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At least 1,351 records · Page 75Linked to original sources
PubMed1987

Impaired kinetic properties of hypoxanthine-guanine phosphoribosyl transferase as a cause of uric acid nephropathy in early infancy.

A 6-month-old infant presented with failure to thrive, hyperuricaemia and renal insufficiency. The hyperuricaemia was due to uric acid over-production. The level of hypoxanthine-guanine phosphoribosyltransferase (HGPRT) activity was found to be normal. However, a two-fold increase in the Km of the enzyme to hypoxanthine as well as in the Vmax values was observed. It seems therefore, that in cases of uric acid over-production, screening tests of HGPRT activity may be insufficient and additional kinetic properties of the enzyme should be tested.

Acute Kidney Injury↗
PubMed1984

Dissolution of uric acid calculi with systemic alkalization.

We treated 14 patients with uric acid calculi in the renal pelvis and calices (10) or ureter (4) with constant intravenous infusion of a one-sixth molar lactate solution. Dissolution was successful in all but 2 cases. The success of therapy is believed to be related to the sustained urinary alkalization obtained with intravenous infusion compared to the intermittent alkalization that occurs when oral agents are used.

Adult↗
PubMed2001

[Evaluation of glucose, insulin, C-peptide uric acid serum levels in patients with psoriasis].

The aim of our study was to estimate the serum levels of glucose, insulin, C-peptide and uric acid in patients with psoriasis before and after treatment. The study included 12 males with active form of psoriasis and 15 control subjects carefully matched to the psoriatic patients for age and BMI. All measured parameters were in patients with psoriasis significantly increased and dependent on the BMI. Compared with pretreatment values of glucose and uric acid were significantly lower during therapy. The increase in the mean C-peptide and insulin levels after psoriasis therapy was constant and independent from clinical stage of disease. The results of the present study have provided evidence for the importance of impaired glucose and purine metabolism in patients with psoriasis in the increase risk of development of diabetes mellitus and hypertension.

Adult↗
PubMed1983

Stimulation of uric acid production and depression of increase in plasma glutamine concentration by insulin in chickens infused with ammonia.

1. A single intraportal injection of insulin remarkably stimulated uric acid production in the chicken infused with ammonium acetate and significantly depressed the increase in plasma glutamine concentration by the infusion of ammonia (P less than 0.01 at 20 min, P less than 0.05 at 40 min after the start of infusion). 2. The increases in ammonia concentration in the blood and kidney during the infusion of ammonia were not affected by the insulin pretreatment. 3. The depressive effect of insulin on the increase in plasma glutamine concentration by ammonia may be due to the acceleration by insulin of incorporation of glutamine into biosynthetic pathway of uric acid in the chicken.

Acetates↗
PubMed2007

Effect of elevated serum uric acid on cisplatin-induced acute renal failure.

Marked hyperuricemia is known to cause acute renal failure via intrarenal crystal deposition. However, recent studies suggest mild hyperuricemia may have vasoactive and proinflammatory effects independent of crystal formation. We therefore tested the hypothesis that mild hyperuricemia might exacerbate renal injury and dysfunction in a model of cisplatin-induced acute renal failure in the rat. Cisplatin was administered to normouricemic and hyperuricemic rats (the latter generated by administering the urate oxidase inhibitor, oxonic acid). Recombinant urate oxidase (rasburicase) was administered in a third group to assess the effect of lowering uric acid on outcomes. Other control groups include normal rats and hyperuricemic rats without cisplatin-induced injury. Cisplatin induced injury of the pars recta (S3) segment of the proximal tubule in association with a mild monocyte infiltration. Hyperuricemic rats showed significantly greater tubular injury and proliferation with significantly greater macrophage infiltration and increased expression of monocyte chemoattractant protein-1. However, renal function was not different between normouricemic and hyperuricemic rats with cisplatin injury. Treatment with rasburicase reversed the inflammatory changes and lessened tubular injury with an improvement in renal function (relative to the hyperuricemic group). No intrarenal crystals were observed in any groups. These data provide the first experimental evidence that uric acid, at concentrations that do not cause intrarenal crystal formation, may exacerbate renal injury in a model of acute renal failure. The mechanism may relate to a proinflammatory pathway involving chemokine expression with leukocyte infiltration.

Acute Kidney Injury↗
PubMed1979

[Uric acid stones in children. Identification and therapy of a newly detected defect of adenine-phosphoribosyltransferase (author's transl)].

APRT deficiency, a new cause of supposed "uric acid" stones in young children may be benign or life threatening. This stresses the importance of early recognition and diagnosis. The renal failure, severe in some instances, is preventable because 2,8-DHA formation, the precipitating factor in all, may be controlled by allopurinol preferably without alkali. A low purine diet is advised. "Uric acid" stones in children should always be subjected to sophisticated analysis, and regarded with suspicion in young adults. Diagnosis from red cell APRT activity will be impossible in transfused subjects.

Adenine Phosphoribosyltransferase↗
PubMed2000

Quantification of allantoin, uric acid, xanthine and hypoxanthine in ovine urine by high-performance liquid chromatography and photodiode array detection.

A HPLC method for the determination of allantoin, uric acid, hypoxanthine and xanthine (purine metabolites) in ovine urine without the disadvantages inherent in derivatization is described. After dilution 1:6 with water, urine samples were injected onto the column. Separation and quantification of purine metabolites was achieved using two Nova-Pak C18 columns (4 microm, 250x4.6 mm, Waters). A binary gradient program and UV detection were used for purine metabolites analysis. Clear resolution of purine metabolites was obtained in less than 15 min. Allantoin, uric acid, hypoxanthine and xanthine in the effluent were monitored at 225, 284, 250 and 267 nm, respectively. The average recoveries of purine metabolite standards added to urine samples were satisfactory (100.2-102.9%). The low coefficients of variation (0.29-0.73%) as well as the low detection (0.16-0.70 nmol) and quantification (0.52-2.32 nmol) limits indicate satisfactory precision, reproducibility and sensitivity of the proposed method. This procedure is suitable for routine quantification of purine metabolites in a large number of urine samples.

Allantoin↗
PubMed2005

Determination of uric acid in urine, saliva and calcium oxalate renal calculi by high-performance liquid chromatography/mass spectrometry.

A very simple and direct method for determination of uric acid, in various biological matrices, based on high-performance liquid chromatography and mass spectrometry is described. Chromatographic separations were performed with a stationary phase Zorbax Sax Column, an anion exchange resin, with 50% sodium citrate 1 mM at pH 6.5 and 50% acetonitrile as mobile phase delivered at a flow rate of 1 ml/min. The detector counted negative ions by monitoring m/z 167.1, which corresponds to the urate anion. The method does not use an internal standard but quality control samples were used. Intra-day precision ranged between 1.1 and 1.5%, whereas inter-day precision was between 1.3 and 2.8% (n=5) working with some selected standards. Recovery tests of added standard have been successfully performed in urine and saliva samples, thus showing an appropriate accuracy of the method. The limit of quantitation found was 70 microg/l. Different urine and saliva samples were analyzed using an alternative analytical methodology based on an enzymatic reaction and photometric detection at 520 nm, resulting both methods comparable at a 95% confidence level. The method has been also applied to the determination of trace amounts of uric acid in the core of some selected calcium oxalate renal calculi.

Calcium Oxalate↗
PubMed1979

[Uric acid in the tissues and blood of chick embryos].

In the liver, kidney and skeletal muscle of the shank, blood plasma and blood cells of 90 chick embryos of the initial breed Leghorn White, commercial hybrid Primant, uric acid was found in all the intervals within the studied ontogenetic seqeuence. Uric acid was determined colorimetrically in tissue homogenate supernatant; in the blood plasma and in the blood cells it was determined colorimetrically on the 10th, 15th and 20th day of incubation. A significant rise (p less than 0.05) of this metabolite was ascertained in all the samples tested.

Animals↗
PubMed1987

The treatment of uric acid calculi with extracorporeal shock wave lithotripsy.

A review of the first 1000 patients treated with extracorporeal shock wave lithotripsy (ESWL) at UCLA revealed 21 patients with uric acid renal or ureteric calculi. Using the combination of ESWL and oral urinary alkalinisation, 16/21 patients (76%) were stone-free at follow-up 3 months later and 19 patients were stone-free at 5 months. ESWL and urinary alkalinisation are complementary methods for the non-invasive treatment of uric acid renal calculi.

Adult↗
PubMed1997

Identification and quantitative determination of uric acid in human urine and plasma by capillary electrophoresis with amperometric detection.

Application of capillary zone electrophoresis with electrochemical detection to the identification and quantitative determination of uric acid in human urine as well as plasma is described. This work was carried out in a 30 cm x 25 microm I.D. fused-silica capillary with tricine buffer and a carbon fiber bundle was employed as a working electrode, the working voltage in amperometric detection was set at +0.80 V (vs. SCE). The sample constituent is identified by stopped flow-linear sweep voltammetry. Under optimal conditions, a lower detection limit of 0.48 fmol was obtained for uric acid.

Buffers↗
PubMed1962

Serum uric acid in mongolism.

A highly significant increase (P < .01) in average uric acid level was found in the blood serum of mongoloids when levels were compared with those in normal control subjects or nonmongoloid, mentally retarded subjects. The possible relationship of these findings to other abnormalities known to exist in mongolism is discussed.

Asian People↗
PubMed2003

Phosphoribosylpyrophosphate synthetase overactivity as a cause of uric acid overproduction in a young woman.

Overactivity of phosphoribosylpyrophosphate synthetase (PRS) is an X chromosome-linked disorder of purine metabolism that is characterized by gout with uric acid overproduction and, in some families, neurodevelopmental impairment. We present the case of a 24-year-old Spanish woman with renal colic and hyperuricemia, which first manifested at age 11 years. Results of enzymatic and genetic studies supported the view that accelerated purine nucleotide and uric acid production in this woman resulted from defective allosteric regulation of PRS activity, which is, in turn, a consequence of a mutation in one of the patient's PRPS1 genes: an A-to-T substitution at nucleotide 578, encoding leucine for histidine at amino acid residue 192 of the mature PRS1 isoform. A previous example of disordered regulation of PRS1 activity in a family with a different substitution at the same amino acid residue strengthens this proposed mechanism. This is the first reported instance of PRS overactivity in which the propositus and sole affected family member is a woman.

Adult↗
PubMed1998

Serum uric acid is a strong predictor of stroke in patients with non-insulin-dependent diabetes mellitus.

BACKGROUND AND PURPOSE: Patients with non-insulin-dependent diabetes mellitus (NIDDM) are at increased risk for stroke. Hyperuricemia is a common finding in NIDDM, but its significance as an independent risk factor for cardiovascular disease has remained uncertain. Therefore, we investigated serum urate as a predictor of stroke in NIDDM patients free of clinical nephropathy (ie, with a serum creatinine level of < or = 120 micromol/L). METHODS: In this population-based study, cardiovascular risk factors were determined in 1017 patients (551 men and 466 women) with NIDDM, aged 45 to 64 years at baseline. The patients were followed up for 7 years with respect to stroke events. RESULTS: During the follow-up period, 31 NIDDM patients (12 men [2.2%] and 19 women [4.1%]) died from stroke and 114 NIDDM patients (55 men [10.0%] and 59 women [12.7%]) had a fatal or nonfatal stroke. The incidence of stroke increased significantly by quartiles of serum uric acid levels (P<.001). High uric acid level (above the median value of > 295 micromol/L) was significantly associated with the risk of fatal and nonfatal stroke by Cox regression analysis (hazard ratio, 1.93 [1.30 to 2.86]; P=.001). This association remained statistically significant even after adjustment for all cardiovascular risk factors (hazard ratio, 1.91 [1.24 to 2.94]; P=.003). CONCLUSIONS: Our results indicate that hyperuricemia is a strong predictor of stroke events in middle-aged patients with NIDDM independently of other cardiovascular risk factors.

Cerebrovascular Disorders↗
PubMed1993

Uric acid and didanosine compliance in AIDS clinical trials: an analysis of AIDS Clinical Trials Group protocols 116A and 116B/117.

An analysis is presented that promotes the use of uric acid levels as an indicator of patients didanosine (ddI) use. Logistic regression techniques were used on data from two test groups that best represent patients entered on ACTG protocols 116A and 116B/117. Two classification functions resulted that are based on serial uric acid measurements and were used to classify patients to one of two groups: those treated with zidovudine (ZDV) and those treated with ddI. These functions correctly classified well over 70% of the patients in each of these two studies. Implications of these results with respect to the assessment of ddI compliance and limitations in the use of these classification functions are discussed.

Adult↗
PubMed1989

Allopurinol inhibits uric acid accumulation in the rat brain following focal cerebral ischemia.

Uric acid (UA) in the rat brain was measured by HPLC with an electrochemical detector following focal ischemia. At 24 h after the operation, the UA level in the ischemic center was 105.47 +/- 8.39 nmol/g tissue, whereas it was 8.36 +/- 1.86 in the sham-operated group. Allopurinol, xanthine oxidase inhibitor, almost completely inhibited this UA accumulation. These data demonstrate that the UA increase in the ischemic brain is due to the xanthine oxidase reaction.

Allopurinol↗
PubMed1976

Isolation and characterization of uricine from uric acid stones.

Uricine was found to be present in all uric acid stones tested, although another physiochemically related pigment was occasionally present. Uricine is of low molecular weight (28.2) and a preliminary analysis of its structure suggests that it is formed by two pyrrolic rings. It is a yellow pigment whose color is pH-dependent, shifting from reddish-yellow to green at pH 1.0. It is water soluble, but its solubility increases in alkaline solutions. Preliminary evidence suggests that uricine is related metabolically to bilirubin-like compounds.

Chemical Phenomena↗