Dietary Antioxidant Supplements and Uric Acid in Chronic Kidney Disease: A Review

Roumeliotis, Stefanos; Roumeliotis, Athanasios; Dounousi, Evangelia; Eleftheriadis, Theodoros; Liakopoulos, Vassilios

doi:10.3390/nu11081911

Cited by 97 publications

(83 citation statements)

References 123 publications

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“…In addition, the key urate-producing enzyme XDH was significantly increased in the HPD group compared with the CON group and was positively correlated with the serum urate levels. Hyperuricemia is closely associated with kidney excretion disorders [14,48]. We also detected MSU on the kidney surface, which indicates that inflammation occurred in the renal tissue.…”

Section: Discussionmentioning

confidence: 58%

High-Protein Diet Induces Hyperuricemia in a New Animal Model for Studying Human Gout

Hong

Zheng

et al. 2020

IJMS

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Hyperuricemia is a central risk factor for gout and increases the risk for other chronic diseases, including cardiometabolic disease, kidney disease, and hypertension. Overproduction of urate is one of the main reasons for hyperuricemia, and dietary factors including seafoods, meats, and drinking are contributed to the development of it. However, the lack of a suitable animal model for urate metabolism is one of the main reasons for the delay and limitations of hyperuricemia research. Combining evolutionary biological studies and clinical studies, we conclude that chicken is a preferred animal model for hyperuricemia. Thus, we provided chickens a high-protein diet (HPD) to evaluate the changes in the serum urate levels in chickens. In our study, the HPD increased the serum urate level and maintained it at a long-term high level in chickens. Long-term high serum urate levels induced an abnormal chicken claw morphology and the precipitation of monosodium urate (MSU) in joint synovial fluid. In addition, a long-term HPD also decreased the glomerular filtration rate and induced mild renal injury. Most importantly, allopurinol and probenecid displayed the positive effects in decreasing serum urate and then attenuated hyperuricemia in chicken model. These findings provide a novel model for hyperuricemia and a new opportunity to further investigate the effects of long-term hyperuricemia on other metabolic diseases.

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Section: Discussionmentioning

confidence: 58%

High-Protein Diet Induces Hyperuricemia in a New Animal Model for Studying Human Gout

Hong

Zheng

et al. 2020

IJMS

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“…This is associated with several factors, such as malnutrition, dietary restrictions, or loss of vitamins and trace elements occurring during HD or PD (Liakopoulos et al, 2017Roumeliotis et al, 2019a). Implementing lifestyle interventions, such as administration of exogenous antioxidants, in patients with CKD on dialysis may downregulate the inflammation and oxidative stress associated with CVD-linked morbidity and mortality even in early stages of CKD (Liakopoulos et al, 2019a,b;Roumeliotis et al, 2019b). Indeed, several studies have investigated the possible benefits of exogenous antioxidant administration in both HD and PD patients.…”

Section: Changes In Cellular Balance Of Reactive Oxygen Species Can Cmentioning

confidence: 99%

“…CKD (Liakopoulos et al, 2019a,b;Roumeliotis et al, 2019b). However, further studies in large cohorts of HD and PD patients are necessary to determine the causality between antioxidant supplementation and clinical hard end-points of CVDs and allcause mortality.…”

Section: Changes In Cellular Balance Of Reactive Oxygen Species Can Cmentioning

confidence: 99%

Mechanisms of Cardiovascular Disorders in Patients With Chronic Kidney Disease: A Process Related to Accelerated Senescence

Carracedo

Alique

Vida

et al. 2020

Front. Cell Dev. Biol.

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Cardiovascular diseases (CVDs), especially those involving a systemic inflammatory process such as atherosclerosis, remain the leading cause of morbidity and mortality in patients with chronic kidney disease (CKD). CKD is a systemic condition affecting approximately 10% of the general population. The prevalence of CKD has increased over the past decades because of the aging of the population worldwide. Indeed, CVDs in patients with CKD constitute a premature form of CVD observed in the general population. Multiple studies indicate that patients with renal disease undergo accelerated aging, which precipitates the appearance of pathologies, including CVDs, usually associated with advanced age. In this review, we discuss several aspects that characterize CKD-associated CVDs, such as etiopathogenic elements that CKD patients share with the general population, changes in the cellular balance of reactive oxygen species (ROS), and the associated process of cellular senescence. Uremiaassociated aging is linked with numerous changes at the cellular and molecular level. These changes are similar to those observed in the normal process of physiologic aging. We also discuss new perspectives in the study of CKD-associated CVDs and epigenetic alterations in intercellular signaling, mediated by microRNAs and/or extracellular vesicles (EVs), which promote vascular damage and subsequent development of CVD. Understanding the processes and factors involved in accelerated senescence and other abnormal intercellular signaling will identify new therapeutic targets and lead to improved methods of diagnosis and monitoring for patients with CKD-associated CVDs.

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“…It has been demonstrated that hyperuricemia is not only a risk factor for gout and chronic kidney disease, but also a risk factor for hypertension, hyperlipidemia, diabetes and cardiovascular disease, which are conditions that seriously affects human health (11)(12)(13)(14)(15)(16)(17). Therefore, xanthine oxidase inhibitors are commonly used in clinical practice to inhibit the synthesis of uric acid (18,19), but the effect is not as good as expected and has serious side effects (20)(21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

Construction and expression of recombinant uricase‑expressing genetically engineered bacteria and its application in rat model of hyperuricemia

Cai

Deng

et al. 2020

Int J Mol Med

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At present, the treatment of hyperuricemia is designed primarily to decrease the production of uric acid using xanthine oxidase inhibitors; however, the therapeutic effect is not satisfactory. Therefore, the key to the successful treatment of hyperuricemia is to increase the excretion of uric acid. The aim of present study was to construct uricase-expressing genetically engineered bacteria and analyze the effects of these engineered bacteria on the lowering of uric acid levels in a rat model of hyperuricemia. The uricase expression vector was constructed by gene recombination technology and transfected into Escherichia coli. The expression and activity of uricase were analyzed by SdS-PAGE analysis and Bradford assay. The water consumption, food intake, body weight, eosinophil count and intestinal histology, in addition to the levels of serum uric acid (SUA) and allantoin in the feces of the rats, were assessed. The intestinal contents of the rats were analyzed by 16S rdNA sequencing technology. The results demonstrated that uricase-expressing genetically engineered bacteria secreted active uricase. All rats exhibited a natural growth trend during the entire experiment, and the SUA of hyperuricemic rats treated with uricase-expressing engineered bacteria was significantly decreased. In conclusion, these results indicate that uricase secreted by recombinant uricase-expressing genetically engineered bacteria served an important role in decreasing SUA levels in a rat model of hyperuricemia.

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Dietary Antioxidant Supplements and Uric Acid in Chronic Kidney Disease: A Review

Cited by 97 publications

References 123 publications

High-Protein Diet Induces Hyperuricemia in a New Animal Model for Studying Human Gout

High-Protein Diet Induces Hyperuricemia in a New Animal Model for Studying Human Gout

Mechanisms of Cardiovascular Disorders in Patients With Chronic Kidney Disease: A Process Related to Accelerated Senescence

Construction and expression of recombinant uricase‑expressing genetically engineered bacteria and its application in rat model of hyperuricemia

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