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PubMed2002

Prevention and treatment of hyperuricemia in hematological malignancies.

The standard prophylactic and treatment regimen for hyperuricemia in patients with hematological malignancies previously included vigorous hydration, urinary alkalinization, and a xanthine oxidase inhibitor, allopurinol, which blocks the conversion of hypoxanthine and xanthine to uric acid. However, xanthine is less soluble than uric acid, and preexisting uric acid is not affected by allopurinol. The enzyme urate oxidase, not present in mammals, converts uric acid to allantoin, which is 5-10 times more soluble than uric acid. A new recombinant form of urate oxidase, rasburicase, has recently been developed. In a phase I/II study of rasburicase in children and young adults with hematological malignancies, rasburicase was demonstrated to be well tolerated at 0.2 mg/kg/day intravenously, had a mean T1/2 of 21.2 +/- 12.0 hours, and induced a median decrease in uric acid from 9.7 mg/dL to 1.0 mg/dL (P < 0.001). We recently demonstrated, in a randomized prospective trial comparing rasburicase versus allopurinol in children with hematological malignancies at high risk of tumor lysis syndrome, that rasburicase significantly lowered the mean uric acid area under the curve 0 to 96 hours (128 +/- 70 mg/dL/hour vs. 329 +/- 129 mg/dL/hour; P < 0.001) and 4 hours post uric acid by 86% versus 12% (P < 0.001). Furthermore, in the hyperuricemic group, the baseline creatinine level decreased from 144% to 102% by 96 hours following rasburicase compared to an increase from 132% to 147% following allopurinol. Although the difference in effect on creatinine levels is not significant, the study was not designed or powered to question this effect. Lastly, in 510 patients with hematological malignancies at risk for tumor lysis syndrome who received rasburicase, only 2 (0.4%) have developed new renal complications requiring hemodialysis. In summary, in the prevention and treatment of hyperuricemia, patients with hematological malignancies at risk of tumor lysis syndrome appear to benefit significantly from the use of a recombinant urate oxidase (rasburicase).

Allopurinol↗
PubMed2004

[Prognostic value of hyperuricemia in chronic heart failure].

BACKGROUND: Hyperuricemia has been proposed as a risk marker in chronic heart failure, but its value as an independent prognostic is not well established. AIM: To determine the prognostic value of hyperuricemia, in patients with chronic stable heart failure. PATIENTS AND METHODS: Forty six male patients with chronic heart failure, aged 62 +/- 13 years, were studied. Their election fraction was less than 40% and their serum creatinine was less than 2 mg/dl. Serum uric acid and catecholamines, maximal oxygen consumption (VO2 max) and left ventricular ejection fraction were measured. Mortality and the need for cardiac transplant were recorded as endpoints during a mean follow up of 39 +/- 18 months. The relationship between basal measures and the occurrence of events was analyzed using univariate and multivariate methods. RESULTS: Basal VO2 max and left ventricular ejection fraction were 16 +/- 4.6 ml/kg/min and 22 +/- 7% respectively. Eighteen patients died and three required transplantation during the follow up. Patients reaching these endpoints had a lower VO2 max and left ventricular ejection fraction and higher uric acid levels. Multivariate analysis accepted left ventricular ejection fraction (relative risk 0.89, 95% CI 0.82-0.97) and serum uric acid (relative risk 1.335 95% CI 1.02-1.74) as significant predictors of events. The relative risk for cardiac transplantation was 7.07 times higher among those with a serum uric acid over 7 mg/dl. CONCLUSIONS: A high serum uric acid is an independent predictor of bad prognosis in patients with stable chronic heart failure.

Analysis of Variance↗
PubMedDate not supplied

[An exceptionally severe hyperuricemia in acute renal failure caused by spontaneous tumor lysis syndrome (TLS)].

Acute tumor lysis syndrome (TLS) is a catastrophic complication of the treatment of certain neoplastic disorders. It most commonly occurs in association with hematologic malignancies and manifests a few hours to a few days after initiation of specific chemotherapy. Acute spontaneous TLS has been described in leukemia and lymphoma and in some patients with solid tumors prior to institution of therapy. The findings that may be seen in acute TLS include hyperphosphatemia, hypocalcemia, hyperuricemia, hyperkalemia, and acute oliguric or anuric renal failure due to uric acid precipitation within the tubules (acute uric acid nephropathy) and to calcium phosphate deposition in the renal parenchyma and vessels. We report here a case of acute spontaneous TLS (high grade B-cell lymphoma of the right colon) in which serum uric acid concentration attained exceptionally high levels (36.7 mg/dL). The patient underwent acute oliguric renal failure soon after right colectomy. He was treated by means of a large infusion of saline. The renal function recovered in such a rapid way that no dialysis treatment was required. In conclusion the present case report has two peculiarities: that of being one of the rare examples of spontaneous TLS, and that of showing an exceptionally severe hyperuricemia, probably the highest ever reported in the literature. The administration of a large volume of saline was able to ensure a complete recovery of renal function. Therefore, hydration with saline remains the keystone in the prevention and treatment of acute TLS.

Acute Kidney Injury↗
PubMed2004

Hypertension was the major risk factor leading to development of cardiovascular diseases among men with hyperuricemia.

OBJECTIVE: A 7-year followup study among men with hyperuricemia was conducted to study the longterm relationships between serum uric acid concentrations and cardiovascular diseases. Any interaction between uric acid levels and other risk factors (e.g., obesity, hypertension) on the development of cardiovascular diseases was also examined. METHODS: A total of 391 men with hyperuricemia aged 30 and over screened from the community-based Kinmen study in 1991-92 (the baseline study) were followed in 1997-98, with a 75% followup rate. Demographic, clinical, and biochemical data were collected in both baseline and followup periods. RESULTS: After followup for 7 years, the significant risk factors of coronary heart disease were age, increase of uric acid level at followup, baseline systolic blood pressure, and increase of systolic blood pressure at followup. Factors independently associated with left ventricular hypertrophy included baseline systolic blood pressure and increase of systolic blood pressure at followup. Gouty syndrome, age, baseline fasting plasma glucose level, and increase of systolic blood pressure followup were significantly related to cardiac arrhythmia. After adjusting for baseline serum uric acid level, we found that hyperuricemic men with hypertension, especially overt hypertension stage 2 and stage 3, would predict cardiovascular disease incidence synergistically with uric acid level. CONCLUSION: There is a positive and statistically significant relationship between gout and subsequent cardiac arrhythmia. Moreover, hypertension was the major risk factor leading to aggravation of development of atherosclerosis among hyperuricemic subjects. Gout and elevated uric acid level seemed not to be an independent risk factor for most cardiovascular diseases. Nevertheless, blood pressure level was predictive for cardiovascular disease incidence synergistically with serum uric acid level.

Adult↗
PubMed2005

Unusual presentation of thyrotoxicosis as bradycardia, acute renal failure and hyperuricemia in an elderly patient.

Bradycardia with renal system involvement in patients with thyrotoxicosis has rarely been reported. We report a 72-year-old woman with unusual presentations of sinus bradycardia and normothermia accompanied by acute renal failure and hyperuricemia in thyrotoxicosis. The electrocardiogram changes in this patient included sinus bradycardia (50 beats per minute), followed by atrial fibrillation (84 beats per minute), and finally sinus rhythm with T wave inversion (80 beats per minute). Her renal function and hyperuricemia completely recovered after appropriate antithyroid therapy. A high index of suspicion is needed for early diagnosis and antithyroid treatment in patients with unusual manifestations of thyrotoxicosis in general clinical practice.

Acute Kidney Injury↗
PubMed2005

[Hyperuricemia in hypertension: any clinical implication?].

Twenty-five percent of untreated hypertensive patients are hyperuricemic. The causal role of uric acid in the pathogenesis of hypertension has not been clearly demonstrated in humans. An elevated serum uric acid appears to be predictive of the development of hypertension. Serum uric acid has also been considered as a cardiovascular risk factor but this issue is controversial. A high serum uric acid is associated with an increased cardiovascular morbidity and mortality in men. Thus, hyperuricemia in hypertensive patients should be considered as a sign of increased risk leading to a more intensive management of all other risk factors. When managing hypertensive patients with hyperuricemia, physicians should know the impact of antihypertensive drugs on serum uric acid to prevent a further increase in uric acid and the development of gout.

Antihypertensive Agents↗
PubMed2006

Dose adjustment of allopurinol according to creatinine clearance does not provide adequate control of hyperuricemia in patients with gout.

OBJECTIVE: Published guidelines state that allopurinol doses should be adjusted according to creatinine clearance. We investigated whether such dosing provides adequate control of hyperuricemia. METHODS: We studied 250 patients with gout attending rheumatology clinics in South Auckland from 2001 to 2004. Allopurinol dose, creatinine clearance, and serum uric acid (SUA) level were recorded. We analyzed the relationship between recommended allopurinol dose and SUA lowering to <or= 0.36 mmol/l. RESULTS: For patients taking allopurinol, 70.9% were taking recommended doses, based on published allopurinol dosing guidelines. There were 4 (1.6%) patients with cutaneous hypersensitivity reactions to allopurinol, but none of these patients were taking higher than recommended allopurinol doses. The proportion of patients achieving SUA <or= 0.36 mmol/l was lower in those taking recommended doses, compared with those taking higher than recommended doses (19% vs 38.1%; p < 0.01). CONCLUSION: Adherence to published allopurinol dosing guidelines led to suboptimal control of hyperuricemia in this population of patients with gout. Further work is required to clarify the safety and efficacy of allopurinol dose escalation, particularly in patients with renal impairment.

Adult↗
PubMed2006

[Preclinical diagnosis of the familial nephropathy associated to hyperuricemia].

We describe one patient with the pre-symptomatic diagnosis of the disease named afamilial nephropathy associated to hyperuricemia)) (OMIM 162000; FJHN). This is a hereditary disease, autosomic dominant, characterized by its progression to renal insufficiency. Several mutations in the gene that codifies uromodulin or Tannn-Horsfall protein (UMOD) have been identified in some families. The clinical presentation is heterogeneous. In some cases the disease appears as juvenile hyperuricemia due to a diminished renal urate excretion, with or without gout, but in some other cases the first manifestation is renal insuffciency. The study of the UMOD gene shows that patient is heterozygous for the mutation C869 --> A, which results in C255Y change, and enabled to establish the diagnosis of FJHN. This patient shows the possibility to identify the genetic alteration associated to FJHN in early stages. This fact implies a clinical follow-up and eventual treatment to reduce the inexorable progression to renal insuffciency.

Child↗
PubMed1978

Hyperuricemia in congenital heart disease.

Gout is rarely noted as a clinical problem in secondary polycythemia-- even if profound polycythemia exists, as in cyanotic congenital heart disease. A retrospective study of 81 patients with congenital heart disease was done to assess the incidence of hyperuricemia. Twenty of 46 patients with cyanotic congenital heart disease had serum levels of uric acid greater than 8 mg/dl. Thirteen of 16 (81%) cyanotic male patients more than 15 years old had serum levels greater than 8 mg/dl. For cyanotic patients, serum levels of uric acid were related directly to the degree of polycythemia (r = .44; P less than .02). Impaired renal function or drug therapy did not seem to account for the hyperuricemia. Because levels of uric acid greater than 10 mg/dl probably are nephropathic, many of these patients may be incurring subclinical uric acid nephropathy.

Adolescent↗
PubMed1998

Medullary cystic kidney disease with hyperuricemia and gout in a large Cypriot family: no allelism with nephronophthisis type 1.

We describe a large Cypriot family with an interstitial type of nephropathy, inherited as an autosomal dominant trait that led to end stage renal failure between 51 to 78 years of age (mean 62.2 years). Twenty-three people are known to be affected, but several younger relatives with normal renal function may remain undiagnosed because of the absence of precise clinical and laboratory diagnostic criteria. This nephropathy is associated with medullary renal cysts, hypertension, hyperuricemia, and gout. Several relatives have typical medullary cystic disease (MCD), while in the others the findings are compatible with this diagnosis. Due to the similarity of clinical and pathologic findings, earlier reports had suggested that MCD may be allelic to autosomal recessive familial juvenile nephronophthisis, which was mapped recently to chromosome band 2q13. Linkage analysis of the present family with a closely linked marker excluded linkage to the above locus. Linkage was also excluded to the PKD1 locus of adult polycystic kidney disease type 1, and up to 5 cM on either side, on chromosome 16. We suggest that because of the element of hyperuricemia and gout found in this family, although with reduced penetrance, it may represent a variant of autosomal dominant MCD of the adult type. This variability may be the result of allelic or locus heterogeneity. Molecular genetic approaches including linkage analysis on appropriate families will certainly assist in classifying such related genetically heterogeneous disorders.

Adult↗
PubMed2002

Childhood hyperuricemia and acute renal failure resulting from a missense mutation in the HPRT gene.

A 6-year-old boy was determined to have partial hypoxanthine phosphoribosyl transferase (HPRT) enzyme deficiency without the phenotypic features of Lesch-Nyhan syndrome. He presented with recurrent acute renal failure (ARF) from hyperuricemia. Treatment with allopurinol prevented further attacks of renal failure. T lymphocyte cultures were used to sequence the HPRT cDNA and a novel single nucleotide substitution at codon 65 in exon 3 was found (193C>T, 65leu>phe). This mutation was confirmed by genomic DNA sequencing and was also detected in his heterozygous, asymptomatic mother and sister. Unlike the cells from patients with classic Lesch-Nyhan syndrome, the in vitro cultures of our patient's T-lymphocytes did not proliferate in the presence of purine analogue 6-thioguanine (TG). This report highlights the unusual occurrence of recurrent ARF in a child with partial HPRT enzyme deficiency. The absence of TG resistance in vitro with this mutation shows that even small alterations in enzyme activity in vivo can result in disease symptoms, in this instance, hyperuricemia sufficient to cause ARF. Atypical HPRT mutations should also be considered in cases of unusual renal failure, because correct diagnosis can allow appropriate treatment, as well as informed genetic counseling.

Acute Kidney Injury↗
PubMed1995

Myogenic hyperuricemia: what can we learn from metabolic myopathies?

The association of muscle glycogenosis with hyperuricemia led to the identification of a unique purine disorder. Myogenic hyperuricemia is ascribed to excessive degradation of muscle purine nucleotides, secondary to impaired ATP generation. Although this pathophysiological condition has been observed not only in glycolytic defects but also in mitochondrial diseases affecting lipid and carbohydrate oxidation, it is most common and prominent in muscle phosphofructokinase deficiency, in which neither glycogen nor glucose can be used as metabolic fuels. The first key reaction of muscle purine degradation is catalysis by AMP deaminase. Numerous studies have indicated that AMP deaminase may play an important role in energy metabolism in contracting muscle. Arguments against this hypothesis have emerged through analyses on muscle AMP deaminase deficiency. According to a recent study, the mutant allele is extremely frequent among Caucasians and African-Americans, suggesting that many individuals with this enzyme defect may be clinically asymptomatic. Further study is required to explain the significance of muscle purine degradation in energy metabolism.

AMP Deaminase↗
PubMed2001

Hyperuricemia in Saudi Arabia.

The objective of this prospective study was to determine the prevalence of hyperuricemia and gout in a sample of Saudi individuals and their relationship to certain risk factors, namely, obesity, serum glucose, triglycerides, cholesterol, age, and sex. A total of 487 Saudis (250 males and 237 females) from 14 primary care clinics were interviewed, examined, and investigated. The mean age for the males was 46.89 +/- 17.01 years (range 14-83) and for the females 45.08 +/- 13.67 years (range 21-80). Serum uric acid (SUA) values above 420 micromol/l for males and 360 micromol/l for females were considered to be high. Of the 487 individuals, 41 (8.42%; 20 males and 21 females) had hyperuricemia. The mean SUA was 308.41 +/- 90.64 micromol/l for males and 254.59 +/- 85.79 micromol/l for females. In females, uric acid levels correlated significantly with age, body mass index (BMI), serum creatinine, and the erythrocyte sedimentation rate (ESR), but not with serum cholesterol or triglycerides. In males, uric acid levels only correlated significantly with BMI and serum creatinine. No case of gout was found.

Adolescent↗
PubMed2001

Hyperuricemia and renal function.

Increased serum urate concentration is commonly seen in clinical practice. It does not represent a specific disease, nor is it an indication for therapy. Hyperuricemia can be the consequence of increased uric acid production and/or decreased renal capacity to excrete uric acid. In essential hypertension, it has been described in up to one third of patients and is directly related to an increase in renal vascular resistance and inversely correlated with renal plasma flow. In other words, abnormal renal hemodynamics, commonly seen in the initial stages of the disease, account for the increased serum urate concentration. This can be maintained if a decrease in glomerular filtration rate takes place. The increase in uric acid has been shown to be a potent predictor of the development of cardiovascular events and death. In addition, uric acid, particularly when elevated, could represent an independent risk factor. On the other hand, an altered renal function predicts in an independent manner a higher cardiovascular risk. For this reason, the predictive capacity of uric acid could be partly dependent on the fact that hyperuricemia runs in parallel with a deranged renal function.

Cardiovascular Diseases↗
PubMed2002

Pathogenesis of hyperuricemia: recent advances.

The literature on the pathogenesis of hyperuricemia have been limited to the discussion of metabolic syndromes associated with risk factors for atherosclerosis and hyperuricemia and the genetics of the juvenile form of hyperuricemic nephropathies. A few new mutations in the hypoxanthine-guanine phosphoribosyltransferase gene, which result in Lesch-Nyhan syndrome, have been described. In addition, some new insight has been gained in the renal handling of uric acid by the human kidney.

Humans↗
PubMed1976

Hyperuricemia in pre-eclampsia. A reappraisal.

Seventeen pre-eclamptic (PE), 22 hypertensive (H), and 13 normal pregnant women (C), all in the third trimester, were studied to examine the relationship of blood lactate (L) to the hyperuricemia characteristic of PE. The parameters measured were: serum and urinary uric acid, and creatinine, and lactate (L), and pyruvate (P) in the blood. Uric acid clearance (Cur), and creatinine clearance (Ccr), and fractional uric acid clearance (Fract. Cur) as well as L/P ratios were calculated. Some of the patients, from the three groups, were infused with approximately equal to 100 mEq. of sodium lactate during the course of 50 minutes. "Preinfusion," "midinfusion," and "postinfusion," determinations were compared, as well as the per cent change in the different parameters as the result of the infusion and after its discontinuation. The results showed that serum urine acid is elevated, and Cur is impaired in PE; however, L was lower in PE than in control subjects. There was no correlation between L or L/P and Cur. Lactate infusion caused comparable impairment of Cur in all groups. There was no significant difference in the response of the parameters studied, to the infusion, between the different groups. Our data cast serious doubts on the postulated role of blood lactate in the etiology of hyperuricemia in PE. Contracted plasma volume and/or local release of angiotensin II in the kidney of pre-eclamptic patients probably play a more important role.

Absorption↗
PubMed1985

Hyperuricemia and hypertriglyceridemia: metabolic basis for the association.

Hypertriglyceridemia has been reported frequently in patients with hyperuricemia and gout. The current studies have evaluated this relationship. To examine whether hypertriglyceridemia leads to hyperuricemia, IV intralipid was given to three gouty patients. Triglycerides increased from 169 to 700 mg/dl for three hours but caused no change in serum urate level or urine uric acid and oxypurine excretion. We next examined whether high carbohydrate intake increases serum urate and triglyceride levels. Four obese patients were placed on a 2000 kcal/d sucrose diet for seven days. The serum urate increased from 6.3 +/- 1.7 to 7.9 +/- 2.0 mg/dL. The percent uric acid clearance to creatinine clearance decreased from 5.9 +/- 1.3 to the lowest mean value of 3.7 +/- 1.2, while serum triglycerides increased from 106 +/- 33 to 252 +/- 57 mg/dL and blood lactate from 607 +/- 227 to 1167 +/- 381 mumol/L. A 3000 kcal/d glucose diet in four other obese subjects produced no change in serum urate levels but increased lactate and triglyceride levels. During an isocaloric sucrose diet in two normal men, the serum urate level increased from 5.3 and 4.0 to peak values of 9.5 and 7.4 mg/dL. The percent uric acid to creatinine clearance decreased from 5.6 and 6.6 to 2.9 and 3.3. The uric acid turnover did not increase. In three gouty patients the mean serum urate increased from 8.5 +/- 1.5 to 10.6 +/- 1.4 mg/dL following an isocaloric sucrose diet. The urine uric acid excretion increased from 0.30 and 0.25 to 0.37 and 0.38 mg/mg creatinine in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Hyperuricemia in rats during acute carbon monoxide poisoning.

The effect of carbon monoxide (CO) inhalation on plasma levels of uric acid and hypoxanthine in rats was investigated. Exposure to 3% CO caused respiratory arrest within about 2 minutes. The plasma uric acid level of CO-treated rats increased to 157% above that of ether-treated rats. When rats were exposed to 1% or 0.8% CO, the exposure periods until the onset of respiratory arrest were prolonged, and plasma uric acid levels at respiratory arrest were further elevated. Plasma uric acid levels at respiratory arrest increased with prolongation of the exposure periods. Under our experimental conditions, hypoxanthine or xanthine was not detected in plasma of CO-treated rats. These results are discussed in relation to the hyperuricemia in hemorrhagic shock or hypoxemia: CO-induced hyperuricemia can be attributed to the stimulated degradation of adenine nucleotides under tissue anoxia, and thus could be an excellent parameter of tissue anoxia.

Adenine Nucleotides↗