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At least 19 recordsLinked to original sources
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↗
PubMedDate not supplied

[The prevalence of gout and hyperuricemia among the workers of a meat-packing plant complex].

An attempt was made to study the incidence of gout and hyperuricemia among the workers of the Moscow meat-packing plant exposed to high food purine loads. Using extensive clinical material (535 men and 1121 women) the authors established that gout was diagnosed 33 times more often in men of this plant than in the muscular population of other towns of the country. Moderate hyperuricemia was revealed in every second of the examinees. Marked hyperuricemia was noted 1.8 times more often, it being 3.4 times more often in men working at this plant as compared to the whole muscular population of the country. There was a direct dependence of the level of hyperuricemia in men working in this industry on their service record. The levels of moderate hyperuricemia in all groups of men and in some groups of women directly depended on the amount of daily purine loads. Marked hyperuricemia among the examined men is a factor of risk in the development of load and among the examined women an indicator of risk (i. e. warning) of possible metabolic changes which require an adequate dietetic and therapeutic correction.

Age Factors↗
PubMed1988

[Hyperlipoproteinemia in primary gout and asymptomatic hyperuricemia].

More than 800 patients suffering from primary gout or asymptomatic hyperuricemia were examined for the values of total cholesterol and triglycerides and the pattern of lipoproteins. The values for HDL (high-density-lipoprotein = alpha-lipoprotein), LDL (low-density-lipoprotein = beta-lipoprotein) and VLDL (very-low-density-lipoprotein = pre-beta-lipoprotein), found in lipid electrophoresis, were significant abnormal as well in the group of patients with gout (n = 147) as in the group of patients with asymptomatic hyperuricemia (n = 700) versus the healthy controls. It was remarkable, that the values of lipoproteins in asymptomatic hyperuricemia almost were abnormal just as often as in primary gout. Approximately 80% of both groups showed an increased LDL, around 35% a decreased HDL, and an increased VLDL was found in 72% of patients with gout and in 54% of asymptomatic hyperuricemia. Pathological changes of all lipoproteins (HDL, LDL and VLDL) appeared in 23% of patients with gout and in 20% of patients with asymptomatic hyperuricemia. Only 2.7% of patients with gout and 4.8% with hyperuricemia showed a normal lipometabolism.

Adolescent↗
PubMed1992

[First indications of decrease in the incidence of hyperuricemia in North Germany].

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).

Adult↗
PubMed1990

Renal dysfunction and hyperuricemia at presentation and relapse of acute lymphoblastic leukemia.

Hyperuricemia is an unusual presenting feature of acute lymphoblastic leukemia (ALL) and is generally associated with a large leukemic cell burden. We describe three children with T-cell ALL who presented with acute renal failure and very high serum uric acid concentrations, despite a relatively small leukemic cell burden. Two of the three patients had normal complete blood counts without circulating blasts or other physical evidence of leukemia. An isolated renal relapse in one case was associated with hyperuricemia, increased renal excretion of uric acid, and renal dysfunction. An unusually high rate of purine catabolism of the lymphoblasts may cause hyperuricemia in these cases. Unexplained hyperuricemia should prompt a search for occult malignancy.

Acute Kidney Injury↗
PubMed1992

Hyperuricemia and gout among heart transplant recipients receiving cyclosporine.

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.

Arthritis, Gouty↗
PubMed1990

Underexcretory-type hyperuricemia, disproportionate to the reduced glomerular filtration rate, in two boys with mild proteinuria.

Two unrelated boys with mild persistent proteinuria and underexcretory-type hyperuricemia of more than 9.0 mg/dl (535 mumols/l) are described. The proteinuria was detected at age 10 and 6 years, respectively. The fractional excretion of uric acid in both was low at 2-3%, when the creatinine clearance was decreased by about 50%. Tissue examination revealed focal interstitial fibrosis in both patients and medullary urate crystals in one patient in whom medullary tissue was obtained on biopsy. An immunofluorescence study was negative for immunoglobulins, complements and fibrin. Treatment of hyperuricemia did not prevent further deterioration of their renal function. One of them underwent a renal transplantation and then his serum uric acid level returned to the normal range. Neither patient had a family history of hyperuricemia, gout or inherited progressive renal disease. Both patients are likely to be sporadic cases of familial nephropathy with gout, an autosomal dominant disease, due to a new mutation. Hyperuricemia due to diminished uric acid clearance may be a risk factor or predictor for the development of progressive renal disease in some subjects.

Child↗
PubMed1992

The epidemiology of gout and hyperuricemia in a rural population of Java.

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.

Adolescent↗
PubMed1988

[Neonatal oliguria associated with hyperuricemia].

Acute renal failure syndrome in the newborn has many etiologic factors. Hyperuricemia as unique etiology of this syndrome has been seldom cited in literature, although is a well know factor operating together with others. From nine newborns with oliguria, hyperuricemia vas a contributing factor in appearance of the syndrome in seven. In the other two cases hyperuricemia was the sole possible etiologic factor in development of oliguria which was classified as functional. Hyperuricemia alone may be the unique etiologic factor in functional oliguria of the newborn being further investigations needed to understand its precise mechanism.

Acute Kidney Injury↗
PubMed1987

Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study.

To quantify the consequences of asymptomatic hyperuricemia, this study examined rates for a first episode of gouty arthritis based on 30,147 human-years of prospective observation. A cohort of 2,046 initially healthy men in the Normative Aging Study was followed for 14.9 years with serial examinations and measurement of urate levels. With prior serum urate levels of 9 mg/dl or more, the annual incidence rate of gouty arthritis was 4.9 percent, compared with 0.5 percent for urate levels of 7.0 to 8.9 mg/dl and 0.1 percent for urate levels below 7.0 mg/dl. With urate levels of 9 mg/dl or higher, cumulative incidence of gouty arthritis reached 22 percent after five years. Incidence rates were three times higher for hypertensive patients than for normotensive patients (p less than 0.01). The strongest predictors of gout in a proportional hazards model were age, body mass index, hypertension, and cholesterol level, and alcohol intake. When the serum urate level became a factor in the model, none of these variables retained independent predictive power. At the final examination, only 0.7 percent of participants had a serum creatinine level of 2.0 mg/dl or more, with no evidence of renal deterioration attributable to hyperuricemia. These data support conservative management of asymptomatic hyperuricemia.

Adult↗
PubMed1987

Myogenic hyperuricemia. A common pathophysiologic feature of glycogenosis types III, V, and VII.

To identify the mechanism of hyperuricemia in glycogen storage diseases (glycogenoses) that affect muscle, we studied the effects of exercise and prolonged rest on purine metabolism in two patients with glycogenosis type III (debrancher deficiency), one patient with type V (muscle phosphorylase deficiency), and one patient with type VII (muscle phosphofructokinase deficiency). All had hyperuricemia except for one patient with glycogenosis type III. Plasma concentrations of ammonia, inosine, and hypoxanthine increased markedly in all the patients after mild leg exercise on a bicycle ergometer. The plasma urate concentrations also increased, but with a delayed response. Urinary excretion of inosine, hypoxanthine, and urate increased greatly after exercise, consistently with the increases in plasma levels. Hypoxanthine and urate concentrations were extremely high in the plasma and urine of the patient with glycogenosis type VII. With bed rest, the plasma hypoxanthine level returned to normal within a few hours, and the plasma urate concentration decreased from 18.6 to 10.6 mg per deciliter (1106 to 630 mumol per liter) within 48 hours. Similarly, the urinary excretion of these purine metabolites was reduced by bed rest. These findings indicate that muscular exertion in patients with glycogenosis types III, V, and VII causes excessive increases in blood ammonia, inosine, and hypoxanthine due to accelerated degradation of muscle purine nucleotides. These purine metabolites subsequently serve as substrates for the synthesis of uric acid, leading to hyperuricemia.

Adult↗
PubMed1989

Cyclosporine-induced hyperuricemia and gout.

To evaluate the frequency and the pathogenesis of hyperuricemia and gout during cyclosporine therapy, we studied renal-transplant recipients who were treated with either cyclosporine and prednisone (n = 129) or azathioprine and prednisone (n = 168). Among the patients with stable allograft function and serum creatinine concentrations below 265 mumol per liter, hyperuricemia was more common in the cyclosporine group than in the azathioprine group (84 percent vs. 30 percent; P = 0.0001). Gout developed in nine patients (7 percent) in the cyclosporine group, but no episodes occurred in the azathioprine group. Serum urate levels became elevated in 90 percent of the patients in the cyclosporine group who were treated with diuretics, as compared with 60 percent of those not treated with diuretics (P = 0.001); in the azathioprine group, the corresponding values were 47 percent and 15 percent (P = 0.0001). Serum urate levels did not correlate with trough blood cyclosporine levels in a selected subgroup (n = 40) of patients from the cyclosporine group, who were studied from 4 to 96 weeks after transplantation. Detailed studies of urate metabolism in six cyclosporine-treated patients revealed normal turnover rates for urate and decreases in creatinine and urate clearance, as compared with seven control subjects. We conclude that hyperuricemia is a common complication of cyclosporine therapy and is caused by decreased renal urate clearance. Gouty arthritis is the cause of considerable morbidity among renal-transplant recipients who receive cyclosporine.

Adult↗