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PubMed2002

High prevalence of hyperuricemia in adolescent Taiwan aborigines.

OBJECTIVE: To explore the prevalence and related factors of hyperuricemia among adolescent Taiwan aborigines in tribes with a high prevalence of adult gout, compared with adolescents of low prevalence aboriginal and non-aboriginal tribes. METHODS: The participants were aborigines and non-aborigines in Taiwan, age 12 to 15 years and free of gout. Each participant provided information on sex, age, and parents' tribal background as well as body weight and height. Serum samples were analyzed for biochemical markers. A logistic regression model was used to study factors related to hyperuricemia. RESULTS: In total 940 adolescents participated. The hyperuricemia rate in tribes with high gout prevalence (57.7%) was higher than in non-aborigines (48.2%) and in aboriginal tribes with low gout prevalence (34.0%). Factors statistically significantly related to hyperuricemia were tribe, sex, obesity, creatinine, and cholesterol levels in preliminary analysis. After adjustment by the logistic regression model, obese boys with higher creatinine were most likely to have hyperuricemia. Adolescents whose parents originated from tribes with high gout prevalence had a tendency to have hyperuricemia, and those aborigines from tribes with low gout prevalence had a low prevalence of hyperuricemia compared to non-aborigines. CONCLUSION: The prevalence of hyperuricemia in aboriginal adolescents mirrors the incidence of adult gout, implying a predisposition for adult gout in childhood, with genetic and/or environmental components presumably contributing to the differences between tribes; this may be of potential benefit to preventive efforts.

Adolescent↗
PubMed2004

Recent trends of hyperuricemia and obesity in Japanese male adolescents, 1991 through 2002.

The aim of the present study was to determine the change of serum uric acid (UA) levels in male adolescents and to characterize the relationship between UA levels and obesity or its related factors. This study was conducted in 17,155 students at enrollment in Okayama University from 1991 through 2002, in which the mean serum UA level as a whole was 5.64 +/- 0.009 mg/dL (mean +/- SEM) and the incidence of hyperuricemia (>/=7.6 mg/dL) was 4.13%. Serum UA levels were correlated with obesity-related indicators, including body mass index (BMI; r = 0.282, P <.0001) and skin-fold thickness (r = 0.286, P <.0001). The incidence of hyperuricemia was increased in parallel with BMI. In the last 4 years (1999 through 2002) of the study period, serum UA levels (5.76 mg/dL) and the incidence of hyperuricemia (4.5%) were significantly increased compared with those in the earlier period (1991 through 1994: 5.50 mg/dL and 3.5%, respectively). However, BMI has been rather gradually decreased throughout 12-year observation in all the subjects. Hyperuricemia was related to the presence of other risk factors, including hypercholesterolemia, liver function abnormality, and hypertension. The frequencies of such abnormalities were higher than euuricemic subjects and this trend was notable in the most recent students enrolled from 1999 through 2002. Hyperuricemia was even found in the group of non-obese male adolescents. Taking into consideration that hyperuricemia is associated with a high prevalence of lifestyle-related diseases in adults, it is of great importance to prevent hyperuricemia at the early stage in Japanese adolescents.

Adolescent↗
PubMed2004

Reduced incidence of hyperuricemia, gout, and renal failure following liver transplantation in comparison to heart transplantation: a long-term follow-up study.

BACKGROUND: Hyperuricemia and gout are common complications of heart transplantation, reaching a prevalence of 84% and 30%, respectively, in heart transplant recipients. In contrast, they are seldom reported following orthotopic liver transplantation (OLT). METHODS: We retrospectively evaluated 75 consecutive liver transplant recipients and 47 consecutive heart transplant recipients, followed for at least 3 years after transplantation in a single transplantation center in Jerusalem, Israel. Data was collected on demographic and clinical variables, levels of uric acid, the occurrence of gout, renal function, and variables effecting hyperuricemia, such as weight and medications. RESULTS: Clinical gout was significantly more prevalent in heart recipients than in liver recipients (25.5% and 2.6%, respectively). Hyperuricemia was present in 100% of heart recipients, with an average uric acid level of 451 micromol/l, as compared with 85.7% and 403 micromol/l for liver recipients (P < 0.001 for both variables). Univariate analysis identified several parameters which significantly influenced the difference in hyperuricemia and gout among the two groups including age, gender, rejection episodes, hypertension, diabetes mellitus, the level of uric acid prior to transplantation, and the use of cyclosporine A, diuretics, steroids, and aspirin. Use of tacrolimus and azathioprine were associated with decreased incidence of hyperuricemia and gout. Multivariate analysis identified the type of transplantation as the only independent risk factor predicting the development of hyperuricemia and gout. CONCLUSION: Clinical gout and hyperuricemia were significantly more prevalent in heart recipients than in liver recipients. The disparity can be explained by differences in age, gender and renal function among the groups, as well as by the use of different medication regimens.

Adult↗
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↗
PubMed2005

Hyperuricemia induces endothelial dysfunction.

BACKGROUND: Hyperuricemia has been linked to cardiovascular and renal diseases, possibly through the generation of reactive oxygen species (ROS) and subsequent endothelial dysfunction. The enzymatic effect of xanthine oxidase is the production of ROS and uric acid. Studies have shown that inhibiting xanthine oxidase with allopurinol can reverse endothelial dysfunction. Furthermore, rat studies have shown that hyperuricemia-induced hypertension and vascular disease is at least partially reversed by the supplementation of the nitric oxide synthase (NOS) substrate, L-arginine. Therefore, we hypothesized that uric acid induces endothelial dysfunction by inhibiting nitric oxide production. METHODS: Hyperuricemia was induced in male Sprague-Dawley rats with an uricase inhibitor, oxonic acid, by gavage; control rats received vehicle. Allopurinol was placed in drinking water to block hyperuricemia. Rats were randomly divided into four groups: (1) control, (2) allopurinol only, (3) oxonic acid only, and (4) oxonic acid + allopurinol. Rats were sacrificed at 1 and 7 days, and their serum analyzed for serum uric acid and nitrites/nitrates concentrations. The effect of uric acid on nitric oxide production was also determined in bovine aortic endothelial cells. RESULTS: Oxonic acid induced mild hyperuricemia at both 1 and 7 days (P < 0.05). Allopurinol reversed the hyperuricemia at 7 days (P < .001). Serum nitrites and nitrates (NO(X)) were reduced in hyperuricemic rats at both 1 and 7 days (P < .001). Allopurinol slightly reversed the decrease in NO(X) at 1 day and completely at 7 days (P < .001). There was a direct linear correlation between serum uric acid and NO(X) (R(2)= 0.56) and a trend toward higher systolic blood pressure in hyperuricemic rats (P= NS). Uric acid was also found to inhibit both basal and vascular endothelial growth factor (VEGF)-induced nitric oxide production in bovine aortic endothelial cells. CONCLUSION: Hyperuricemic rats have a decrease in serum nitric oxide which is reversed by lowering uric acid levels. Soluble uric acid also impairs nitric oxide generation in cultured endothelial cells. Thus, hyperuricemia induces endothelial dysfunction; this may provide insight into a pathogenic mechanism by which uric acid may induce hypertension and vascular disease.

Animals↗
PubMed2005

High prevalence of hyperuricemia in elderly Taiwanese.

Serum urate status, the prevalence of hyperuricemia and their relationship to the metabolic syndrome in elderly Taiwanese were described using data from the Elderly Nutrition and Health Survey in Taiwan (1999-2000), in which a stratified multi-stage clustered sampling scheme was applied. Complete data from biochemical assays and anthropometric measures for 1225 males and 1167 females were included in the analysis. The mean urate level and 95% confidence interval was 411 (398, 424) microM for males and 357 (347, 367) microM for females. Males had significantly higher serum urate levels than females across all age groups (P<0.05). No significant difference in mean serum urate was found among the four age groups of males. On the other hand, females of 75-79 years had significantly higher serum urate levels (376 microM) than that of the 65-69 and>or=80 age groups. The overall prevalence of hyperuricemia (>or=416.7 microM (7.0 mg/dL) in the elderly was 36% (46% for males and 26% for females). Among the participants, 4.2% of males and 1.1% of females were taking medication to lower uric acid. The elderly (males 455 microM; females 416 microM) of the Mountain areas, mainly indigenes, had the highest mean serum urate overall, however, the highest prevalence of hyperuricemia in males was found in the PengHu islands (62%) and that for females in the Mountain areas (51%). The odds ratio (OR) for hyperuricemia was 2.84 for males in the PengHu islands and 4.33 for females in Mountain areas, compared with their counterparts in the third stratum in the northern areas. Adjusting for obesity, alcohol and other related covariates did not alter the relative rank of the ORs in the various strata. Elderly males (22%) had a significantly lower rate of metabolic syndrome (MS) than females (39%) (P<0.05). For both genders, those with MS had a significantly higher mean serum urate (males 436 microM vs. 405 microM; females 389 microM vs. 338 microM) and prevalence of hyperuricemia (males 56% vs. 43%; females 38% vs.19%) (P<0.05). The population attributable risk for MS from hyperuricemia was 18.8% in men and 15.5% in women. In conclusion, the mean serum urate and prevalence of hyperuricemia in the elderly in Taiwan were higher than those found in other populations and was significantly associated with MS. Gene-environmental interaction may play a key role since great geographical variation exists within various Han Chinese groups in Taiwan and between Han Chinese and Taiwanese indigenes.

Age Factors↗
PubMed2005

[Study on hyperuricemia with hyperlipaemia, high blood sugar and hypertension in 1320 elderly people].

OBJECTIVE: To investigate the prevalence of hyperuricemia with hyperlipaemia, high blood sugar and hypertension among elderly people. METHODS: Serum uric acid (SUA), cholesterol, triglycerides, blood sugar and blood pressure were detected in 1320 elderly people and 6107 people at young and middle age. RESULTS: The mean SUAs in elderly male and female groups were significantly higher than that in young and middle aged male groups respectively (P < 0.05). The prevalence rates of hyperuricemia in elderly male and female groups were significantly higher than in young and middle aged male groups respectively (P < 0.05). The prevalence rates of hyperlipaemia, high blood sugar and hypertension in the elderly people of hyperuricemia were significantly higher than that in the elderly people of normal serum uric acid (P < 0.05). The prevalence rates of hyperuricemia in the elderly people were complicated by hyperlipaemia, high blood sugar and hypertension which was significantly higher than that in young and middle aged people of hyperuricemia (P < 0.05). CONCLUSION: Hyperuricemia is a common disease in elderly people and more attention should be paid to the closer relations among hyperuricemia with hyperlipaemia, high blood sugar and hypertension among the elderly.

Aged↗
PubMed1980

The natural history of hyperuricemia among asymptomatic relatives of patients with gout.

1. Hyperuricemia is common among the gouty relatives as reported by others (8-11). It is of interest to note that serum urate fluctuates periodically. Hyperuricemia is not necessarily maintained in a steady state throughout the years. Thus a single determination of serum uric acid can be misleading. 2. Development of gout from asymptomatic hyperuricemia is often correlated with the degree of hyperuricemia as observed from population or family studies (12-14). The data presented indicate that unequivocal hyperuricemia is more often accompanied by excessive excretion of uric acid, diminished excretion of ammonia and abnormally high plasma glutamic acid. All are undoubtedly important risk factors for gout. 3. The elevated glutamate could be due to a deficiency of glutamic dehydrogenase, as postulated by Pagliara and Goodman (15). In presence of intracellular accumulation of glutamate in glutamic dehydrogenase deficiency, renal production of ammonium may be reduced due to its inhibitory action on glutaminase 1. As a result of a renal block of ammonia formation, the glutamine in surplus may be diverted for uric acid synthesis. 4. Long-term studies indicate serum urate in most hyperuricemia relatives of gout can be modified by environmental factors, such as diet, weight and changes of life style. When hyperuricemia is under better control, the potential hazard of developing symptomatic gout may be circumvented.

Amino Acids↗
PubMed1988

Hyperuricemia after renal transplantation.

Hyperuricemia is common in cyclosporine-treated renal allograft recipients. An increased incidence of gout in patients receiving both diuretics and cyclosporine has been reported, but the effect of hyperuricemia on renal allograft function has not been studied. In a prospective, randomized trial of cyclosporine and prednisone versus azathioprine, prednisone, and antilymphocyte globulin for immunosuppression in renal allograft recipients, 105 of 131 cyclosporine and prednisone-treated patients (80 percent) experienced hyperuricemia (serum uric acid level above 8 mg/dl) and 13 of 131 (10 percent) were severely hyperuricemic (serum uric acid level above 14 mg/dl). In contrast, hyperuricemia developed in 63 of 115 patients (55 percent) treated with azathioprine, prednisone, and antilymphocyte globulin (p less than 0.002). Despite the frequent occurrence of hyperuricemia, gout was rare. Clinical gout developed in six patients in the cyclosporine and prednisone group and in 0 patients in the azathioprine, prednisone, and antilymphocyte globulin group between 1 and 43 months (median 22.5 months) after transplantation. Neither severe hyperuricemia nor diuretic therapy were associated with a significantly increased incidence of gout. The mean serum creatinine concentration of severely hyperuricemic patients (all on cyclosporine and prednisone) was similar to that of normouricemic cyclosporine and prednisone patients (1.8 mg/dl versus 1.6 mg/dl, p greater than 0.2), and the severely hyperuricemic patients had a 4-year graft survival rate of 90 percent. Asymptomatic hyperuricemia after renal transplantation does not adversely affect allograft function, requires no specific therapy, and is not a contraindication to use of diuretics.

Antilymphocyte Serum↗
PubMed1999

Reappraisal of the pathogenesis and consequences of hyperuricemia in hypertension, cardiovascular disease, and renal disease.

An elevated uric acid level is associated with cardiovascular disease. Hyperuricemia is predictive for the development of both hypertension and coronary artery disease; it is increased in patients with hypertension, and, when present in hypertension, an elevated uric acid level is associated with increased cardiovascular morbidity and mortality. Serum uric acid level should be measured in patients at risk for coronary artery disease because it carries prognostic information. Hyperuricemia is caused by decreased renal excretion. In this article, we suggest that this may be mediated by intrarenal ischemia with lactate generation and the inhibition of the secretion of urate by the anion-exchange transport system. The possibility that hyperuricemia directly contributes to cardiovascular or renal disease needs to be reconsidered. Although hyperuricemia is associated with a number of cardiovascular or renal risk factors, several studies have found uric acid level to be independently associated with increased mortality by multivariate analysis. If hyperuricemia is directly toxic, the most likely site is the kidney. Chronic hyperuricemia is strongly associated with chronic tubulointerstitial disease, and many of these patients have decreased renal function. Although it is possible that the hyperuricemia could simply be the consequence of the renal disease, further studies are necessary to rule out a pathogenic role for uric acid in the development of renal disease and salt-dependent hypertension.

Cardiovascular Diseases↗
PubMed1998

Relations of hyperuricemia with the various components of the insulin resistance syndrome in young black and white adults: the CARDIA study. Coronary Artery Risk Development in Young Adults.

PURPOSE: To assess the association of hyperuricemia with the various components of the Insulin Resistance Syndrome (IRS) in a biracial cohort of young adults. METHODS: Cross-sectional study in 4053 young black and white adults aged 18-30 years from the Coronary Artery Risk Development in Young Adults (CARDIA) study. RESULTS: Body mass index (BMI), fasting insulin, and triglycerides were significantly higher, and high density lipoprotein (HDL)-cholesterol lower in subjects with hyperuricemia (uric acid > or = 7.0 mg/dl in males; > or = 6.0 mg/dl in females) (all p < 0.001). BMI showed the strongest positive correlation with uric acid among the IRS components. Significant associations of hyperuricemia with these risk factors were observed in all sex-race groups, which persisted after controlling for possible confounders including age, education, physical activity, smoking, alcohol intake, oral contraceptive use, and creatinine. Further adjustment for BMI and/or waist-to-hip ratio caused a large decrease in the strength of the associations. Adjustment for insulin also lead to decreases; however, the influence of fasting insulin appeared weaker than obesity. Even after controlling for obesity, insulin, and the other components of the IRS, male subjects in both races in the upper tertile of triglycerides were still more likely to have hyperuricemia. CONCLUSIONS: The association of hyperuricemia with most aspects of the IRS may result predominantly from their covariation with adiposity and secondarily with insulin level. Elevated triglyceride level seems to have an independent relationship with hyperuricemia in males. The relationship between hyperuricemia and cardiovascular disease observed in previous studies may be secondary to its association with the IRS.

Adult↗
PubMed2001

Predictors for development of hyperuricemia: an 8-year longitudinal study in middle-aged Japanese men.

To identify the factors responsible for increases in serum uric acid (SUA), a cohort of 1,312 hyperuricemia-free (SUA < 7.5 mg/dL and no medication for hyperuricemia or hypertension) male office workers aged 30 to 52 years were examined annually for 8 successive years. Subjects who were found to have become hyperuricemic (SUA > or = 7.5 mg/dL) or who started medication for hyperuricemia during repeat surveys were defined as incidence cases. The SUA trend was also examined in 1,062 subjects for whom 9 consecutive SUA values were available and who did not start medication for hyperuricemia or hypertension during the observation period. Multivariate analyses, excluding the baseline SUA level as a factor in the Cox proportional-hazards model, indicated that age (negative), body mass index (BMI), log triglyceride level, hemoglobin A(1c) (HbA(1c)) level (negative), white blood cell count, and alcohol intake at study entry were significantly associated with the incidence of hyperuricemia. In the model including the baseline SUA level, baseline SUA level was the strongest factor for the incidence of hyperuricemia, and BMI, white blood cell count, and alcohol intake at study entry remained as independent factors. From stepwise linear regression analyses for SUA slope, excluding the baseline SUA level as a factor, significant correlates with SUA slope were, in order of their relative importance, slopes of BMI, HbA(1c) (negative), blood urea nitrogen, log triglyceride level, total protein, and baseline levels of hematocrit (negative), white blood cells, and HbA(1c) (negative). In stepwise linear regression analyses, including the baseline SUA level as a factor, SUA level (negative) and alcohol intake at study entry emerged as significant factors for SUA slope. The cumulative percentage of variation for SUA slope was 25.6%. In conclusion, obesity, alcohol intake, and multimetabolic disorders were determined to be independent predictors for the development of hyperuricemia. In addition, the white blood cell level may be a contributory factor.

Adult↗
PubMed2002

Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure-independent mechanism.

Hyperuricemia is associated with hypertension and vascular disease, but whether this represents a causal relationship or an epiphenomenon remains unknown. We recently reported a model of mild hyperuricemia in rats that results in increased blood pressure and mild renal fibrosis. In this study, we examined the effect of hyperuricemia on the renal vasculature. Rats fed 2% oxonic acid and a low-salt diet for 7 wk developed mild hyperuricemia (1.8 vs. 1.4 mg/dl, P < 0.05), hypertension [147 vs. 127 mmHg systolic blood pressure (SBP), P < 0.05], and afferent arteriolar thickening, with a 35% increase in medial area (P < 0.05). Allopurinol or benziodarone prevented the hyperuricemia, hypertension, and arteriolopathy. Hydrochlorothiazide treatment did not prevent the hyperuricemia or arteriolopathy despite controlling blood pressure. In contrast, the arteriolopathy and hypertension were prevented by both enalapril and losartan. Uric acid also directly stimulated vascular smooth muscle cell proliferation in vitro, and this was partially inhibited by losartan. Thus hyperuricemia induces a renal arteriolopathy in rats that is blood pressure independent and involves the renin-angiotensin system.

Administration, Oral↗
PubMedDate not supplied

Hyperuricemia and gout in thyroid endocrine disorders.

OBJECTIVE: A significant correlation between thyroid function and purine nucleotide metabolism has been established in hypothyroidism. On the contrary, the relationship between hyperthyroidism and purine metabolism is more controversial. The present study evaluates the prevalence of hyperuricemia and gout in patients affected by primary hypothyroidism and hyperthyroidism. METHODS: We studied 28 patients with primary hypothyroidism and 18 patients with primary hyperthyroidism, all hospitalized because of endocrine dysfunction. All underwent a series of clinical, biochemical and instrumental evaluations; in particular, thyroid-stimulatin hormone (TSH), free thyroxine (fT4), blood urea, serum creatinine, creatinine clearance, serum and urinary uric acid levels were measured. RESULTS: In comparison to the prevalence reported in the general population, a significant increase of both hyperuricemia and gout was found in the hypothyroid patients, and of hyperuricemia in the hyperthyroid patients. In hyperthyroidism the hyperuricemia is due to the increased urate production, while in hypothyroidism the hyperuricemia is secondary to a decreased renal plasma flow and impaired glomerular filtration. CONCLUSIONS: Ourfindings confirm the data in the literature concerning the high prevalence of hyperuricemia and gout in hypothyroidism. It shows that hyperthyroidism can cause a significant increase in serum uric acid, as well, although lower than the hyperuricemia due to thyroid hormone deficiency.

Adult↗
PubMed2006

Prevalence of hyperuricemia and its relationship with metabolic syndrome in Thai adults receiving annual health exams.

BACKGROUND: Associations between hyperuricemia, metabolic syndrome, cardiovascular disease and diabetes have been reported. Limited information, however, is available concerning the prevalence and correlates of hyperuricemia among Thai men and women. We sought to estimate the prevalence of hyperuricemia among a population of patients receiving annual health exams and to evaluate its relationship with metabolic syndrome (MetS). METHODS: We conducted a cross-sectional study of 1,381 patients (376 men and 1,005 women) who first participated in annual health examinations at the Preventive Medicine Clinic of the King Chulalongkorn Memorial Hospital in Bangkok, Thailand during the period July 1999 through February 2000. Hyperuricemia was defined as >7.0 mg/dL in men and >6.0 mg/dL in women. MetS was defined using the modified ATP III criteria. RESULTS: The overall prevalence of the hyperuricemia was 10.6%. The condition was more common in men than in women (18.4 vs. 7.8%). Among women, serum uric acid was statistically significantly correlated with body mass index (BMI), systolic and diastolic blood pressure, high-density lipoprotein-cholesterol, triglyceride and fasting plasma glucose (all p <0.05). Men with serum uric acid concentrations >6.7 mg/dL (upper quartile) had a 3.91-fold increased in risk of MetS (95% CI:1.36-11.23), as compared with those who had concentrations <5.1 mg/dL (lowest quartile). Among women, the risk of MetS increased at least 2-fold for concentration of serum uric acid concentrations >4.0 mg/dL (p for trend <0.001). CONCLUSIONS: Hyperuricemia is prevalent among Thai men and women receiving routine health exams. Additionally, serum uric acid is positively associated with MetS.

Adult↗
PubMed2006

Hyperuricemia and associated diseases.

After introduction of urate-lowering therapy, asympotomatic hyperuricemia was treated with allopurinol or uricosuric agents in the belief that hyperuricemia and/or gout caused chronic kidney disease. Epidemiologic studies in the 1970s, however, failed to confirm the view that hyperuricemia and gout were independent risk factors for chronic kidney disease. As a result, urate-lowering pharmacotherapy is generally not recommended at the present time in the management of asymptomatic hyperuricemia even though recent epidemiological, experimental, and clinical studies have prompted reexamination of a causal role for hyperuricemia (with or without gout) in chronic kidney disease as well as other important disorders including cardiovascular disease, hypertension, and metabolic syndrome. The issue of such a role remains unresolved and this article reviews the current status of the relationship between hyperuricemia and associated disorders.

Animals↗
PubMed2005

Pharmacological treatment of acute and chronic hyperuricemia in kidney diseased patients.

Several trials argued the possibility that hyperuricemia may have a direct effect on cardiovascular and renal disease. It has been shown that an elevated serum uric acid concentration is a predictor of cardiovascular events such as myocardial infarction. It also predicts the development of hypertension and in hypertensive patients, hyperuricemia is associated with increased cardiovascular morbidity and mortality. Hyperuricemia is a complication often seen in patients with chronic and acute renal disease. The relationship between serum uric acid level and the appearance or progression of renal dysfunction has been debated in the last years. During chemotherapy for hematological malignancies or more rarely for solid tumors, acute renal failure, secondary to a sudden marked increase in uric acid, is not such a rare complication. The therapeutic intervention includes hyper hydration, urinary alkalinization, and the use of uric acid decreasing agents such as allopurinol and rasburicase, a recent recombinant-urate oxidase. In our personal experience, patients with acute renal failure due to hyperuricemia, showed a better renal prognosis with rasburicase than allopurinol. Chronic hyperuricemia is also associated with chronic tubulo-interstitial disease with glomerular sclerosis, and renal dysfunction. Experimental trials showed that uric acid can affect kidneys through different mechanisms at glomerular, tubulo-interstitial and vascular level. Although allopurinol is often the drug of choice, caution must be used to avoid serious side effects. New therapeutic options, for treating hyperuricemia are needed in patients with renal dysfunction for slowing the progression to end stage kidney disease.

Acute Disease↗
PubMed2003

Recombinant urate oxidase for prevention of hyperuricemia and tumor lysis syndrome in lymphoid malignancies.

Hyperuricemia is a common manifestation of lymphoid malignancies at diagnosis or after the start of chemotherapy. When accompanied by other metabolic abnormalities and/or organ failure, hyperuricemia may be a manifestation of tumor lysis syndrome (TLS). Patients at particularly high risk of such complications include those with acute lymphoblastic leukemia and advanced stage non-Hodgkin's lymphoma. Conventional measures to prevent hyperuricemia and TLS are comprised of hydration, alkalinization of body fluids, and administration of allopurinol. Although these measures are usually effective in preventing or managing hyperuricemia, approximately 20% of patients at high risk of TLS require dialysis, and many cannot receive chemotherapy as planned. Rasburicase, a recombinant form of the enzyme urate oxidase, has recently become available and may further reduce the morbidity of hyperuricemia and TLS. In this review, we provide an overview of hyperuricemia and TLS and discuss the impact of rasburicase in the overall management of these complications.

Clinical Trials as Topic↗