The role of uric acid in renal damage - A history of inflammatory pathways and vascular remodeling

Russo, Elisa; Verzola, Daniela; Cappadona, Francesca; Leoncini, Giovanna; Garibotto, Giacomo; Pontremoli, Roberto; Viazzi, Francesca

doi:10.20517/2574-1209.2021.11

Cited by 15 publications

(18 citation statements)

References 100 publications

(132 reference statements)

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“…(2) insulin resistance: obesity or extra body fat may be linked with elevated sUA production and insufficient excretion due to insulin resistance, resulting in impaired UA metabolism and even hyperuricemia [11]. Additionally, in the state of insulin resistance, the body can activate the reninangiotensin-aldosterone system, causing a decrease in renal blood flow, resulting in a decrease in UA excretion and an increase in the sUA [12,13]. (3) endocrine role of adipokines: a variety of adipokines (such as adiponectin, leptin, etc.)…”

Section: Discussionmentioning

confidence: 99%

Correlation of obesity, dietary patterns, and blood pressure with uric acid: data from the NHANES 2017–2018

et al. 2022

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Background Prevalence rates of hyperuricemia and gout are increasing. Clinical investigations of hyperuricemia-related risk factors aid in the early detection, prevention, and management of hyperuricemia and gout. Ongoing research is examining the association of obesity, dietary patterns, and blood pressure (BP) with serum uric acid (sUA). Methods A cross-sectional study was conducted based on the National Health and Nutrition Examination Survey. The exposures included body mass index (BMI), dietary patterns, and BP. The outcome variable was sUA level. The weighted multivariate linear regression models and smooth curve fittings were used to assess the association of BMI, dietary patterns, and BP with sUA. Results There was a significantly positive correlation between BMI and sUA (β = 0.059, 95% CI: 0.054 to 0.064, P < 0.00001). Overweight and obese individuals had higher sUA levels than those with the normal BMI (β = 0.451, 95% CI: 0.357 to 0.546, P < 0.00001; β = 0.853, 95% CI: 0.760 to 0.946, P < 0.00001; respectively). Dietary energy intake was positively correlated with sUA (β = 0.000, 95% CI: 0.000 to 0.000, P = 0.01057). Dietary intake of carbohydrate and fiber were negatively correlated with sUA (β = − 0.001, 95% CI: − 0.002 to − 0.000, P < 0.00001; β = − 0.008, 95% CI: − 0.011 to − 0.004, P = 0.00001; respectively). Moreover, systolic BP was positively correlated with sUA (β = 0.006, 95% CI: 0.003 to 0.009, P = 0.00002). However, no statistical differences were found about the associations of dietary intake of total sugars, protein, total fat, cholesterol, and diastolic BP with sUA. Conclusions The current cross-sectional investigation of a nationally representative sample of US participants showed that BMI, dietary energy intake, and systolic BP were positively correlated with sUA levels; dietary carbohydrate and fiber intake were negatively correlated with sUA levels. The findings might be helpful for the management and treatment of hyperuricemia and gout.

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Section: Discussionmentioning

confidence: 99%

Correlation of obesity, dietary patterns, and blood pressure with uric acid: data from the NHANES 2017–2018

et al. 2022

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“…There are several pathophysiological mechanisms linking uric acid to inflammation and oxidative stress, which contribute to the development and progression of endothelial dysfunction and vascular damage. 33 In endothelial cells, elevated UA level stimulates the receptor for advanced glycation end products (RAGE) signaling pathway and activates nuclear factor kappa B (NF‐κB). This process leads to the extracellular release of high‐mobility group protein‐1 (HMGB1) and its interaction with RAGE contributes to the amplification of the inflammatory response, finally inducing endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Genetic risk of hyperuricemia in hypertensive patients associated with antihypertensive drug therapy: A longitudinal study

et al. 2022

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Elevated serum uric acid (UA) level has been shown to be influenced by multiple genetic variants, but it remains uncertain how UA-associated variants differ in their influence on hyperuricemia risk in people taking antihypertensive drugs. We examined a total of 43 UA-related variants at 29 genes in 1840 patients with hypertension from a community-based longitudinal cohort during a median 2.25-year follow-up (including 1031 participants with normal UA, 440 prevalent hyperuricemia at baseline, and 369 new-onset hyperuricemia). Compared with the wild-type genotypes, patients carrying the SLC2A9 rs3775948G allele or the rs13129697G allele had decreased risk of hyperuricemia, while patients carrying the SLC2A9 rs11722228T allele had increased risk of hyperuricemia, after adjustment for cardiovascular risk factors and correction for multiple comparisons; moreover, these associations were modified by the use of diuretics, β-blockers, or angiotensin converting enzyme inhibitors. The rs10821905A allele of A1CF gene was associated with increased risk of hyperuricemia, and this risk was enhanced by diuretics use. The studied variants were not observed to confer risk for incident cardiovascular events during the follow-up.In conclusion, the genes SLC2A9 and A1CF may serve as potential genetic markers for hyperuricemia risk in relation to antihypertensive drugs therapy in Chinese hypertensive patients.

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“…Patients with chronic kidney disease (CKD) and smokers were found to have an increased risk of developing atherosclerosis [187,188] . The enhanced process of carbamylation explains these patterns in patients due to increased concentrations of urea and thiocyanate.…”

Section: Mechanism Of Ldl Carbamylationmentioning

confidence: 99%

A novel insight into the nature of modified low-density lipoproteins and their role in atherosclerosis

2023

Vessel Plus

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Atherosclerosis plays a significant role in the development of cardiovascular diseases, the leading cause of death worldwide. Modification of low-density lipoproteins (LDLs) is a critical event in atherogenesis. Native LDL undergoes several modifications that can lead to the formation of atherogenic modified LDLs. LDL modifications change their physicochemical and biological properties. Possible modifications include changes in the lipoprotein particle's structure, size, charge, and composition. Uptake and utilization of modified LDLs are impaired in cells. Macrophages take up modified LDLs that promote forming of foam cells, one of the critical cellular components of atherosclerotic lesions. Nevertheless, the direct role of each atherogenic LDL modification in atherogenesis remains uncertain. This review highlights LDL's most critical atherogenic modifications, including oxidized, enzymemodified, non-oxidative, desialylated, glycated and carbamylated LDLs. Studying the role of each type of LDL modification will clarify the unknown elements of atherosclerosis progression and facilitate the development of effective methods for its diagnosis, treatment, and prevention.

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The role of uric acid in renal damage - A history of inflammatory pathways and vascular remodeling

Cited by 15 publications

References 100 publications

Correlation of obesity, dietary patterns, and blood pressure with uric acid: data from the NHANES 2017–2018

Correlation of obesity, dietary patterns, and blood pressure with uric acid: data from the NHANES 2017–2018

Genetic risk of hyperuricemia in hypertensive patients associated with antihypertensive drug therapy: A longitudinal study

A novel insight into the nature of modified low-density lipoproteins and their role in atherosclerosis

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