Suppression of Uric Acid Secretion in a Patient with Renal Hypouricemia

1974 ◽  
pp. 723-728 ◽  
Author(s):  
Peter A. Simkin ◽  
Maurice D. Skeith ◽  
L. A. Healey
Keyword(s):  
Uric Acid ◽  
Acid Secretion ◽  
Renal Hypouricemia ◽  
Uric Acid Secretion

scholarly journals Uric Acid Secretion from Adipose Tissue and Its Increase in Obesity

2013 ◽  
Vol 288 (38) ◽  
pp. 27138-27149 ◽  
Author(s):  
Yu Tsushima ◽  
Hitoshi Nishizawa ◽  
Yoshihiro Tochino ◽  
Hideaki Nakatsuji ◽  
Ryohei Sekimoto ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Uric Acid ◽  
Acid Secretion ◽  
Acid Production ◽  
Culture Medium ◽  
Dependent Manner ◽  
Obese Mice ◽  
Subsequent Increase ◽  
Dose Dependent ◽  
Uric Acid Secretion

Obesity is often accompanied by hyperuricemia. However, purine metabolism in various tissues, especially regarding uric acid production, has not been fully elucidated. Here we report, using mouse models, that adipose tissue could produce and secrete uric acid through xanthine oxidoreductase (XOR) and that the production was enhanced in obesity. Plasma uric acid was elevated in obese mice and attenuated by administration of the XOR inhibitor febuxostat. Adipose tissue was one of major organs that had abundant expression and activities of XOR, and adipose tissues in obese mice had higher XOR activities than those in control mice. 3T3-L1 and mouse primary mature adipocytes produced and secreted uric acid into culture medium. The secretion was inhibited by febuxostat in a dose-dependent manner or by gene knockdown of XOR. Surgical ischemia in adipose tissue increased local uric acid production and secretion via XOR, with a subsequent increase in circulating uric acid levels. Uric acid secretion from whole adipose tissue was increased in obese mice, and uric acid secretion from 3T3-L1 adipocytes was increased under hypoxia. Our results suggest that purine catabolism in adipose tissue could be enhanced in obesity.

scholarly journals Bioactive Compounds from Plant-Based Functional Foods: A Promising Choice for the Prevention and Management of Hyperuricemia

Foods ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 973
Author(s):  
Lin-Lin Jiang ◽  
Xue Gong ◽  
Ming-Yue Ji ◽  
Cong-Cong Wang ◽  
Jian-Hua Wang ◽  
...  
Keyword(s):  
Uric Acid ◽  
Side Effects ◽  
Bioactive Compounds ◽  
Functional Foods ◽  
High Serum ◽  
Pharmacological Effects ◽  
Pharmaceutical Drugs ◽  
Natural Remedies ◽  
Obesity Hypertension ◽  
Uric Acid Secretion

Hyperuricemia is a common metabolic disease that is caused by high serum uric acid levels. It is considered to be closely associated with the development of many chronic diseases, such as obesity, hypertension, hyperlipemia, diabetes, and cardiovascular disorders. While pharmaceutical drugs have been shown to exhibit serious side effects, and bioactive compounds from plant-based functional foods have been demonstrated to be active in the treatment of hyperuricemia with only minimal side effects. Indeed, previous reports have revealed the significant impact of bioactive compounds from plant-based functional foods on hyperuricemia. This review focuses on plant-based functional foods that exhibit a hypouricemic function and discusses the different bioactive compounds and their pharmacological effects. More specifically, the bioactive compounds of plant-based functional foods are divided into six categories, namely flavonoids, phenolic acids, alkaloids, saponins, polysaccharides, and others. In addition, the mechanism by which these bioactive compounds exhibit a hypouricemic effect is summarized into three classes, namely the inhibition of uric acid production, improved renal uric acid elimination, and improved intestinal uric acid secretion. Overall, this current and comprehensive review examines the use of bioactive compounds from plant-based functional foods as natural remedies for the management of hyperuricemia.

scholarly journals The Role of Hyperuricemia in the Pathogenesis and Progressivity of Chronic Kidney Disease

2021 ◽  
Vol 9 (F) ◽  
pp. 428-435
Author(s):  
Gede Wira Mahadita ◽  
Ketut Suwitra
Keyword(s):  
Chronic Kidney Disease ◽  
Uric Acid ◽  
Kidney Disease ◽  
Serum Uric Acid ◽  
Filtration Rate ◽  
Stage Iv ◽  
Review Of The Literature ◽  
The Relationship ◽  
Uric Acid Secretion

In humans, the end product of purine metabolism is uric acid. Over 70% of uric acid is excreted through the kidneys. When renal function is impaired, uric acid secretion is also impaired. This directly correlates the prevalence of hyperuricemia with the severity of chronic kidney disease (CKD). It has been reported that the prevalence of hyperuricemia in patients with Stage I-III CKD is 40–60% and up to 70% in patients with Stage IV-V CKD. Some studies found a link between serum uric acid levels and decreased glomerular filtration rate (GFR), an independent risk factor for CKD development. Because CKD and serum uric acid levels are related, the relationship between the two frequently generates controversy. As such, this review of the literature discusses the role of uric acid in the pathogenesis and progression of CKD.

Familial Renal Hypouricemia with Intact Reabsorption of Uric Acid

Nephron ◽  
1987 ◽  
Vol 45 (1) ◽  
pp. 40-42 ◽  
Author(s):  
Hiromu Nakajima ◽  
Masahiro Gomi ◽  
Sayomi Iida ◽  
Norio Kono ◽  
Kaname Moriwaki ◽  
...  
Keyword(s):  
Uric Acid ◽  
Renal Hypouricemia

scholarly journals A Proposal for Practical Diagnosis of Renal Hypouricemia: Evidenced from Genetic Studies of Nonfunctional Variants of URAT1/SLC22A12 among 30,685 Japanese Individuals

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 1012
Author(s):  
Yusuke Kawamura ◽  
Akiyoshi Nakayama ◽  
Seiko Shimizu ◽  
Yu Toyoda ◽  
Yuichiro Nishida ◽  
...  
Keyword(s):  
Uric Acid ◽  
Serum Uric Acid ◽  
Fractional Excretion ◽  
Accurate Diagnosis ◽  
Health Examination ◽  
Regression Analyses ◽  
Genetic Studies ◽  
Renal Hypouricemia ◽  
High Frequencies ◽  
Low Serum

Background: Renal hypouricemia (RHUC) is characterized by a low serum uric acid (SUA) level and high fractional excretion of uric acid (FEUA). Further studies on FEUA in hypouricemic individuals are needed for a more accurate diagnosis of RHUC. Methods: In 30,685 Japanese health-examination participants, we genotyped the two most common nonfunctional variants of URAT1 (NFV-URAT1), W258X (rs121907892) and R90H (rs121907896), in 1040 hypouricemic individuals (SUA ≤ 3.0 mg/dL) and 2240 individuals with FEUA data. The effects of NFV-URAT1 on FEUA and SUA were also investigated using linear and multiple regression analyses. Results: Frequency of hypouricemic individuals (SUA ≤ 3.0 mg/dL) was 0.97% (male) and 6.94% (female) among 30,685 participants. High frequencies of those having at least one allele of NFV-URAT1 were observed in 1040 hypouricemic individuals. Furthermore, NFV-URAT1 significantly increased FEUA and decreased SUA, enabling FEUA and SUA levels to be estimated. Conversely, FEUA and SUA data of hypouricemic individuals are revealed to be useful to predict the number of NFV-URAT1. Conclusions: Our findings reveal that specific patterns of FEUA and SUA data assist with predicting the number of nonfunctional variants of causative genes for RHUC, and can also be useful for practical diagnosis of RHUC even before genetic tests.

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