5.1%) infants. UA concentrations on day 1 (obtained at 16 +/- 4 hours) were 7.9 +/- 2.8 mg/dl and increased to 9.5 +/- 2.58 mg/dl on day 2. UA concentrations on day 1 were higher in infants with severe IVH/PVL versus those in infants with neither condition: 10.2 vs 7.3 mg/dl (p = 0.005). Infants with hyperkalemia on the second postnatal day had higher UA concentrations on the first day versus infants with normal potassium levels: 11.7 +/- 2 mg/dl versus 6.8 +/- 1.8 mg/dl (p < 0.0005). Infants with severe IVH/PVL had higher potassium levels on day 2 versus infants with neither condition: 11.9 vs 6.9 mg/dl (p < 0.048). By univariate analysis UA concentrations were significantly related to gestational age (p = 0.005) and birth weight (p = 0.03). Only UA concentration (p = 0.004) and gestational age (p = 0.02) were related to IVH/PVL. By multivariate analysis UA remained significantly related to IVH/PVL even when adjusted for other clinical variables, with an odds ratio estimate of 1.63 (95% confidence interval 1.16 to 2.31). In conclusion, higher UA concentrations on the first postnatal day were associated with the subsequent development of severe IVH/PVL and with subsequent hyperkalemia. Elevated UA concentrations in the first postnatal day may help to identify a subset of premature infants at greatest risk for having subsequent hemorrhagic ischemic injury.
Birth Weight↗
Pool size, turnover rate, and rapidity of equilibration of injected isotopic uric acid in normal and pathological subjects.
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Humans↗
Bilirubin interference with determination of uric acid, cholesterol, and triglycerides in commercial peroxidase-coupled assays, and the effect of ferrocyanide.
We examined the effect of bilirubin on measurement of serum uric acid, cholesterol, and triglyceride in the BMD-8700, Hitachi 705, Multistat III, CentrifiChem, Cobas-Bio, Ektachem 400, aca II, and RA-1000 analyzers. In general, bilirubin interferes more in peroxidase-coupled assays than in either direct methods or those coupled to NAD(P)+. The degree of interference, which can be spectral or chemical, varies and depends on the chromogen and wavelength used. We present data to show the origin and extent of the interference by bilirubin in these systems and demonstrate how ferrocyanide can provide a satisfactory resolution in some cases.
Adult↗