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At least 883 records · Page 49Linked to original sources
PubMed2001

Serum uric acid levels: a useful but not absolute marker of compliance with fenofibrate treatment.

The purpose of our study was to investigate whether measurement of serum uric acid levels is a reliable method to assess adherence to fenofibrate treatment. This was a 21 week, open-label study conducted in our lipid clinic. After an 8 week dietary baseline phase, we implemented a treatment phase, during which patients received 200 mg/day micronized fenofibrate for 3 months. Serum lipid profiles, including levels of lipoprotein(a) and fibrinogen, serum uric acid, as well as muscle and liver enzymes, were measured after the dietary phase, and at the end of the 3 month treatment period. Compliance was assessed using a clinical interview. A significant decrease in serum uric acid levels was observed in the compliant, while no significant change was noticed in the non-compliant. The compliant had lower serum uric acid concentrations compared to the non-compliant (P < 0.01) after fenofibrate treatment. Furthermore, they demonstrated lower levels of triglycerides and higher high-density lipoprotein (HDL) cholesterol concentrations (P < 0.05 for both parameters). The results show that serum uric acid concentrations may be used as a useful tool to assess compliance with fenofibrate therapy.

Adult↗
PubMed2006

Uric acid status and its correlates in Hangzhou urban population.

The aim of this study was to investigate the uric acid status and its correlates in relation to selected cardiovascular risk factors in a cross-sectional study in Hangzhou, China. In this cross-sectional study, 186 male (56 +/- 14 yrs) and 85 female (55 +/- 11 yrs) free-living subjects were recruited from the Hangzhou metropolitan area, China. Their physiological parameters were measured. Each subject gave fasting blood, urine and faeces samples, from which serum uric acid and other parameters of biochemistry and haematology were measured by standard methods. Serum uric concentration was 329 +/- 69 micromol/L for male and 237 +/- 53 micromol/L for female (P < 0.0001). Compared with female subjects, males had significantly higher BMI (P = 0.0215), serum triacylglycerol (TAG) (P = 0.0012) and creatinine (P<0.0001), and significantly lower total cholesterol (TC) (P = 0.0013) and HDL-C (P < 0.0001). In the partial correlation analysis, after controlling for sex, age and BMI, serum uric acid was significantly positively correlated with serum concentrations of TC (r = 0.205, P = 0.001), LDL-C (r = 0.229, P < 0.001),TAG (r = 0.172, P = 0.008) and creatinine (r = 0.330, P < 0.001). The results from the present study indicated that prevalence rates of hyperuricaemia are lower in Hangzhou than in Beijing; increased serum uric acid concentration was associated with a cluster of cardiovascular risk factors for the Hangzhou urban population.

Body Mass Index↗
PubMed1976

Uric acid excretion by the pig kidney.

The handling of uric acid by the pig kidney has been investigated during continuous urate infusion in unrestrained, unanesthetized animals. Urate-to-inulin clearance rates in excess of 1 were found under all experimental conditions, demonstrating only net secretion by the pig kidney. The demonstration of a secretory maximum was precluded owing to a progressive reduction in the GFR associated with high rates of urate infusion. Urate clearance was independent of urine flow rate up to 10 ml/min. The administration of probenecid inhibited urate secretion, but urate-to-inulin clearance ratios below unity were not observed. Pyrazinamide or pyrazinoic acid, at doses which either inhibited secretion or promoted uricosuria in other species, did not alter urate excretion in the pig. Probenecid together with pyrazinamide exerted the same inhibitory effect on urate secretion as probenecid alone. Pyrazinoic acid was reabsorbed at all infusion rates. It is concluded that the pig kidney eliminates uric acid by filtration and secretion only.

Animals↗
PubMed1989

Ammonia production from uric acid, urea, and amino acids and its absorption from the ceca of the cockerel.

Experiments were conducted in situ and in vitro in the ceca to measure ammonia production from uric acid, urea, and amino acids and its absorption. When uric acid was injected into a cecal sac containing mixed cecal microfloras, 77% disappeared within 1 hour, with a concomitant increase in ammonia concentration. When [15N]uric acid was added to the ceca in situ, 28% was converted to ammonia after 30 minutes. About 92% of the ammonia introduced into a cecal sac disappeared from the lumen fluid within 30 minutes. About 43% of each of urea nitrogen and glutamine-amide nitrogen was converted to ammonia-nitrogen, and 25% of uric acid-nitrogen and epsilon nitrogen of the arginine was found in ammonia. The conversion of aminonitrogen of glutamic acid and glycine to ammonia amounted to 19-20%, whereas that of alpha-alanine totaled 11%. It is concluded that dietary and urinary nitrogenous compounds that find their way into the ceca are useful nitrogen sources for ammonia production by microflora in the ceca of the chicken, and that ammonia is absorbed rapidly from the ceca.

Amino Acids↗
PubMed2006

Use of allopurinol in slowing the progression of renal disease through its ability to lower serum uric acid level.

BACKGROUND: Hyperuricemia is associated strongly with the development of hypertension, renal disease, and progression. Allopurinol decreases serum uric acid levels by inhibiting the enzyme xanthine oxidase. We hypothesized that administrating allopurinol to decrease serum uric acid levels to the normal range in hyperuricemic patients with chronic kidney disease may be of benefit in decreasing blood pressure and slowing the rate of renal disease progression in these patients. METHODS: We conducted a prospective, randomized, controlled trial of 54 hyperuricemic patients with chronic kidney disease. Patients were randomly assigned to treatment with allopurinol, 100 to 300 mg/d, or to continue the usual therapy for 12 months. Clinical, hematologic, and biochemical parameters were measured at baseline and 3, 6, and 12 months of treatment. We define our study end points as: (1) stable kidney function with less than 40% increase in serum creatinine level, (2) impaired renal function with creatinine level increase greater than 40% of baseline value, (3) initiation of dialysis therapy, and (4) death. RESULTS: One patient in the treatment group dropped out because of skin allergy to allopurinol. Serum uric acid levels were significantly decreased in subjects treated with allopurinol, from 9.75 +/- 1.18 mg/dL (0.58 +/- 0.07 mmol/L) to 5.88 +/- 1.01 mg/dL (0.35 +/- 0.06 mmol/L; P < 0.001). There were no significant differences in systolic or diastolic blood pressure at the end of the study comparing the 2 groups. There was a trend toward a lower serum creatinine level in the treatment group compared with controls after 12 months of therapy, although it did not reach statistical significance (P = 0.08). Overall, 4 of 25 patients (16%) in the allopurinol group reached the combined end points of significant deterioration in renal function and dialysis dependence compared with 12 of 26 patients (46.1%) in the control group (P = 0.015). CONCLUSION: Allopurinol therapy significantly decreases serum uric acid levels in hyperuricemic patients with mild to moderate chronic kidney disease. Its use is safe and helps preserve kidney function during 12 months of therapy compared with controls. Results of this study need to be confirmed with an additional prospective trial involving a larger cohort of patients to determine the long-term efficacy of allopurinol therapy and in specific chronic kidney disease subpopulations.

Adult↗
PubMed2006

Does Tamm-Horsfall protein-uric acid binding play a significant role in urate homeostasis?

BACKGROUND: Mutations in Tamm-Horsfall protein (THP), also known as uromodulin, lead to a group of diseases known as the uromodulin storage disorders. Clinically, these diseases present with tubulo-interstitial damage, progressive renal dysfunction, hyperuricaemia, and gout. However, it remains unclear how a mutation in THP, a protein produced in the thick ascending limb, can cause hyperuricaemia when most of the uric acid transport is believed to occur in the proximal tubule. However, one study in humans suggests that uric acid could also be secreted in the distal tubule. Thus, an attractive hypothesis could be that THP would bind to uric acid in the distal tubule, and decrease its subsequent reabsorption in the distal nephron. METHODS: We screened for uric acid binding to THP using four independent binding assays. RESULTS: There was no evidence that uric acid could bind to THP. CONCLUSION: THP-uric acid binding does not seem to play a significant role in the regulation of urate homeostasis.

Albumins↗
PubMed1976

Effect of KC1 on renal uric acid excretion.

The effect of two days' KC1 administration per os (total amount 11 g, i.e. 140 mEq potassium) on renal uric acid excretion was studied in healthy subjects under conditions of water diuresis. A significant increase in the uric acid excretory fraction (CUA/CCr..100) was found, from 8.04% in the control test to 10.31% under experimental conditions. Elevated renal uric excretion led to a significant drop in the plasma uric acid level from 4.9 mg% to 4.2 mg% after the administration to KC1. The findings suggest that KC1 influences the tubular transport of uric acid, but the mechanism of its action is still obscure.

Adult↗
PubMed2006

Uric acid in multiple sclerosis.

Peroxynitrite, a reactive oxidant formed by the reaction of nitric oxide with superoxide at sites of inflammation in multiple sclerosis (MS), is capable of damaging tissues and cells. Uric acid, a natural scavenger of peroxynitrite, reduces inflammatory demyelination in experimental allergic encephalomyelitis. Some studies reported lower serum levels of uric acid in MS patients compared with controls, whereas other studies found no difference. A critical appraisal of these studies favors the view that reduced uric acid in MS is secondary to its peroxynitrite scavenging activity during inflammatory disease activity, rather than a primary deficiency. Serum uric acid levels could be used as a biomarker for monitoring disease activity in MS. Therapeutic strategies aimed at raising serum uric acid levels may have a glial/neuroprotective effect on MS patients.

Animals↗
PubMed1994

Chronic musculoskeletal complaints and subgroups with special reference to uric acid.

In a previous article from a cross-sectional study of 737 men and 771 women (40-42 years old) in Norway, we found a higher mean serum uric acid in persons with than without chronic musculoskeletal complaints. Furthermore, the odds ratio for chronic complaints increased by increasing uric acid level. Persons with chronic complaints are heterogenous. The scope of the present study was to inquire whether a further breakdown of the material would shed more light upon our previous findings, and thereby contribute to the understanding of the pathogenesis of chronic complaints. Among persons with such complaints, we wished to characterize the ones with the highest serum uric acid. As possible explanatory factors we used the former fibromyalgia minor criteria and modulating factors, and the presence or absence of widespread complaints judged from the Nordic form body map. Persons with chronic widespread weather-dependent complaints had the highest values. The odds ratios for this subgroup increased by increasing uric acid level to a greater extent than reported in our previous article. Some hypotheses about possible action mecanism are put forward, and the relation to fibromyalgia are briefly discussed. Uric acid needs attention in future studies on chronic widespread musculoskeletal complaints.

Adult↗
PubMed2002

Effect of the angiotensin II receptor antagonist losartan on uric acid and oxypurine metabolism in healthy subjects.

OBJECTIVE: The acute effects of the angiotensin II receptor antagonist losartan on uric acid and oxypurine metabolism were evaluated. METHODS: Losartan (50 mg) was administered orally to 6 healthy males. Blood and urine samples for uric acid and oxypurine were collected before and up to 6 hours after losartan administration. The same examinations were performed later using enalapril (5 mg). RESULTS: Losartan decreased the serum uric acid concentration (from 5.9 +/- 0.9 to 5.2 +/- 1.0 mg/dl) and increased its fractional clearance, which reached a maximum after 2 hours, while enalapril did not. Losartan also induced an increase in the plasma concentration of hypoxanthine, peaking in the fourth hour, and a decrease in its urinary clearance, while the plasma xanthine concentration and its urinary clearance were unchanged. The extent of uric acid excretion was much greater than that of the oxypurines. CONCLUSIONS: Losartan, which has a high affinity for the urate/anion exchanger, has a transient uricosuric effect. Our data indicate that losartan induces a significant decrease in the urinary excretion of hypoxanthine without changes in xanthine.

Adult↗
PubMed1995

Separation and determination of liver uric acid and allantoin.

We previously described the only satisfactory procedure yet achieved for separating uric acid and allantoin from rat liver. The procedure was based on trichloroacetic acid (TCA) extraction, acid hydrolysis, treatment with Hg-acetate, and cation- and anion-exchange chromatography. After separation, allantoin was quantified by a colorimetric method, and uric acid enzymatically using uricase. Since this procedure is too time-consuming, we propose an improved version which avoids the need for anion-exchange chromatography and the complex assay of catabolic compounds. The new method consists of a very fast and simple HPLC separation and direct determination of uric acid and allantoin at 220 nm. The method can be used for fresh tissue or after treatment of the tissue with labeled precursor.

Allantoin↗
PubMed2000

Levels of uric acid, urea and creatinine in Iraqi children with sickle cell disease.

OBJECTIVE: To determine the levels of serum uric acid, urea and creatinine in subjects with sickle cell disease and compare them to those reported in literature. SETTING: Department of Paediatrics, College of Medicine, University of Basrah. METHODS: Plasma uric acid, urea and creatinine was estimated by Varley's method, group of 65 sickle cell patients (35 Hb AS, 30 Hb SS) aged between 2-11 years. The results were compared with those obtained in a group of 45 age and sex-matched controls with normal haemoglobin (Hb AA). RESULTS: The uric acid level was elevated in sickle cell patients as compared with the normal control group. The 95% confidence intervals for differences in the mean of the two groups: HbAA vs HbAS was 4.22 (0.3), while for HbAA for HbSS was 3.4 (0.06), both being statistically highly significant [p < 0.0001]. Urea and creatinine levels were considerably lower in the sickle cell disease patients. The difference in the patient's mean for urea compared to the mean in the normal group (Hb AA) was 9.64 (1.95) and 8.55 (1.76) for HbSS and HbAS, respectively. Like wise, the difference in the mean for creatinine in HbSS group was 0.71 (0.12) and in HbAS was 0.76 (0.12), which was statistically significant [p < 0.0001]. CONCLUSION: Raised serum uric acid levels were found in Iraqi children with sickle cell disease, creatinine clearance studies will be valuable to assess renal function.

Child↗
PubMed1979

[Excretion of uric acid in cardiac decompensation].

The role of hyperuricemia is confirmed, in literature, as a risk factor in ischemic heart disease and in the development of atherosclerotic complications. The problem of uric acid concentration in serum is still not elucidated as well as the role of the eventual hyperuricemia as a risk factor and its excretion from the kidneys of patients with heart diseases in a decompensation stage. Thirty five patients with different heart diseases in various decompensation stages were observed. In all patients, the uric acid concentration in serum were studied as well as the clearance of uric acid, reabsorption percentage in tubules and glomerular filtration according to the clearance of endogenous creatinine. The results obtained revealed that hyperuricemia (over 7 mg%) is found in a great number of the patients (40%) with heart decompensation. The hyperuricemia established resulted primarily from the reduced filtration of glomeruli. In some of the cases, an increased reabsorption of uric acid in tubules was found. In other, single cases, data exist about uric acid secretion in tubules. The problem of heart patients treatment in decompensation stage with the presence of hyperuricemia is discussed. In those cases, very likely, prophylactic measures should be undertaken due to the fact that hyperuricemia is a factor, secondarily leading to atherosclerotic heart alterations.

Adolescent↗
PubMed1976

Serum uric acid, cholesterol, and psychological moods throughout stressful naval training.

Navy recruits, all 51 volunteers for a preliminary underwater demolition team (UDT) training program, were followed through 4 weeks of training; 27 men passed and 24 failed the training course. Serum uric acid and serum cholesterol levels, as well as psychological moods data were collected on all volunteers at the start of training and at the end of each of the four training weeks. Men who passed training were compared to those who failed. In addition, these same measures were carried out with a control group of 66 naval recruits. Pre-UDT trainees who passed the program demonstrated high levels of positive moods, early peaks in serum uric acid level, and stable serum cholesterol levels throughout training. These findings supported previous work with successful UDT trainees. Pre-UDT trainees who failed the program demonstrated intermediate levels of positive moods, a midtraining period peak in serum uric acid, and a significant rise in serum cholesterol during the final 2 weeks of the course. The serum cholesterol rise seen during a period shortly prior to failure substantiates previous findings. A comparison group showed low levels of positive moods, an initial peak in serum uric acid, and stable serum cholesterol levels. Two mood scales had siginificant correlations with serum uric acid for only men who passed training. A motivation scale, given at the start of training, correlated with serum uric acid levels for men who failed training.

Cholesterol↗
PubMed2006

Frequency of hyperuricemia and effect of calcineurin inhibitors on serum uric acid levels in liver transplanted children.

Hyperuricemia is common after renal and cardiac transplantations, but it is rarely reported after liver transplantations. The aim of this study is to determine the frequency of hyperuricemia in children following orthotopic liver transplantation and the effects of calcineurin inhibitors tacrolimus and cyclosporine) on blood uric acid levels. Between September 1997 to January 2004, 76 liver transplantations were performed in 70 children (male/female; 39/31) at Ege University, Organ Transplantation Center (37 deceased donation and 39 live donors). Patients who had been transplanted within the last three months and patients who died within six months after liver transplantation were excluded from the study. Finally 59 patients were included in this study. Uric acid levels were measured before transplantation and after transplantation within six months intervals for two yr. In these series 17 cases had increased uric acid levels after liver transplantation (28.8%). Serum uric acid levels in both groups (tacrolimus or cyclosporine) were detected to be significantly higher than initial values at 12th months (p < 0.05). Hyperuricemia developed in eight patients receiving cyclosporine (eight of 11; 72%) whereas nine patients receiving tacrolimus developed hyperuricemia (nine of 48; 18%). However, the rate of having high uric acid levels was significantly higher in cyclosporine group compared tacrolimus group (p = 0.001, OR: 11.5, CI 95% 2.5-52.4). Uric acid levels were also significantly higher in cyclosporine group in 12th and 18th months (respectively, p = 0.003 and p = 0.003). Serum creatinine levels at 12th, 18th and 24th months were significantly higher in cyclosporine group than tacrolimus group (respectively, p = 0.009, p = 0.04 and p = 0.02). Hyperuricemia is a common complication after liver transplantation in children. Cyclosporine may cause hyperuricemia more often in respect to tacrolimus and this may be related to the impairment of renal functions. Complications developing because of hyperuricemia such as gout disease or renal calculi are quite rare in children.

Adolescent↗
PubMed1986

Uric acid uptake in erythrocytes of beagle and dalmatian dogs.

Uric acid uptake by erythrocytes of Beagle and Dalmatian dogs has been measured, using (2-14C) uric acid. Uptake was characterized by a fast and a slow component. Urate uptake was inhibited by certain purine and pyrimidine derivatives and by anion transport inhibitors. It was dependent on intraerythrocyte glycolysis. Temperature only influenced uptake by the slow component (Q10 = 2.6). Urate uptake by the slow component is apparently due to the transport into the erythrocytes by facilitated diffusion (Km = 6.6 mmol/l, Vmax = 390 mumol/l/min), whereas the fast component exhibits an adsorption of urate on erythrocyte surface. No difference of urate uptake by erythrocytes of Beagle and Dalmatian dogs has been observed.

Animals↗
PubMed1983

Variation in the potassium needs of chickens selected genetically for variation in blood uric acid concentrations.

Two strains of sex-linked dwarf chickens that have been selected genetically for divergence in plasma uric acid concentrations were found to differ in their requirements for potassium. The rates of growth of chicks from both strains were similar when nutritionally adequate levels of potassium were provided. However, the growth of chicks having normal plasma uric acid concentrations was significantly poorer than that of hyperuricemic chicks when the chicks received potassium-deficient diets, and the retention of dietary potassium was less in the former group. There were no consistent strain differences in response to sodium deficiency. Because the two strains previously were found to differ in the renal tubular transport of uric acid, the strain difference in potassium requirement may reflect an association of potassium with uric acid excretion.

Animals↗
PubMed1976

Uric acid lithiasis associated with altered kinetics of hypoxanthine-guanine phosphoribosyltranferase.

1. A patient is described who had uric acid calculi which obstructed both kidneys. Serum uric acid was 34 mg/100 ml upon admission to hospital, and evidence of precipitation of uric acid in joints was obtained. 2. Total activity of hypoxanthine-guanine phosphoribosyltransferase in erythrocytes lysates from this patient was 44% of normal. Kinetic studies revealed that the apparent Michaelis constant of this enzyme for phosphoribosyl pyrophosphate was elevated 15-fold, while these values for hypoxanthine and guanine were in the normal range.

Adult↗