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PubMed2002

Mild hyperuricemia induces glomerular hypertension in normal rats.

Mildly hyperuricemic rats develop renin-dependent hypertension and interstitial renal disease. Hyperuricemia might also induce changes in glomerular hemodynamics. Micropuncture experiments under deep anesthesia were performed in Sprague-Dawley rats fed a low-salt diet (LS group), fed a low-salt diet and treated with oxonic acid (OA/LS group), and fed a low-salt diet and treated with oxonic acid + allopurinol (OA/LS/AP group) for 5 wk. The OA/LS group developed hyperuricemia and hypertension compared with the LS group: 3.1 +/- 0.2 vs. 1.1 +/- 0.2 mg/dl (P < 0.01) and 143 +/- 4 vs. 126 +/- 2 mmHg (P < 0.01). Hyperuricemic rats developed increased glomerular capillary pressure compared with the LS rats: 56.7 +/- 1.2 vs. 51.9 +/- 1.4 mmHg (P < 0.05). Pre- and postglomerular resistances were not increased. Histology showed afferent arteriolar thickening with increased alpha-smooth muscle actin staining of the media. Allopurinol prevented hyperuricemia (1.14 +/- 0.2 mg/dl), systemic (121.8 +/- 2.8 mmHg) and glomerular hypertension (50.1 +/- 0.8 mmHg), and arteriolopathy in oxonic acid-treated rats. Linear regression analysis showed that glomerular capillary pressure and arteriolar thickening correlated positively with serum uric acid and systolic blood pressure. Glomerular hypertension may be partially mediated by an abnormal vascular response to systemic hypertension due to arteriolopathy of the afferent arteriole.

Animals↗
PubMed2000

Improvement of renal function in patients with chronic gout after proper control of hyperuricemia and gouty bouts.

AIM: To evaluate the effect of nonsteroidal anti-inflammatory drug (NSAID) withdrawal on renal function in patients with chronic gout after proper control of hyperuricemia and gouty symptoms. METHODS: Patients with chronic gout, who regularly used NSAIDs to control gouty symptoms prior to urate-lowering therapy, were prospectively followed up in an observational study. Risk factors for renal function impairment were recorded, and the clearance of creatinine (Ccr) was initially measured while on colchinine therapy to prevent gouty bouts. Therapy with urate-lowering drugs was started in order to keep serum urate levels under 6.0 mg/dl (275 micromol/l), and the Ccr was monitored during the follow-up period. Final assessment of the renal function was made after 1 year free from gouty bouts and without NSAID therapy during this period. RESULTS: 87 patients completed a 1-year period of NSAID withdrawal. Low initial Ccr was related to age, hypertension, hypertriglyceridemia and the presence of previous renal diseases. After proper control of gout and NSAID withdrawal during 1 year, the mean Ccr significantly raised from 94 to 104 ml/min. The improvement was especially significant in patients whose initial Ccr was under 80 ml/min. Their mean Ccr rose from 60 to 78 ml/min, and 12 of 29 patients achieved normal Ccr at the end of the study. No risk factor correlated with improvement of the renal function. CONCLUSIONS: Renal function impairment in patients with chronic gout is mainly related to vascular risk factors, but improvement of the renal function was observed after proper control of hyperuricemia and NSAID withdrawal. Optimal control of hyperuricemia and, therefore, of symptoms of gout should be especially considered in patients with vascular risk factors in order to avoid renal function loss due to NSAID use.

Adult↗
PubMed1984

Severe hyperuricemia in patients with volume depletion.

Profound hyperuricemia (19-42 (27 +/- 3.3) mg/dl) was noted in seven adult patients with volume depletion and marked prerenal azotemia (SUN, 155 +/- 30 mg/dl and serum creatinine 5.2 +/- 1.1 mg/dl). The serum level of uric acid returned to normal following the administration of 3.2 +/- 0.4 liters of saline/day over a period of 3.4 +/- 0.6 days. Throughout the course of the illness, there were significant correlations (r = 0.83, p less than 0.01) between the serum levels of both urea nitrogen and creatinine and those of uric acid. Because of the rapid reversibility of this hyperuricemia with hydration, it should be differentiated from other clinical conditions associated with acute renal failure and profound hyperuricemia.

Adult↗
PubMed1996

Mechanisms of hyperuricemia in cyclosporine-treated renal transplanted children.

Mechanisms of hyperuricemia were investigated in 19 pediatric renal transplant recipients 6 months after transplantation. 51Cr-EDTA, PAH, lithium and sodium clearances, 24-hour urinary creatinine and urate excretions were measured. Ten patients had hyperuricemia. The hyperuricemic patients had lower EDTA, PAH, and urate clearances (mean 69.5 vs. 92.5, p < 0.05, 234 vs. 421, p < 0.05 and 4.3 vs. 10.6 ml/min/1.73 m2, p < 0.001, respectively). Serum urate concentration correlated with cyclosporine dose (r = 0.46, p < 0.05) and inversely with urate (r = -0.88, p < 0.001), and lithium (r = -0.55, p < 0.05) clearances. Urate clearance showed a significant positive correlation with lithium clearance (r = 0.66, p = 0.01) and an inverse correlation with fractional proximal tubular reabsorption (r = -0.63, p = 0.02). Results were not influenced by diuretic administration. Our data support increased proximal tubular urate reabsorption rather than decreased secretion as the mechanism in cyclosporine-induced hyperuricemia.

Azathioprine↗
PubMed1977

The pathogenesis of hyperuricemia in glycogen storage disease, type I.

After the infusion of fructose, 0.25 g/kg body weight, blood uric acid levels were significantly increased above the mean basal value in five patients with glycogen storage disease (GSD), type I (P less than 0.02-P less than 0.05). The mean fasting blood inorganic phosphate (Pi) level in the patients was 3.9 +/- 0.3 mg/100 ml and was significantly lower than the mean Pi value of 4.8 +/- 0.3 mg/100 ml of the control subjects (P less than 0.05). Blood Pi levels were significantly lower in the patients than in the control subjects at varying times after the administration of fructose (P less than 0.005-P less than 0.05). Uric acid excretion did not increase significantly in the patients after fructose was given. In contrast to normal children, the mean peak blood uric level in the patients increased significantly after the administration of glucagon (P less than 0.001). In both patients (P less than 0.005) and control subjects (P less than 0.05), mean blood Pi concentrations decreased significantly after the administration of glucagon; however, the blood Pi concentrations in the patients were significantly lower than in the control subjects. Uric acid excretion increased after glucagon administration in both patients and control subjects, but the differences in uric acid excretion between the two groups were not significant. The data in our patients after fructose and glucagon administration suggest that hyperuricemia in GSD results from enhanced nucleotide catabolism. The concentrations of hepatic Pi and ATP may be low in patients with GSD; hepatic Pi and ATP content would therefore be further diminished by the administration of fructose and glucagon. By a mechanism similar to that of fructose-induced hyperuricemia, diminished hepatic Pi and ATP content might increase the breakdown of adenine nucleotides with resultant hyperuricemia.

Adolescent↗
PubMed1991

Hyperuricemia induced by the uricosuric drug probenecid in rats.

Stimulation of uric acid production by the well-known uricosuric drug probenecid was studied using potassium oxonate-treated rats and eviscerated rats subjected to functional hepatectomy. In oxonate-treated rats, probenecid was hyperuricosuric, increasing the glomerular-filtered amounts of uric acid and causing marked hyperuricemia. This could be completely blocked by combination dosing with allopurinol, an inhibitor of xanthine oxidase. In eviscerated rats subjected to functional hepatectomy, probenecid also increased plasma uric acid and urinary uric acid excretion, but when given together with allopurinol, the increase of plasma uric acid was abolished with a remarkable increase of plasma hypoxanthine and xanthine. When probenecid was given by combination dosing with propranolol, a beta adrenoceptor antagonist, the hyperuricemia was also completely blocked. Thus, probenecid is concluded to stimulate uric acid production, probably via some interaction with endogenous catecholamine, resulting in hyperuricemia in rats, although it is a practical hypouricemic drug in humans.

Allopurinol↗
PubMed1991

[The role of hyperinsulinemia on the renal mechanism of hyperuricemia in overweight patients with essential hypertension].

The aim of the present study was to investigate the role of insulin on the renal mechanism of hyperuricemia in overweight patients with essential hypertension. Thirty-four essential hypertensives(EHT), receiving a regular diet containing 120mEq of sodium, 75mEq of potassium and 2000 kilocalories daily, were divided into two groups of non-obese(NHT) and obese(OHT) EHT. NHT as categorized as a body mass index (BMI) less than, and OHT as a BMI equal to or more than, 25 kg/m2 in male patients and 24 kg/m2 in female patients. In the early morning after overnight fast, renal uric acid and sodium clearance were examined while the patients remained in a supine position. During the two-hour clearance period, mean arterial pressure(MAP), heart rate(HR), endogenous creatinine clearance(Ccr), immunoreactive insulin(IRI), serum uric acid(SUA), fractional excretion of uric acid(FEUA) and sodium(FENa) were measured. Although there were no significant differences in age, MAP, HR, Ccr, nor SUA between the two groups, a higher ratio of female to male patients was found in OHT than in NHT. On the other hand, higher SUA and IRI and lower FEUA and FENa were observed in OHT than in sex-and Ccr-matched NHT. SUA was negatively correlated with FEUA in all patients (r = -0.392, p less than 0.05) and in NHT (r = -0.553, p less than 0.05), unlike in OHT. A significant negative correlation between BMI and FEUA was revealed in all EHT (r = -0.441, p less than 0.01) and in OHT (r = -0.597, p less than 0.01) but not in NHT. FEUA was positively correlated with FENa in all EHT (r = 0.554, p less than 0.001) as well as in NHT (r = 0.548, p less than 0.05) and OHT (r = 0.507, p less than 0.05). Moreover, there was a significant negative correlation between IRI and FENa in all EHT (r = -0.361, P less than 0.05) and in OHT (r = -0.470, p less than 0.05). However, no significant relation was demonstrated between IRI and SUA or FEUA in NHT or OHT. From these results, it is concluded that an attenuated renal excretion of uric acid related to natriuretic ability may play an important role in hyperuricemia in EHT. However, the role of hyperinsulinemia, which contributes to the blunting of natriuresis, might be relatively small in the renal mechanism of hyperuricemia in EHT, particularly in OHT.

Female↗
PubMed1992

Renal handling of urate in two patients with hyperuricemia and primary hyperparathyroidism.

Two patients with primary hyperparathyroidism had hyperuricemia due to the decrease in urate clearance. In analysis by 4-component model system, the tubular secretion of urate commonly decreased without changes in either filtered urate or presecretory reabsorption of urate. Both patients had a reduction of urea clearance, and both parathyroidectomy in the former case and intravenous infusion of saline in the latter case could reduce the serum urate level associated with the increase in the ratio of urate clearance to creatinine clearance. It is of interest that the former case with a higher serum urate level had a relatively higher postsecretory reabsorption, even with the decrease in tubular secretion of urate. However, the latter patient with a lower serum urate level had a decrease in postsecretory reabsorption of urate in proportion to the decrease in tubular secretion. These results suggest that in hyperuricemia patients with primary hyperparathyroidism, the reduction of tubular urate secretion via hypoperfusion of the capillary network is typically present, however, the severity of the hyperuricemia might be dependent on the dysfunction of the postsecretory reabsorption of urate.

Aged↗
PubMed1978

Asymptomatic hyperuricemia: the case for conservative management.

The management of asymptomatic hyperuricemia is controversial. Reported benefits from treatment prevention of acute gouty arthritis, chronic tophaceous gout, urolithiasis, or gouty nephropathy. A review of experimental and clinical data suggests that the risks of asymptomatic hyperuricemia are small or unknown and the efficacy of long-term treatment in preventing gout or renal disease is unproved. The costs and risks of prolonged drug administration and practical considerations such as patient compliance mitigate against long-term therapy in asymptomatic persons. We offer some recommendations for an expectant approach to the management of asymptomatic hyperuricemia.

Gout↗
PubMed2001

Diet and medication in the treatment of hyperuricemia in hypertensive patients.

OBJECTIVE: To evaluate the effects of diet and medication, either isolated or associated, on serum levels of uric acid in patients with hyperuricemia. METHODS: We studied patients from the Hypertension Unit of the University of Goias who had hyperuricemia (men > or =8.5 mg/dL and women > or =7.5 mg/dL). We divided the patients into three groups: G1 (low purine diet), G2 (low purine diet + medication), and G3 (medication only). Patients received allopurinol, 150 mg/day titrated up to 300 mg/dL when necessary. Patients were evaluated with regards to their lifestyles (diet, smoking, physical, activity, alcohol consumption), uric acid, blood pressure, use of medication, body mass index, cholesterol, and triglyceride. Follow-up took place in weeks 0 (M1), 6 (M2), 12 (M3) during the intervention and in week 36 (M4) after the study was completed. RESULTS: Fifty-five patients participated in the study, 31 women, mean age 54.4+/-10.6 years, body mass index 28.6+/-3.9 kg/m2. A similar reduction (p<0.001) in uric acid levels occurred in the three intervention groups. In week 36 (M4), after 24 weeks without intervention, a tendency toward elevation of uricemia was noted in G2 and G3, and a continuous drop in uricemia was noted in G1. No significant modifications were observed in the other variables analyzed. CONCLUSION: Considering the cost x benefit relationship, a diet low in purine should be the 1st therapeutic option for controlling hyperuricemia in patients with similar characteristic to the ones presented in this study.

Allopurinol↗
PubMedDate not supplied

[Study of hyperuricemia in Tahiti. 31 cases hospitalized at the Territorial Hospital Center in Papeete (Tahiti)].

Frequency of gout in French Polynesia has induced us to define a type of "hyperuricemia Polynesian" from a population of patients admitted in a general Medicine Ward. Each admitted patient gets immediately a blood check-up. A figure higher than 70 mg/l in male and 60 mg/l in female is considered as pathological. In such a case, uricemia and uraturia are tested every 24 h for three days and we consider the mean value of these three tests. On the other side, some admitted patients non-hyperuricemic, are examined according to the same protocol. So, we have two groups: 31 hyperuricemics and 20 non-hyperuricemics, secondarily grouped according to age, sex, ethnic. We did not consider some secondary causes of hyperuricemia (chronic renal insufficiency diuretic treatment, psoriasis etc.). 1. Within the hyperuricemic population, mean uricemia is 85.35 mg/l versus 52.65 mg/l in the second sample. In the hyperuricemic group (21 males and 10 females) 48% are gouty and 13% of them are females. Articular manifestations are acute arthritis, affecting mainly inferior limbs, ankles, knees). We did not notice any significant divergence between uricemia and uraturia of gouty and non gouty people. Within the group of gouty people, percentage of individual hyper excretion is 53% (uraturia greater than 600 mg/24 h) with no significant divergence with the non-gouty group: Nephrolithiasis is rare (3%). There is no significant divergence between urinary pH of gouty and non-gouty people. Associated metabolic troubles are: diabetes (26%) high triglyceridemia (43%) three syndromes associated together (hyperuricemia + diabetes + hypertriglyceridemia) in 19.5%, total cholesterol is normal (2.07 g/l) but a low cholesterol (0.30 g/l).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Familial hyperuricemia and renal insufficiency.

A kindred is described in which hyperuricemia and renal insufficiency were observed in three generations. The hyperuricemia appeared to precede the renal diseases. Lowering the serum uric acid level to normal did not decrease the progression of renal insufficiency. This suggested that the hyperuricemia was a marker of a familial nephropathy and possibly not the cause.

Adolescent↗
PubMed1978

[Uptake of 2-C14 urate by erythrocytes in hyperuricemia and in gout (author's transl)].

The uptake of 2-C14 urate by erythrocytes was measured in 19 patients with primary hyperuricemia, 6 patients with secondary hyperuricemia, 17 patients with primary gout and 30 controls. The uptake of urate in patients with primary gout was significantly lower than in the controls. In contrast no such difference could be observed in patients with primary and secondary hyperuricemia. The uptake of labeled urate by erythrocytes from gouty patients is especially diminished in the early phase of the uptake kinetics. The possible relevance of this finding for the pathogenesis of urate precipitation in gout is discussed. Further, we consider the application of the tracer urate uptake by erythrocytes as an aid in the early diagnosis of gout.

Erythrocytes↗
PubMed1982

[Life-threatening hyperuricemia during cytostatic leukemia therapy].

In 25 children with lymphoblastic leukemia is shown that prophylactic treatment with allopurinol, 48 hours before initial cytostatic therapy, always prevents hyperuricemia. In 4 patients was renounced on this measurement and 2 of 4 patients died of the sequeles of hyperuricemia. In severe ill leukemic patients the parental use of allopurinol is recommended. 2 additional patients developed during remission therapy or after cessation of chemotherapy a moderate hyperuricemia which had to be treated, over years, with allopurinol.

Adolescent↗
PubMed1982

Hyperuricemia and gout.

Although chronic tophaceous gout has become increasingly uncommon, hyperuricemia and acute gout are still common clinical entities. Most patients with hyperuricemia are under-excreters, and many of these cases are drug induced. Since longstanding asymptomatic hyperuricemia does not appear to cause progressive renal insufficiency, and uric acid renal stones are uncommon in underexcreters, these patients generally require no treatment. The minority of patients who overproduce uric acid are at increased risk for urolithiasis, and therapy should be decided on an individual basis. Acute gout is best treated with colchicine or indomethacin. The newer non-steroidal anti-inflammatory drugs (ie, ibuprofen, sulindac) may prove to be equally effective and are associated with fewer gastrointestinal side effects. Prophylaxis should be undertaken in patients with recurrent gout or documented uric acid urolithiasis. Although uricosuric drugs appear to be less toxic than allopurinol, they should not be used in patients who overproduce uric acid or in patients who have a history of urolithiasis or renal insufficiency. The allopurinol hypersensitivity syndrome is being reported with increased frequency and may be fatal.

Allopurinol↗
PubMed1978

Familial occurrence of hyperuricemia, gout, and medullary cystic disease.

We observed hyperuricemia, acute gouty arthritis, and renal medullary cystic disease in three members of a family over two generations. Two of these individuals were women who developed gout by age 20 years. Two teenage sons of one of these patients had severe hyperuricemia, which appeared due to underexcretion of uric acid. To our knowledge the occurrence of hyperuricemia, gout, and renal medullary cystic disease has not been reported previously.

Adolescent↗
PubMed1981

Management of asymptomatic hyperuricemia.

Although the incidence of gout, renal stones, or both is increased in patients with hyperuricemia, there is no evidence that long-term therapy offers any substantial long-term benefits. Recent data also suggest that no clear relationship exists between hyperuricemia and the development of interstitial nephritis (so-called urate nephropathy). Finally, the relationship between elevations in the serum concentration of uric acid and the risk of developing cardiovascular disease remains undefined. It is recommended that, in a patient with asymptomatic hyperuricemia, a conservative approach be taken and hypouricemic therapy not be instituted as a matter of routine.

Acute Disease↗
PubMed1980

[Correlative urinary excretion of sodium-uric acid in hyperuricemia (author's transl)].

Since uricosuria is an essential compensative factor in hyperuricemia, multiple factors exist which can influence on the uric acid excretion in the tubules. Normally, 90% of the uric acid filtered by the glomerulus is reabsorbed, and its active tubular secretion forms the greater part of the uric acid present in the urine. One of the factors observed as leading to urinary excretion of uric acid, is saline overload, although this effect cannot always be achieved. This study is an attempt to assess the importance of hyperuricemia as a determinant of the action of sodium upon the urinary excretion of uric acid. The series were grouped according to the plasma and urinary values of uric acid. In cases studied, the percentage of sodium was similar independent of the excretion percentages obtained for uric acid. Nevertheless, in the groups with increased plasma levels of uric acid, a direct and significant correlation was found between the excretion percentage of sodium and that of uric acid. These data cannot be obtained in groups with normal plasma levels of uric acid. Since saline overload does not always lead to hyperuricosuria, other factors must condition the secondary effect. The obtained results suggest that hyperuricemia can be one of those factors, offering a great amount of uric acid to the renal tubule, a condition in which the sodium may act as a dragging factor which may not be possible with a lesser degree of uric acid.

Adult↗