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PubMed2001

Creatine kinase and uric acid: early warning for metabolic imbalance resulting from disorders of fatty acid oxidation.

UNLABELLED: In eight patients with disorders of fatty acid oxidation, analysis of uric acid and creatine kinase served as indicators of the underlying disorder in episodes of acute metabolic imbalance. Six patients had deficiency of medium-chain acyl-CoA dehydrogenase, one had long-chain hydroxyacyl-CoA dehydrogenase deficiency, and one very long-chain acyl-CoA dehydrogenase deficiency. The most common presentation was with symptomatic hypoglycemia; there was one Reye-like presentation and one of rhabdomyolysis. The mechanism of the elevation of uric acid and creatine kinase appears to be the breakdown of tissue. CONCLUSION: it is concluded that uric acid and creatine kinase provide a useful alerting signal to the presence of a disorder of fatty acid oxidation. Maximal levels of uric acid in this series were 6.2-21.5 mg/dl and of creatine kinase 879-27,557 U/l.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed2002

[The association between uric acid and coronary heart disease].

OBJECTIVE: To determine the association between uric acid and coronary artery disease (CAD) and whether the relationship is gender dependent. METHOD: A cross-sectional study of 355 men and women with or without CAD was performed. Coronary artery angiography was done for all the subjects. Patients treated with diuretics, isopurinol, aspirin, lipid-lowering agents and heparin and patients with renal, hepatic, or thyroid diseases were excluded. Gender, age, body mass index, fasting plasma glucose, total cholesterol, triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, fibrinogen, cigarette smoking consumption, CAD family history, essential hypertension history and CAD severity were analyzed. Cigarette smoking consumption was graded as follows: 0: no smoking, 1: </= 5 pack-year, 2: 5 to 10 pack-year, 3: greater than 10 pack-year. CAD severity was scored angiographically as follows: 0 (absent): no evidence of CAD; 1 (mild): 1-vessel disease with < 50% stenosis; 2 (moderate): 1-vessel disease with >/= 50% stenosis, or 2-vessel disease, both vessels with < 50% stenosis or 1 with < 50% and the other with > 50% stenosis, or 3-vessel disease, all with < 50% stenosis; 3 (severe): 2-vessel disease, both with > 50% stenosis, or 3-vessel disease with >/= stenosis in one vessel > 50%. RESULTS: The upper uric acid qunrtiles in the women group were associated with higher CAD severity than the lower uric acid qunrtiles. The mean CAD severity score according to the uric acid qunrtiles were 2.10 (uric acid 163 approximately 217.5 micro mol/L) 2.27, (uric acid 218.0 approximately 276.0 micro mol/L) 2.36 (uric acid 277.0 approximately 335.0 micro mol/L) and 2.62 (uric acid 336.0 approximately 694.0 micro mol/L). No such relation was found in men. With multiple logistic regression, gender (B = 0.924, P = 0.012, OR = 2.520), fasting plasma glucose (B = 0.391, P = 0.006, OR = 1.478), fibrinogen (B = 0.007, P = 0.000, OR = 1.007) and cigarette smoking consumption grading (B = 0.306, P = 0.018, OR = 1.358) were independently associated with CAD, there was a trend association between age and CAD (B = 0.032, P = 0.056, OR = 1.032), Uric acid (B = 0.002, P = 0.349, OR = 0.998) and other variables did not have significant independent association with CAD. With stepwise multiple regression analysis, fibrinogen, fasting plasma glucose, total cholesterol, gender, age showed significant independent association with CAD severity, but uric acid (B = 0.004, beta = 0.025, t = 0.373, P = 0.709) and other variables did not. In the female group, CAD or CAD severity was independently associated with triglyceride and fibrinogen, but not with uric acid. CONCLUSIONS: The upper uric acid qunrtiles in the women group have higher CAD severity than the lower uric acid qunrtiles. However, with multiple regression, either in women or in men, uric acid was not independently associated with CAD or CAD severity.

Adult↗
PubMed1977

Protein intake, uric acid metabolism and protein efficiency ratio in growing chicks.

Changes in uric acid metabolism in chicks resulting from alterations in dietary protein intake have been correlated with dietary protein quality. Plasma uric acid levels, total uric acid excretion and protein efficiency ratio were measured in growing chicks fed diets containing 11%, 20%, 43% and 80% protein. A second degree polynomial with a coefficient of determination of 93% best described the relationship between dietary protein intake and total uric acid output. A second degree polynomial with a coefficient of determination of 58% best described the relationship between protein intake and dietary protein quality as measured by the protein efficiency ratio method. Plasma uric acid level was correlated, positively and linearly, with dietary protein intake and had a coefficient of determination of 42%. An integration of these relationships with purine biosynthesis and reutilization would enhance our knowledge of the control of uric acid production in the chick and possibly in human gout. The data demonstrate that total uric acid excretion and uric acid concentration in excreta may represent very useful methods of measuring dietary protein quality in the chick. The data also demonstrate that dietary protein level markedly affects uric acid production.

Animals↗
PubMed2003

The effect of a vegetarian and different omnivorous diets on urinary risk factors for uric acid stone formation.

BACKGROUND: About 10-15% of all urinary stones are composed of uric acid. A high urinary uric acid excretion, a low urine volume and an acidic urinary pH value are suggested to be the most important risk factors for uric acid stone formation. AIM OF THE STUDY: The effect of a vegetarian diet and different omnivorous diets on the risk of uric acid crystallization was investigated. METHODS: Ten healthy male subjects ingested a self-selected meat-containing diet (SD) for two weeks, and three different standardized diets for a period of 5 days each. The Westerntype diet (WD) was representative of the usual dietary habits,whereas the balanced omnivorous diet (OD) and the ovo-lacto-vegetarian diet (VD) were calculated according to the requirements. RESULTS: The risk of uric acid crystallization was highest on the ingestion of diets SD and WD, due to the high urinary uric acid excretion and the acidic urinary pH. The relative supersaturation with uric acid declined significantly by 85% on the intake of diet OD, consequent to the decrease in uric acid excretion and concentration and the increase in urinary pH value. The ingestion of the vegetarian diet VD led to a further significant reduction in the risk of uric acid crystallization by 93% compared to diet WD. CONCLUSIONS: The results indicate that the intake of a balanced vegetarian diet with a moderate animal protein and purine content, an adequate fluid intake and a high alkali-load with fruits and vegetables results in the lowest risk of uric acid crystallization compared to the omnivorous diets.

Adult↗
PubMed2004

The metabolic syndrome and uric acid nephrolithiasis: novel features of renal manifestation of insulin resistance.

BACKGROUND: Uric acid nephrolithiasis primarily results from low urinary pH, which increases the concentration of the insoluble undissociated uric acid, causing formation of both uric acid and mixed uric acid/calcium oxalate stones. These patients have recently been described as exhibiting features of insulin resistance. This study was designed to evaluate if insulin resistance is associated with excessively low urinary pH in overtly healthy volunteers (non-stone formers) and if insulin resistance may explain the excessively low urinary pH in patients with uric acid nephrolithiasis. METHODS: Fifty-five healthy volunteers (non stone-formers) with a large range of body mass index and 13 patients with recurrent uric acid nephrolithiasis underwent hyperinsulinemic euglycemic clamp, 24-hour urinary studies, and anthropometric measurements of adiposity. A subgroup of 35 non-stone formers had 2-hour timed urinary collection before and during the hyperinsulinemic phase of the clamp studies. RESULTS: For the non-stone former population, low insulin sensitivity measured as glucose disposal rate significantly correlated with low 24-hour urinary pH (r= 0. 35; P= 0.01). In addition to the previously described acidic urine pH and hypouricosuria, patients with recurrent uric acid nephrolithiasis were found to be severely insulin resistant (glucose disposal rate: uric acid stone-formers vs. normals; 4.1 +/- 1.3 vs. 6.9 +/- 2.1 mg/min/kg of lean body mass, P= 0.008). Acute hyperinsulinemia was associated with higher urinary pH (6.1 +/- 0.7 at baseline to 6.8 +/- 0.7 during hyperinsulinemia; P < 0.0001), urinary ammonia excretion (2.7 +/- 1.6 mEq/2 hr at baseline and 4.0 +/- 2.6 mEq/2 hr P= 0.002) and urinary citrate excretion (48 +/- 33 mg/2 hr at baseline and 113 +/- 68 mg/2 hr P < 0.0001). CONCLUSION: We conclude that one renal manifestation of insulin resistance may be low urinary ammonium and pH. This defect can result in increased risk of uric acid precipitation despite normouricosuria.

Acids↗
PubMed2006

Role of uric acid in different types of calcium oxalate renal calculi.

AIM: The presence of uric acid in the beginning zone of different types of 'pure' calcium oxalate renal calculi was evaluated with the aim of establishing the degree of participation of uric acid crystals in the formation of such calculi. METHODS: The core or fragment of different types of 'pure' calcium oxalate renal calculi was detached, pulverized and uric acid extracted. Uric acid was determined using a high-performance liquid chromatography/mass spectrometry method. RESULTS: In calcium oxalate monohydrate (COM) papillary calculi with a core constituted by COM crystals and organic matter, 0.030+/-0.007% uric acid was found in the core. In COM papillary calculi with a core constituted by hydroxyapatite, 0.031+/-0.008% uric acid was found in the core. In COM unattached calculi (formed in renal cavities) with the core mainly formed by COM crystals and organic matter, 0.24+/-0.09% uric acid was found in the core. In COM unattached calculi with the core formed by uric acid identifiable by scanning electron microscopy (SEM) coupled to X-ray microanalysis, 20.8+/-7.8% uric acid was found in the core. In calcium oxalate dihydrate (COD) unattached calculi containing little amounts of organic matter, 0.012+/-0.004% uric acid was found. In COD unattached calculi containing little amounts of organic matter and hydroxyapatite, 0.0030+/-0.0004% of uric acid was found. CONCLUSIONS: From these results it can be deduced that uric acid can play an important role as inducer (heterogeneous nucleant) of COM unattached calculi with the core formed by uric acid identifiable by SEM coupled to X-ray microanalysis (these calculi constitute the 1.2% of all calculi) and in COM unattached calculi with the core mainly formed by COM crystals and organic matter (these calculi constitute the 10.8% of all calculi).

Calcium Oxalate↗
PubMed1976

The epitaxially induced crystal growth of calcium oxalate by crystalline uric acid.

Seed crystals of anhydrous uric acid were shown to epitaxially induce the crystal growth of calcium oxalate monohydrate from its metastable supersaturated solution. Scanning electron microscopic examination of crystalline material isolated from the kinetic experiments supports the chemical evidence that calcium oxalate had been nucleated by uric acid. In spite of close lattice similarities between some of the faces of the two phases, the induction period required for heterogeneous nucleation by the seed material was about half of that required for precipitation in the absence of potential nucleating agents. This has created some doubt as to whether crystalline uric acid has an influence on the formation of calcium oxalate lithiasis.

Calcium↗
PubMed1997

Specific detection of kappa light chain in uric acid stones.

Proteins were extracted from uric acid stones with 6M guanidine chloride (pH 8.5), which were successively developed by 12% polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate (SDS-PAGE). Amino acid sequence analysis of each band on SDS-PAGE revealed that major components in uric acid stones were immunoglobulin alpha heavy and kappa light chains. Although immunoglobulin heavy chain (gamma and mu, as well as alpha) and a kappa light chain were clearly detected in uric acid stones by Western blotting using their specific antibodies, no lambda chains whatsoever could be detected. The results suggest that immunoglobulins selectively containing kappa light chain might have specific functions in uric acid stone formation as stone matrices.

Amino Acid Sequence↗
PubMed2006

Association between intronic SNP in urate-anion exchanger gene, SLC22A12, and serum uric acid levels in Japanese.

Serum uric acid levels are maintained by urate synthesis and excretion. URAT1 (coded by SLC22CA12) was recently proposed to be the major absorptive urate transporter protein in the kidney regulating blood urate levels. Because genetic background is known to affect serum urate levels, we hypothesized that genetic variations in SLC22A12 may predispose humans to hyperuricemia and gout. We investigated rs893006 polymorphism (GG, GT and TT) in SLC22A12 in a total of 326 Japanese subjects. Differences in clinical characteristics among the genotype groups were tested by the analysis of variance (ANOVA). In male subjects, mean serum uric acid levels were significantly different among the three genotypes. Levels in the GG genotype subjects were the highest, followed by those with the GT and TT genotypes. However, no differences between the groups were seen in the distributions of creatinine, Fasting plasma glucose (FPG), HbA(1c), total cholesterol, triglyceride, HDL cholesterol levels or BMI. A single nucleotide polymorphism (SNP) in the urate transporter gene SLC22CA12 was found to be associated with elevated serum uric acid levels among Japanese subjects. This SNP may be an independent genetic marker for predicting hyperuricemia.

Asian People↗
PubMed1994

Reliability of single urine and serum samples for estimation of 24-hour urinary uric acid excretion in six healthy beagles.

Urine uric acid-to-urine creatinine ratios (UUA:UC), urine uric acid concentrations, urine uric acid concentrations corrected for glomerular filtration rate, and urinary uric acid fractional excretions were compared with 24-hour urinary uric acid excretions measured in 6 healthy adult female Beagles. Comparisons, using correlation analysis, were made when dogs consumed a 10.4% protein (dry weight), casein-based diet and a 31.4% protein (dry weight), meat-based diet. The UUA:UC, urine uric acid concentrations corrected for glomerular filtration rate, and urinary uric acid fractional excretions were not reliable estimates of 24-hour urinary uric acid excretions during consumption of either diet. Urine uric acid concentrations in samples collected 2, 4, 6, and 24 hours after initiation of collection correlated with 24-hour urinary uric acid excretions when dogs consumed the casein-based diet; correlation was not found at any time interval when dogs consumed the meat-based diet. Therefore, determination of 24-hour urinary uric acid excretion is recommended because UUA:UC are unreliable.

Animals↗
PubMed1992

Urine uric acid excretion in patients with insulin-dependent diabetes mellitus.

Serum uric acid has been described as being increased in the prediabetic stage of diabetes mellitus and as being decreased in overt diabetes. In this study we compared the serum uric acid levels of patients with insulin-dependent diabetes mellitus (IDDM) to those of controls matched for sex, age and ethnic origin. Also the correlation between serum uric acid levels and the fractional excretion of uric acid in IDDM patients was investigated, as well as the correlation between glycosuria and the fractional excretion of uric acid. The mean serum uric acid was lower in IDDM patients than in normal controls (4.0 +/- 1.3 vs. 4.3 +/- 1.3 mg/100 ml; p less than 0.03), mainly due to significantly lower levels in male and Ashkenazi IDDM patients, as compared to their respective controls. The fractional excretion of uric acid was found to be elevated in IDDM patients: 13.0 +/- 8.6% (mean +/- SD). A significant negative correlation was found between serum uric acid levels and the fractional excretion of uric acid in IDDM patients (p less than 0.001), although not when the males were examined separately. We found no correlation between the fractional excretion of uric acid and the degree of glycosuria in IDDM patients. In addition, the prevalence of hypouricemia (serum uric acid less than 2.5 mg%) was the same in IDDM patients and controls.

Adult↗
PubMed1992

Relation between creatinine and uric acid excretion.

The relation between creatinine and uric acid metabolism was analysed in 77 male patients with primary gout and 62 healthy male subjects. Significant positive correlations between 24 hour urinary creatinine and uric acid excretion were shown in both groups. The mean urinary creatinine and uric acid excretions in the patients with gout were significantly increased as compared with those of normal male controls. These results suggest that there is a close correlation between creatinine and uric acid synthesis. In addition, it seems that accelerated uric acid synthesis seen in some patients with gout is due to increased creatinine synthesis.

Adult↗
PubMed1983

[Parathyroid function and uric acid metabolism].

In order to elucidate the influence of the parathyroid function on the uric acid metabolism, 24 patients (14 males, 10 females) with primary hyperparathyroidism (PHP) and 17 patients (9 males, 8 females) with idiopathic hypoparathyroidism (IHP) were extensively studied. The mean age was not significantly different between these groups, being 40.3 +/- 2.8 and 39.0 +/- 3.5 respectively. Hyperuricemia was found in 4 patients with PHP, but none of the patients had experienced gout. The serum uric acid levels were significantly higher and uric acid clearances were significantly lower in PHP than in IHP. There was no difference in daily urinary excretion of uric acid and in creatinine clearance between the two groups. In PHP, a positive correlation was observed between the levels of serum uric acid and calcium, both of which negatively correlated to renal uric acid clearance. Although the serum uric acid levels did not correlate to serum PTH levels in PHP, the removal of parathyroid adenoma resulted in a significant fall of serum uric acid levels. In IHP, the administration of PTH induced a small but significant decrease in serum uric acid levels with a coincidental increase in urinary uric acid excretion. Four hours of calcium infusion had no effect on the serum uric acid levels and urinary uric acid excretion. Treatment of IHP with 1 alpha-OH D3 to restore normal serum calcium levels caused significant increase in serum uric acid levels. These data indicate that the parathyroid function influences uric acid metabolism, even in the absence of renal insufficiency, mainly through changes of uric acid clearance. Levels of active vitamin D or chronically abnormal calcium levels in the circulation may be major determinant for uric acid metabolism in parathyroid disorders.

Adolescent↗
PubMedDate not supplied

Predictive value of uric acid in gastric mucosal damage in hemodialysis patients.

BACKGROUND/AIMS: Uric acid, which has an antioxidant effect, is present at very high serum levels in hemodialysis patients, but its effect has not yet been clarified. In this study we investigated whether or not serum uric acid levels could be associated with gastric mucosal damage in hemodialysis patients. METHODOLOGY: We performed endoscopy in 53 patients who were on dialysis for more than two months and determined the relationship between serum uric acid levels, clinical features and gastric mucosal damage. RESULTS: Of 53 patients, gastroduodenal ulcer was found in 13 patients (Ulcer group), gastritis lesions in 25 patients (Gastritis group) and no pathological findings in 15 patients (Normal group). Serum uric acid levels before the dialytic session were remarkably higher in the Ulcer group than in the Normal (P < 0.01) or Gastritis group (P < 0.05). There was also a significant difference between the Gastritis and Normal groups in the serum uric acid levels (P < 0.05). Alcohol intake and noncompliance resulted in a significant increase in both gastric mucosal damage (P = 0.009 and P = 0.010) and serum uric acid levels (P < 0.05 and P < 0.01). Serum uric acid levels were markedly decreased after treatment with a proton pump inhibitor or H2 blocker. CONCLUSIONS: In hemodialysis patients alcohol intake and noncompliance contribute to the increase in serum uric acid levels and gastric mucosal damage, and serum uric acid levels have predictive values in gastric mucosal damage.

Aged↗
PubMed2006

Serum uric acid: a risk factor and a target for treatment?

Serum uric acid was first noted to be associated with increased BP by Frederick Mohamed in the 1870s. Although the link was rediscovered periodically over the years, it generally was dismissed as a surrogate marker for decreased renal function that led to increased uric acid and increased risk for hypertension and cardiovascular (CV) disease. Recently, however, several lines of evidence suggest that increased serum uric acid may be a significant modifiable risk factor. Increased serum uric acid is associated with increased risk for future hypertension in several large longitudinal clinical trials as well as an independent risk factor for poor CV prognosis. Animal model experiments demonstrate that increased serum uric acid causes increased BP that initially is reversible but becomes irreversible, salt sensitive, and uric acid independent over time. The mechanisms include the direct action of uric acid on smooth muscle and vascular endothelial cells. Finally, in adolescents with new-onset essential hypertension, the prevalence of elevated serum uric acid is >90%, and preliminary clinical trial evidence suggests that agents that lower serum uric acid may lower BP in this select population. Although the investigations are still preliminary, serum uric acid represents a possible new and intriguing target for the reduction of morbidity and mortality associated with hypertension and CV disease.

Adolescent↗
PubMed1980

Quantification of renal uric acid synthesis in the rat.

The excretion of nephrogenic uric acid in the urine of Sprague-Dawley rats was estimated by use of the isotope-dilution technique. In nonfasted rats the urine-to-plasma specific activity ratio (SAR) of [14C]uric acid was 0.93, suggesting that a minimum of 7% of the uric acid excreted in the urine is synthesized in the kidney. During hypoxanthine infusion the SAR decreased in a dose-related fashion, indicating that the rat kidney is capable of synthesizing relatively large amounts of uric acid and that circulating precursor levels may in part regulate the renal synthesis of uric acid. During allopurinol infusion the SAR increased to 1.0, demonstrating that the SAR is a valid indicator of the contribution of nephrogenic uric acid excreted into the urine. Results of perfusion studies in isolated rat kidneys suggest that uric acid is the major end product of purine catabolism in the rat kidney and that some uric acid formed in the kidney may be absorbed directly into the circulation.

Allopurinol↗
PubMed1999

[Uric acid as a scavenger in oxidative stress].

Uric acid, the naturally occurring product of purine metabolism, is widely used as a diagnostic parameter in different diseases. The concentration of uric acid may vary between broad ranges without causing symptoms, like idiopathic hyperuricemia, which behind metabolic disorders were always suggested. Recently the uric acid has been shown as a strong scavenger of oxidative stress molecules or radicals. Uric acid was successfully used to treat experimental allergic encephalomyelitis, the mouse model of multiple sclerosis (M. S.). It was shown, that patients with multiple sclerosis had significantly lower levels of serum uric acid than the control persons. In addition, statistical evaluation of more than 20 million patient records for the incidence of MS and hyperuricemic gout revealed, that the hyperuricemia may protect against MS.

Animals↗