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PubMed1978

Metabolism of uric acid in normal and toxemic pregnancy.

The formation, measurement, and excretion of uric acid are reviewed. Since fluctuations in serum uric acid may be as high as 40% over a 24-hour period, a single value must be evaluated with caution. Alterations in the renal handling of uric acid are responsible for the pronounced decrease in serum uric acid over the first 20 weeks of gestation, its gradual increase in the latter part of pregnancy, and its further increase with pregnancy-induced hypertension. Although there is a fair degree of overlap between a normotensive control and a preeclamptic group, the level of serum uric acid generally correlates with the severity of preeclampsia. Possible intrarenal mechanisms that could produce these changes are discussed.

Eclampsia↗
PubMed1998

Purine metabolism of uric acid urolithiasis induced in newborn piglets.

To clarify the relationship between uric acid urolithiasis and purine catabolites in newborn piglets, the incidence of uric acid urolithiasis and the plasma concentrations of xanthine, hypoxanthine, uric acid and allantoin were examined in 32 piglets. The newborn piglets were divided into two groups: normal (over 1.2 kg, n = 18, group N) and low body weight (below 0.9 kg, n = 14, group L). The animals in both groups were given water (non-nutrition, n = 11, treatment W), artificial milk (normal nutrition, n = 12, treatment M), or a combination of water and allopurinol (prophylactic treatment for the urolithiasis, n = 9, treatment A), during the first 60-hr of birth. At necropsy, the incidence of urolithiasis was higher in the piglets that received treatment W than those in the treatment M or A in both the N and L groups. In group L, the plasma xanthine, hypoxanthine and uric acid concentrations were markedly increased in the piglets that underwent treatment W compared with the treatment M. In both the N and L groups, the plasma allantoin concentration was higher in the treatment W piglets as compared with the treatment M piglets. These results suggested that the occurrence of uric acid urolithiasis in the newborn piglets is attributable to increased purine catabolites due to a starvational condition after birth.

Aging↗
PubMed1986

In vitro oxidation of uric acid in serum by methylene blue.

Methylene blue oxidizes uric acid to allantoin in vitro, analogous to the reaction between uric acid and phosphotungstate, although the rate is considerably slower. The reaction requires oxygen and produces hydrogen peroxide. As little as 10 micromol of methylene blue per liter in a serum sample will produce a measurable difference in the apparent uric acid concentration within 4 h at room temperature. Methylene blue may be administered for various medical reasons. If uric acid is to be measured in such sera, the procedure should be performed within 30 min, whatever method of analysis is used.

Aerobiosis↗
PubMed1992

Capillary endothelial transport of uric acid in guinea pig heart.

Much of the adenosine formed in the heart is degraded by endothelial enzymes to uric acid, which is exported across the coronary capillary endothelial cell membrane before renal excretion. Because previous experiments suggested that cell permeability for uric acid is either very high (similar to water) or very low, multiple indicator-dilution experiments were carried out to distinguish between the two possibilities. An intravascular reference tracer, 131I-labeled albumin, and an extracellular reference tracer, L-[3H]glucose, were injected together with [14C]uric acid as a bolus into the coronary inflow, while fractionating the venous outflow for 90 s. Recovery of injected uric acid averaged 99.0 +/- 2.9% (mean +/- SD, n = 12) that of L-glucose. Peak capillary extraction of L-glucose and uric acid averaged 0.38 +/- 0.032 and 0.42 +/- 0.035 (P less than 0.005) compared with albumin. Except at the peaks, the dilution curves for [14C]uric acid and L-[3H]glucose coincided closely, indicating that little uric acid was transported into cells. The dilution curves were analyzed using an axially distributed, multipathway, four region mathematical model, to estimate membrane permeability-surface area (PS) products. Since the endothelial cell PS for uric acid was low (0.12 +/- 0.09 ml.g-1.min-1), approximately 3% of the PS reported for adenosine, the possibility of flow-limited exchange for uric acid is ruled out. To estimate steady-state endothelial concentrations of uric acid in vivo, equations were developed describing electrochemical potential gradients for dissociated and undissociated forms of a weak acid. Despite endothelial production, intracellular concentrations that are lower than outside are expected because the negative membrane potential and lower cellular pH assist uric acid efflux.

Algorithms↗
PubMed2004

Hypouricemia in severely disabled children II: influence of elemental enteral nutrition on the serum uric acid levels.

The previous study showed that both valproic acid (VPA) and a bedridden state decreased the serum uric acid level, and VPA-induced renal tubular dysfunction was suspected to be one cause of hypouricemia in severely disabled children. However, it was uncertain what factor of bedridden state influences the uric acid level in severely disabled children. Among many factors of a bedridden state that might influence the uric acid level, we examined the influence of elemental nutrition on the serum uric acid level in severely disabled children because many severely disabled children with marked hypouricemia receive elemental nutrition. Thirty-one severely disabled children were included in this study, who were divided into two groups-group A: 11 patients with elemental nutrition; group B: 20 patients with non-elemental nutrition. The laboratory data in both groups were analyzed statistically, using the t-test. The uric acid level was significantly decreased in group A compared with group B (p < 0.01) without elevation of urinary excretion of uric acid. Other laboratory data, except phosphate and potassium, did not differ between the two groups significantly. An elemental diet may be one factor that decreases the uric acid level in severely disabled children.

Adolescent↗
PubMed2005

[Uric acid as a marker of pathophysiological mechanisms in patients with cardiovascular disease].

Uric acid can serve as a marker of pathophysiological mechanisms in patients with cardiovascular disease, which may explain why serum uric acid contains prognostic information. Uric acid is the end product of purine degradation. It is catalyzed by the enzyme xanthin oxidase, which is responsible for the production of uric acid and damaging free radicals. This is a central link in the association between serum uric acid and myocardial ischemia, myocardial dysfunction and non-cardial function, which is determined primarily by impaired peripheral blood flow. Inhibition of xanthin oxidase with allopurinol may be used in future treatment of heart patients.

Biomarkers↗
PubMed1998

The effects of eprosartan, an angiotensin II AT1 receptor antagonist, on uric acid excretion in patients with mild to moderate essential hypertension.

The effects of antihypertensive agents, including angiotensin II receptor antagonists, on urine uric acid excretion may have important clinical consequences. Therefore, the effects of single and repeated doses of eprosartan on uric acid excretion were evaluated in 57 male patients with mild-to-moderate essential hypertension in a double-blind, randomized, placebo-controlled, repeated dose, dose-rising, two-period, period-balanced, crossover study conducted in two parts. In part 1 (n = 33), the effects of eprosartan dose regimens of 50 mg, 100 mg, and 350 mg once daily and 150 mg every 12 hours on uric acid excretion were assessed. In part 2 (n = 24), the effects of eprosartan dose regimens of 600 mg, 800 mg, and 1,200 mg once daily on uric acid excretion were assessed. Eprosartan was well tolerated. There were no appreciable changes from predose values in fractional excretion of uric acid (FEua), urine uric acid excretion, urine uric acid to creatinine (Uua/Ucr) ratios, or serum uric acid concentrations after single or repeated doses of eprosartan. Mean Uua/Ucr ratios for eprosartan doses of 50 mg, 100 mg, or 350 mg daily or 150 mg every 12 hours were comparable to those for placebo. Mean FEua values and Uua/Ucr ratios for eprosartan doses of 600 mg, 800 mg, or 1,200 mg daily also were comparable to those for placebo. Single and repeated oral doses of eprosartan ranging from 50 mg to 1,200 mg daily had no effect on serum uric acid concentrations or urine uric acid excretion in patients with mild-to-moderate essential hypertension.

Acrylates↗
PubMedDate not supplied

[Diuretics and uric acid (author's transl)].

Long-term diuretic therapy often increases serum uric acid. The renal metabolism of uric acid is recalled and the factors which lead to diuretic-induced hyperuricemia are discussed. Fluid and sodium loss appears to be the main cause of increased serum uric acid. The authors' experience with management of severe hypertension is consistent with this theory. The effect of tienilic acid which lowers serum uric acid levels is discussed.

Adult↗
PubMed2002

Part 1. Uric acid and losartan.

PURPOSE OF REVIEW: To characterize the mechanism and clinical impact of the angiotensin-receptor blocker losartan on both renal uric acid handling and thereby serum uric acid. RECENT FINDINGS: Losartan effect on serum uric acid has been demonstrated at various stages of renal failure including most recently observations obtained in end-stage renal disease patients. Other angiotensin-receptor blockers do not alter renal handling of uric acid. The uricosuria, which accompanies losartan administration, has not been associated with adverse renal consequences, in part, because of the increase in urinary pH that follows its administration. SUMMARY: Hyperuricemia is closely linked to both hypertension and cardiovascular disease. The development of hyperuricemia and its persistence are clearly renal processes. Likewise, the correction of hyperuricemia is often accomplished by increasing its renal excretion. A number of medications, by way of varying mechanisms, can alter renal urate handling and thereby influence serum uric acid values. Most recently, the angiotensin-receptor blocker losartan has been shown to reduce serum uric acid. The mechanism of this process relates to losartan alone and does not involve the E-3174 metabolite of this compound. This probenecid-like effect of losartan occurs shortly after drug administration, and is both transient and dose-dependent. This property of losartan, touted by some as a meaningful pharmacological distinction among the angiotensin-receptor blockers, remains to be proved, since, to date, the hypothesis that a reduction in serum uric acid alters the natural history of cardiovascular disease has not been formally tested.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

Plasma uric acid level and its association with diabetes mellitus and some biologic parameters in a biracial population of Fiji.

Plasma uric acid was investigated in a population survey on diabetes and cardiovascular risk factors among Melanesians and Asian Indians in Fiji in 1980. Plasma uric acid levels were elevated in men and women with impaired glucose tolerance in both ethnic groups. The lowest plasma uric acid levels were found in diabetic patients, especially in diabetic men. Even though obesity was positively associated with plasma uric acid, it did not explain the high plasma uric acid level in persons with impaired glucose tolerance. Body mass index had a significant and independent impact on plasma uric acid levels both in nondiabetic and diabetic men and women. The strongest predictor of plasma uric acid in the multiple regression analysis in our study populations was plasma creatinine: it alone explained 9% of the variation in men and 2% in women; and 24% in Melanesians and 5% in Asian Indians. Our findings suggest a strong renal involvement in the balance of plasma uric acid and may also reflect certain dietary patterns, such as a high intake of protein, fats, and certain local vegetables. Although the prevalence of hyperuricemia was high, 27% in both Melanesian men and women, 22% in Asian Indian men, and 11% in Asian Indian women, clinical gout was uncommon. Many predictor variables and their interactions were analyzed along with the reasons for the high plasma uric acid levels in persons with impaired glucose tolerance and for the low plasma uric acid levels in diabetic patients.

Adult↗
PubMed1990

Uric acid handling in autosomal dominant polycystic kidney disease with normal filtration rates.

PURPOSE: Patients with autosomal dominant polycystic kidney disease (ADPKD) are alleged to have more frequent or more pronounced alterations of uric acid homeostasis than are seen in most other types of chronic renal diseases. We performed this study to examine the hypothesis that individuals with ADPKD have abnormal uric acid homeostasis that is manifest before the development of renal insufficiency. PATIENTS AND METHODS: We studied 301 subjects, 163 with ADPKD and 138 relatives without ADPKD (NADPKD), by ultrasonography. The subjects were interviewed and examined. Venous blood and two 24-hour urine collections were obtained for uric acid and creatinine determinations. RESULTS: Presence of hyperuricemia, serum uric acid levels, uric acid clearance, and fractional excretion of uric acid did not differ between ADPKD and NADPKD subjects with normal renal function (creatinine clearance greater than 80 mL/minute/1.73 m2). Clearance of uric acid decreased and fractional excretion increased in subjects with decreased renal function in both groups. Female gender enhanced renal excretion of uric acid in both groups and hypertension depressed it except in men with ADPKD, who had higher fractional excretions of uric acid than did hypertensive NADPKD men. CONCLUSIONS: Uric acid homeostasis is preserved in individuals with ADPKD with normal renal function when compared to unaffected family members. Hyperuricemia and decreased renal excretion of uric acid develop as renal function worsens in ADPKD, similar to that in control subjects. The expected depressing effect of hypertension on renal handling of uric acid was not seen in men with ADPKD, speculatively due to an effect of atrial natriuretic factor.

Female↗
PubMedDate not supplied

Serum lipids and uric acid relationship in ischemic thrombotic cerebrovascular disease.

Serum lipids and serum uric acid have been studied in 50 patients with ischemic thrombotic cerebrovascular disease. Patients having diseases known to predispose to hyperuricemia were excluded. Abnormalities of large vessels were present in 14 or 30 cases (46.6%) as a whole, and in 9 of 16 cases (56.5%) below 40 years of age. Thirty percent of the cases showed hyperuricemia. A statistically significant rise in serum triglycerides, pre-beta lipoproteins and serum uric acid was found in all 50 patients and in patients below 40 years of age. In patients above 40 years of age, only the rise in serum triglycerides and pre-beta lipoproteins was found to be statistically significant. A statistically significant rise in serum triglycerides, pre-beta lipoproteins, cholesterols and uric acid was found in patients with abnormal angiograms. A statistically significant correlation was observed between serum uric acid and serum triglycerides in all the groups, between serum uric acid and pre-beta lipoprotein in patients below 40 years of age, and between serum uric acid and serum phospholipids in patients with abnormal angiograms. These factors may be playing a role in the causation of ischemic thrombotic cerebrovascular disease in general and especially in patients below 40 years of age.

Adult↗
PubMed1978

The relationship between uric acid and potassium in normal subjects.

The serum uric acid concentration in normal healthy subjects has been studied in relation to sex, height, weight, lean body mass measured from total body potassium and predicted from the Hume-Weyers formula (1971), total body potassium, plasma potassium and urea, and packed cell volume. The strongest correlation was found with sex, but height, weight, total body potassium, lean body mass (measured and predicted) also correlated significantly with serum uric acid concentration. However, when the sex variable was removed, the other factors lost their significant correlation. Finally, total red blood cell and plasma volumes were predicted (Hume and Goldberg, 1964) and from these an estimate of total plasma uric acid, total plasma potassium, and total red blood cell potassium obtained. Measured total body potassium was found to correlate well with total plasma potassium and total red blood cell potassium independent of sex. Total plasma uric acid correlated well with measured total body potassium when both sexes were considered and when separated into male and female groups the males retained a significant correlation as did the female group.

Adolescent↗
PubMed1977

Effect of methoxyflurane anesthesia on serum uric acid in man.

Serum uric acid levels were significantly increased on the first and third postoperative days following methoxyflurane anesthesia in subjects undergoing various surgical procedures. The increment on each of these days was significantly correlated with the duration of the anesthesia. No such changes were found following halothane or nitrous oxide-oxygen and relaxant anesthesia.

Halothane↗
PubMed2006

Serum uric acid as an obesity-related indicator in early adolescence.

In adults, serum uric acid levels are positively correlated with body mass index (BMI) and hyperuricemia is considered to be a common lifestyle disorder related with obesity. However, the relation of serum uric acid levels with obesity has not been elucidated in children and adolescents. Serum uric acid levels were determined in 1,729 healthy children, consisted of 923 boys and 806 girls, aged 9.1 - 15.0 years. The incidence of hyperuricemia (defined as more than 7.0 mg/dl) in boys and girls were 8.8% and 0.6%, respectively. In 1,281 children out of all subjects, including 684 boys and 597 girls, height, weight, aspartate aminotransferase, and alanine aminotransferase were also determined and the correlations between serum uric acid levels and obesity were analyzed. BMI is popularly used as a standard indicator of obesity in adults. However, BMI increases without fat accumulation as children grow. In Japan, percentage of overweight (POW) is usually used as an alternative indicator for obesity. In general, children are evaluated as obesity, when POW is equal to or more than 20% (>or= 20%). Serum uric acid levels are positively correlated with obesity-related indicators, BMI and POW, in both boys and girls. Serum uric acid levels of the subjects with high POW (>or= 20%) are significantly higher than those of the subjects with low POW (< 20%) in both boys and girls. These results suggest that serum uric acid levels are significantly increased with obesity and could be used as one of obesity-related indicators even in early adolescence.

Adolescent↗
PubMed1999

Evaluation of serum uric acid changes in different forms of hepatic vascular inflow occlusion in human liver surgeries.

Uric acid values in serum have been analyzed as one of the markers to predict cellular damage due to ischemia reperfusion injury in the field of organ transplantation. The present study was conducted to confirm that uric acid values in serum could be an efficient marker of ischemic injury of liver parenchyma following hepatic vascular occlusion in human liver surgery. The changes in serum uric acid values were analyzed at fixed intervals during different liver surgeries. Significant increases in serum uric acid values were observed in patients who received the Pringle's maneuver in which hepatic vascular inflow was manipulated with a repetition of 15 min occlusion and 5 min perfusion, whereas almost no changes in uric acid values were found in both groups of patients who received the hemilobal occlusion of the Glisson's triad in which the right or left vessels were manipulated with a repetition of 30 min occlusion and 5 min perfusion and the "control method" in which the hepatic vessels of the lesion side were previously cut before liver resection. Uric acid values in serum increased in patients of Pringle's maneuver compared to those of the hemilobal occlusion of the Glisson's triad and the control method though these procedures were used in larger hepatectomies rather than Pringle's maneuver. The results indicated that serum uric acid values do not always reflect the severity of ischemia of the liver parenchyma but reflect intestinal congestion because marked intestinal congestion was observed in patients of Pringle's maneuver but not in patients of the hemilobal occlusion of the Glisson's triad and the control method. The evaluation of the severity of the ischemic injury of the liver should be done with caution when uric acid is used as a marker in human liver surgery.

Adolescent↗
PubMed1997

[Variations in the uric acid levels in pregnancy hypertension].

The objective was to analyse the levels of uric acid in the hypertensive disorders of pregnancy. The research involves the study of 137 patients that suffered any hypertensive disease associated with pregnancy, hospitalized on the Luis Castelazo Ayala Hospital. The patients were classified according to the ACOG. The levels of uric acid observed were measured and compared against one control group and between them. The levels of uric acid observed in any hypertensive state of pregnancy are superior to the ones observed in then control group. On patients with chronical hypertension complicated with preeclampsia, the levels of uric acid were above the levels observed on patients with chronic hypertension itself. It is not known with certainty, but some authors think that the problem es rather tubular than glomerular. There is not an exact explanation about uric acid's depuration. Nevertheless, the common characteristic is a reduction of renal perfusion. Uric acid is related with the degree of severity. Moreover, uric acid is a good indicator for the detection of hypertensive states of pregnancy.

Adult↗
PubMed2006

Analysis of excretion fraction of uric acid.

Excretion fraction of uric acid (EFUA), is one of the most important hallmarks for diagnosis of familial juvenile hyperuricemic nephropathy (FJHN) and hereditary renal hypouricemia. EFUA was measured in 20 patients with FJHN. However, low excretion fraction (<6%) was found also in healthy FJHN family members and healthy controls (ref. ranges EFUA: men 6-12%, women 6-20%). Similar finding of low EFUA was reported recently. Distribution of EFUA was further studied in 2,416 healthy controls, which were selected from 6,000 samples and divided according to age. In conclusion, finding of low EFUA in family members is a risk factor for renal damage and indication for purine metabolic investigations with subsequent molecular biology analysis. As EFUA could be found also in healthy controls--it should be interpreted with care and other features of FJHN (such as hyperuricemia, progressive renal disease in family) should be taken to account.

Adolescent↗