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For the first time after onset of the economic miracle since 1948/49 the continuous considerable upward trend of the prevalence of hyperuricemia among the adult population in northern Germany seems to be stopped. In a comparative study of a total of 7169 unselected patients of both sexes, that has been admitted as inpatients for rehabilitation reasons predominantly concerning rheumatic diseases, has been examined which differences result between 1988 and 1990 with respect to the prevalence of hyperuricemia in relation to overweight. Age structure, professions and social levels were comparable in both populations. In comparison with the large upward trend of the risk factor profile between 1976 and 1988 the prevalence of hyperuricemia in males decreased significantly from an average of 17.9 per cent to 15.2 per cent. For females only an insignificant trend to a decrease of the prevalence of hyperuricemia (4.5 per cent vs. 4.2 per cent) was noted. In hyperuricemic males the prevalence of overweight of more than 20 per cent in relation to the individual ideal weight was significantly more frequent than in the whole male population (70.1 per cent vs. 57.7 per cent). Just as for obesity and diabetes mellitus the prevalence of hyperuricemia among the adult population in northern Germany appears to have culminated or crossed its summit. There is further evidence for a small success of public and medical efforts to improve public health. Of a total of 3584 patients who were investigated in 1990 1977 males showed a mean serum uric acid level of 5.71 +/- 1.62 mg/dl whereas in females the corresponding mean value was highly significantly less (4.22 +/- 1.06 mg/dl).
PURPOSE: To determine the frequency and characteristics of hyperuricemia and gouty arthritis among cyclosporine-treated heart transplant recipients. PATIENTS AND METHODS: One hundred ninety-six surviving adult heart or heart/lung transplant recipients were evaluated. Medical records were reviewed to determine peak serum uric acid levels after transplantation, and to evaluate potential risk factors for hyperuricemia. Patients were surveyed by postal questionnaire for a history of gouty arthritis, with positive responses evaluated by telephone interview and/or examination of the patient. RESULTS: Hyperuricemia occurred in 72% of male and 81% of female patients and was not correlated with cyclosporine level, presence of hypertension, or degree of renal insufficiency. Eleven (6%) patients had gout prior to transplantation; 14 (8%) had onset of definite gout and seven (4%) had probable gout a mean of 17 months after transplantation. Polyarticular arthritis and/or tophi developed in six (43%) of the posttransplant-onset definite gout group within a mean of 31 months. CONCLUSION: Both hyperuricemia and gouty arthritis occur with increased frequency among cyclosporine-treated heart or heart/lung transplant recipients. The clinical course of gout in these patients is often accelerated, with management complicated by the patients' renal insufficiency and interaction with transplant-related medications.
The prevalence of gout and hyperuricemia was investigated by a survey of a total population of 4683 rural adults. The successful response rate was 95.2%. Of the respondents 85.3% of the individuals were examined. The prevalence of gout and hyperuricemia in men was 1.7 and 24.3%, respectively. The male to female ratio was 34:1 for gout and 2:1 for hyperuricemia. The observed higher prevalence of gout and hyperuricemia in this male Malayo-Polynesian population compared with Caucasian data, in spite of a lower life expectancy and subsistence economy, suggests that genetic and racial predisposition are key causative factors.
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.
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.
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.
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)
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.
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.
De novo purine biosynthesis has been investigated in circulating blood lymphocytes in vitro. N-formyl-glycinamide ribonucleotide (FGAR) has been mesured using 14C-formate incorporation in the presence of azaserine, a metabolic inhibitor blocking the metabolical pathway at the level of FGAR synthesis. Such a synthesis was measured in 20 healthy controls, 24 patients with primary gout (11 on allopurinol therapy) and 26 patients with chronic renal failure and secondary hyperuricemia (8 on allopurinol therapy). Among gouty patients without allopurinol therapy, FGAR synthesis was normal in 5 and increased in the others. FGAR synthesis was decreased in patients with renal failure whatever the therapy. However, FGAR synthesis remained increased in patients with a primary gout complicated with renal insufficiency. The test we propose for de novo purine biosynthesis measurement is simple and of value to analyse the patho-physiology of hyperuricemia and its therapy. The test allows an acurate discrimination between primary and secondary hyperuricemia in the presence of renal insufficiency.
Hyperuricemia-associated renal injury is closely linked to oxidative stress and inflammation, highlighting the need for safe dietary intervention. This study evaluated the protective effects of a black rice anthocyanin (ATC)-hyaluronic acid complex (HAA) against uric acid (UA)-induced injury. In UA-induced human renal proximal tubular epithelial (HK-2) cells, black rice ATCs, HA, and HAA improved cell viability and antioxidant defenses, as shown by increased glutathione (GSH) levels and catalase (CAT) and superoxide dismutase (SOD) activities. They also reduced malondialdehyde (MDA), reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β). HAA produced a greater reduction in TLR4/NF-κB-related inflammatory gene expression, suggesting that its cytoprotective and anti-inflammatory effects may be associated with modulation of this inflammatory axis. In hyperuricemic mice, HAA lowered serum UA, creatinine, and blood urea nitrogen levels, inhibited hepatic xanthine oxidase and adenosine deaminase activities, and attenuated renal histopathological injury. HAA also reduced the mRNA expression of urate reabsorption-related genes, including GLUT9, OAT4, and OAT10, while increasing that of urate excretion-related genes, including OAT1 and ABCG2, which may contribute to improved urate homeostasis. These findings support the potential of HAA as a functional dietary ingredient for the management of hyperuricemia-associated metabolic disturbances and renal injury.
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.
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.
Six infants and children with medium-chain acyl-coenzyme A dehydrogenase deficiency were found to have hyperuricemia during an acute episode. Hyperuricemia may be a clue to the diagnosis of medium-chain acyl-coenzyme A dehydrogenase deficiency.
Hyperuricemia was induced in rats ingesting a diet supplemented with 2 1/2+ uric acid and 5% oxonic acid (an inhibitor of hepatic uricase activity). After seven days, inulin clearance (CIn) and superficial nephron glomerular filtration rate (SNFR) were significantly lower than values recorded in healthy rats (CIn:0.94 +/- 0.10 vs. 3.61 +/- 0.13 ml/min/kg of body wt; SNFR: 54.9 +/- 3.2 vs. 129.7 +/- 6.7 nl/min/kg of body wt). Filtration rate reduction was accompanied by an increased concentration of urate in renal tissue. Gross examination of the kidney revealed the presence of whitish streaks containing negatively birefringent crystals throughout the medulla and papilla. Histological examination revealed dilatation of the collecting ducts with flattening of the epithelium and intraluminal crystalline deposits. Intraluminal hydrostatic pressure was markedly higher than that observed in healthy rats in both proximal (21.5 +/- 1.7 vs. 11.4 +/- 0.3 mm Hg) and distal convoluted tubules (20.3 +/- 2.0 vs. 7.6 +/- 0.5 mm Hg). In another group of rats ingesting a similar diet, CIn was reduced to 1.49 +/- 0.20 ml/min/kg of body wt. Partial or complete restoration of CIn toward normal was effected within seven additional days by the oral ingestion of a large volume of an alkali solution (CIn:2.63 +/- 0.44 ml/min/kg of body wt) or by the cessation of treatment with oxonic-uric acid (CIn: 4.70 +/- 0.28 ml/min/kg of body wt). These results demonstrate that oxonic/uric acid-induced hyperuricemia is accompanied by severe filtration rate reduction, and they suggest strongly that intraluminal obstruction, via the deposition of uric acid, plays an important role in its pathogenesis.
A patient with severe idiopathic hyperuricemia and hypokalemic alkalosis was followed over a one-year period. A tubulointersitial nephritis consistent with hypokalemic nephropathy was found on biopsy. However, the possibility that the hyperuricemia contributed to the hypokalemia and renal lesion cannot be excluded. Inappropriate urinary loss of potassium could be prevented by administration of spironolactone or triameterene. Six months after initiation of allopurinol therapy with reduction of serum uric acid concentrations to normal concentrations, this potassium wasting was substantially decreased.