Linking uric acid metabolism to diabetic complications

Kushiyama, Akifumi; Tanaka, Kentaro; Hara, Shigeko; Kawazu, Shoji

doi:10.4239/wjd.v5.i6.787

Cited by 77 publications

(50 citation statements)

References 98 publications

(115 reference statements)

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“…As shown in studies, sUA level was not only associated with the risk of diabetes, it was also an independent predictive factor for diabetes complications (e.g., neuropathy, retinopathy, kidney diseases, diabetes mellitus foot and vasculopathy) …”

Section: Methodsmentioning

confidence: 68%

Management of gout and hyperuricemia: Multidisciplinary consensus in Taiwan

Chen

et al. 2018

Int J of Rheum Dis

107

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Gout is an inflammatory disease manifested by the deposition of monosodium urate (MSU) crystals in joints, cartilage, synovial bursa, tendons or soft tissues. Gout is not a new disease, which was first documented nearly 5,000 years ago. The prevalence of gout has increased globally in recent years, imposing great disease burden worldwide. Moreover, gout or hyperuricemia is clearly associated with a variety of comorbidities, including cardiovascular diseases, chronic kidney disease, urolithiasis, metabolic syndrome, diabetes mellitus, thyroid dysfunction, and psoriasis. To prevent acute arthritis attacks and complications, earlier use of pharmacotherapeutic treatment should be considered, and patients with hyperuricemia and previous episodes of acute gouty arthritis should receive long-term urate-lowering treatment. Urate-lowering drugs should be used during the inter-critical and chronic stages to prevent recurrent gout attacks, which may elicit gradual resolution of tophi. The goal of urate-lowering therapy should aim to maintain serum uric acid (sUA) level <6.0 mg/dL. For patients with tophi, the initial goal can be set at lowering sUA to <5.0 mg/dL to promote tophi dissolution. The goal of this consensus paper was to improve gout and hyperuricemia management at a more comprehensive level. The content of this consensus paper was developed based on local epidemiology and current clinical practice, as well as consensuses from two multidisciplinary meetings and recommendations from Taiwan Guideline for the Management of Gout and Hyperuricemia.

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Section: Methodsmentioning

confidence: 68%

Management of gout and hyperuricemia: Multidisciplinary consensus in Taiwan

Chen

et al. 2018

Int J of Rheum Dis

107

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“…The main function of the organ is to excrete metabolic wastes but easily impaired by many factors including drugs like aminoglycosides [1] and some ingredients transformed from body's own materials like uric acid [2]. Uric acid, as the end-product of purine metabolism in human body transformed by a rate-limiting enzyme, xanthine oxidase/xanthine dehydrogenase (XDH/XO) [3], is predominantly excreted through kidney [4]. Uric acid is almost insoluble in body fluids and will be precipitated in kidney tubules, articular cavities, and other peripherial interstitial spaces if the concentration of uric acid is above normal value (above 70 μ g/mL or 420 μ M) for a long time [4].…”

Section: Introductionmentioning

confidence: 99%

Excretory Function of Intestinal Tract Enhanced in Kidney Impaired Rats Caused by Adenine

Gao

et al. 2016

The Scientific World Journal

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The main aim of the study was to prove the compensative effect of intestine for renal function. Rat kidney was impaired by intragastrically administrating adenine (400 mg per day for 5 days). Intestinal tract was harvested and equally divided into 20 segments except cecum. Kidneys were harvested and histologically examined with hematoxylin-eosin staining kits. Uric acid, urea (BUN), and creatinine in serum were determined with assay kits, and BUN and creatinine in every intestinal segment were also determined. The results showed that adenine was able to increase uric acid level in serum from 20.98 ± 6.98 μg/mL to 40.77 ± 7.52 μg/mL and cause renal function damage with BUN (from 3.87 ± 0.62 mM to 12.33 ± 3.27 mM) and creatinine (from 51.48 ± 6.98 μM to 118.25 ± 28.63 μM) increasing in serum and with abnormally micromorphological changes in kidney. The amount of BUN and creatinine distributed in intestinal tract was positively correlated with those in blood. In impaired renal function rats, the amount of BUN (from 4.26 ± 0.21 μMole to 10.72 ± 0.55 μMole) and creatinine (from 681.4 ± 23.3 nMole to 928.7 ± 21.3 nMole) distributed in intestinal tract significantly increased. All the results proved that intestinal tract had excretory function compensative for renal function.

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“…Increased serum UA level is known to predict the risk of hypertension, diabetes mellitus, and cardiovascular disease (CVD) [1][2][3] . More recent data also emphasizes serum UA level to be a risk marker for progression of chronic kidney disease 4,5) and metabolic syndrome (MetS) 6) .…”

Section: Introductionmentioning

confidence: 99%

Changes in alcohol consumption did not affect changes in serum uric acid level in Japanese

Moriyama

2019

Health evaluation and promotion

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Objective Serum uric acid (UA) is associated with obesity, insulin resistance, metabolic syndrome components, hypertension, diabetes mellitus, and renal function. Alcohol is a risk factor for hyperuricemia and gout. Whether changes in alcohol consumption are associated with changes in serum UA levels and factors affecting changes in UA levels remain unclear. Methods Subjects were 5,327 Japanese who underwent two annual health examinations (mean interval, 2.7 years). They were stratified according to changes in serum UA levels and alcohol consumption. Results The change in body mass index, waist circumference (WC), low-density lipoprotein cholesterol (LDL-C), UA, aspartate transaminase (AST), and alanine transaminase gradually increased as changes in UA increased for both men and women. In men, the proportion of subjects who consumed ≥ 25 g ethanol/day in the ≥ 0.3 mg/dL UA change group was not particularly higher than that of in non-drinker (17.4% versus 19.7%) at baseline. In women, the proportion of subjects who consumed ≥ 25 g ethanol/day in the ≥ 0.3 mg/dL UA change group was lower than that of in non-drinker (19.3% versus 17.8%) at baseline. Multiple linear regression analysis revealed that changes in WC, LDL-C, triglyceride, AST and γ-glutamyltranspeptidase were associated with changes in UA. When changes in serum UA levels stratified by changes in UA levels and alcohol consumption were investigated, changes in alcohol consumption did not affect UA level changes; however, regardless of alcohol consumption change, anthropometric measures, lipid levels, renal function, and transaminases were worse in the increased UA level group. Subjects who increased alcohol consumption and had increased UA levels showed the worst anthropometry, BP, lipid levels, UA and transaminases changes. Conclusion Changes in UA level correlated with changes in anthropometry, lipid levels, renal function, and transaminases. Changes in alcohol consumption did not affect changes in UA level; however, subjects who increased alcohol consumption and had increased UA levels had the worst metabolic profile changes.

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Linking uric acid metabolism to diabetic complications

Cited by 77 publications

References 98 publications

Management of gout and hyperuricemia: Multidisciplinary consensus in Taiwan

Management of gout and hyperuricemia: Multidisciplinary consensus in Taiwan

Excretory Function of Intestinal Tract Enhanced in Kidney Impaired Rats Caused by Adenine

Changes in alcohol consumption did not affect changes in serum uric acid level in Japanese

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