Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (738 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
An oxidation product, via xanthine oxidase, of oxypurines such as xanthine and hypoxanthine. It is the final oxidation product of purine catabolism in humans and primates, whereas in most other mammals urate oxidase further oxidizes it to allantoin.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Acid, Uric; 2,6,8-Trihydroxypurine; Trioxopurine; Ammonium Acid Urate; Acid Urate, Ammonium; Urate, Ammonium Acid; Potassium Urate; Urate, Potassium.
Where it fits in the MeSH classification
- Broader topics
- Xanthines
Related concepts
- Xanthine Oxidase
- Xanthine
- Hypoxanthine
- Urate Oxidase
- Allantoin
Research landscape
PubMed indexes 31,884 records tagged with the MeSH heading “Uric Acid” (counts retrieved 2026-10-31). 7,336 of them (23.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 13,080 records.
Reviews account for 2,749 records (8.6%) and meta-analyses for 370. Randomized controlled trials number 1,088 (3.4%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 13,080 |
| 2000-2009 | 3,891 |
| 2010-2019 | 7,577 |
| 2020 onward | 7,336 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,749 | 8.6% |
| Meta-analyses | 370 | 1.2% |
| Randomized controlled trials | 1,088 | 3.4% |
Method: PubMed query "Uric Acid"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Impact of lifestyle factors and dietary patterns on serum uric acid levels and disease activity in gout: a systematic review | 2025 | Systematic review Design not recorded in structured metadata | 9 | cc by PMID 40605100 · DOI · PMC12225473 |
| Serum Uric Acid as a Mediator of Insulin Resistance: Molecular Mechanisms and Metabolic Pathways | 2026 | Review article Design not recorded in structured metadata | 9 | cc by PMID 41521685 · DOI · PMC12793067 |
| Urate-lowering therapy and kidney outcomes in patients with chronic kidney disease and hyperuricemia | 2025 | Research article Design not recorded in structured metadata | 7 | cc by PMID 41361176 · DOI · PMC12686408 |
Impact of lifestyle factors and dietary patterns on serum uric acid levels and disease activity in gout: a systematic review [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundGout is a common type of inflammatory arthritis caused by monosodium urate (MSU) crystal deposition in the joints.
- Closing excerpt
- Further research is required to establish clinical recommendations to improve patient outcomes.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (269 words)
BackgroundGout is a common type of inflammatory arthritis caused by monosodium urate (MSU) crystal deposition in the joints. This leads to pain, swelling, and restricted motion. Although pharmacological treatments are effective, lifestyle and dietary factors play crucial roles in managing gout and its flares.AimThis systematic review aimed to assess the effect of lifestyle factors, physical activity, and dietary patterns on serum uric acid levels and gout activity.MethodsA search of PubMed, BMJ journals, and Google Scholar identified eight studies (five prospective cohort studies, two case-cross-over studies, and one randomized controlled trial), involving 47,879 participants (predominantly males [78.5-95.3%], aged 55-66 years). Eligible studies focused on adults with gout and examined the lifestyle or dietary factors affecting uric acid levels or gout activity. The review followed a pre-specified protocol (PROSPERO registration CRD42024594359). To optimize the quality, the bias risk was assessed using the Newcastle-Ottawa scale for observational studies and the Cochrane Risk of Bias 1.0 tool for randomized controlled trials.ResultsThe findings suggest that consuming polyunsaturated fatty acid-rich fish, regular physical activity, and increased vegetable intake may reduce gout flares. Conversely, high purine intake (especially animal sources), excessive alcohol consumption, and obesity are risk factors for gout exacerbation. Some studies have reported reduced serum uric acid levels with dietary changes, whereas others have found no significant effect. Despite the variability and recall bias, dietary and lifestyle modifications may help manage gout and reduce disease activity.ConclusionThe findings of this systematic review emphasize the importance of dietary and lifestyle factors in managing serum uric acid levels and reducing the risk of gout flares. Further research is required to establish clinical recommendations to improve patient outcomes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40605100 · DOI · PMC12225473
Serum Uric Acid as a Mediator of Insulin Resistance: Molecular Mechanisms and Metabolic Pathways [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundInsulin resistance (IR) is a key factor in metabolic conditions such as type 2 diabetes (T2D) and metabolic syndrome, which significantly impact global health.
- Closing excerpt
- Despite these findings, the precise molecular interactions between SUA and insulin signaling remain incompletely understood, underscoring the need for further translational and mechanistic research.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (223 words)
BackgroundInsulin resistance (IR) is a key factor in metabolic conditions such as type 2 diabetes (T2D) and metabolic syndrome, which significantly impact global health. Serum uric acid (SUA), is the end product of purine catabolism, has increasingly been recognized as a potential modulator of insulin sensitivity.MethodsA comprehensive narrative review was conducted to synthesize current evidence on SUA-mediated insulin resistance, with a focus on underlying molecular mechanisms, clinical implications, and key gaps warranting future investigation. Relevant experimental, translational, and clinical studies examining the role of SUA in insulin resistance, its mechanistic pathways, and therapeutic potential were critically analysed.ResultsEmerging evidence indicates that elevated SUA levels are associated with disturbances in insulin signaling pathways. Mechanistically, high SUA levels can lead to oxidative stress, endothelial dysfunction, inflammation, and impaired function of adipocytes-all of which collectively impede insulin receptor activity and downstream signaling. Key pathways involved include activation of the NLRP3 inflammasome, suppression of AMP-activated protein kinase (AMPK), and induction of mitochondrial dysfunction. These mechanisms contribute to altered insulin sensitivity in both hepatic and adipose tissues. Clinically, higher SUA levels are associated with increased risk of developing metabolic syndrome, T2D, and cardiovascular diseases, highlighting SUA's potential as both a biomarker and a therapeutic target. Despite these findings, the precise molecular interactions between SUA and insulin signaling remain incompletely understood, underscoring the need for further translational and mechanistic research.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41521685 · DOI · PMC12793067
Urate-lowering therapy and kidney outcomes in patients with chronic kidney disease and hyperuricemia [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Hyperuricemia is considered a modifiable risk factor for the development and progression of chronic kidney disease (CKD).
- Closing excerpt
- Large randomized clinical trials with refined designs are needed to assess the effect of ULT in these patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (246 words)
Hyperuricemia is considered a modifiable risk factor for the development and progression of chronic kidney disease (CKD). There remains controversy over the effects of urate-lowering therapy (ULT) on kidney outcomes in patients with CKD and hyperuricemia. We conducted a cohort study using a sequential target trial emulation framework to evaluate the composite kidney outcomes in patients with CKD and hyperuricemia initiating ULT versus supportive care alone (control). A total of 269,831 eligible person trials (56,936 unique persons) with CKD and hyperuricemia who had received supportive care were included from the China Renal Data System database. The primary outcome was a composite kidney outcome defined as a greater than 40% decline in the estimated GFR or end-stage kidney disease (ESKD). The 3-year cumulative incidence rates of the composite kidney outcomes were 19.69% and 23.22% in the ULT group and the control group, respectively, with a risk difference of -3.53% (95% CI, -5.25% to -1.94%). The estimated 3-year risk differences for ESKD, all-cause mortality, and cardiovascular mortality were -1.88% (-3.28% to -0.45%), -2.25% (-3.02% to -1.51%), and -0.69% (-1.33% to -0.05%), respectively, all of which favor the ULT group. The estimates from the subgroup and sensitivity analyses were consistent with those from the primary analysis. Thus, ULT is associated with a significantly lower risk of kidney disease progression and mortality in patients with stage 3 or higher CKD and hyperuricemia. Large randomized clinical trials with refined designs are needed to assess the effect of ULT in these patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41361176 · DOI · PMC12686408
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Hyperuricemia and its related diseases: mechanisms and advances in therapy [4]
- Research article Serum uric acid and the risk of cardiovascular and renal disease [5]
- Research article Uric acid and cardiovascular disease [6]
- Research article Uric acid and risk of heart failure: a systematic review and meta-analysis [7]
- Research article Uric Acid in Inflammation and the Pathogenesis of Atherosclerosis [8]
- Research article Serum Uric Acid Levels and Risk of Metabolic Syndrome: A Dose-Response Meta-Analysis of Prospective Studies [9]
References
- Mustafa M, Alshamrani S, Alghamdi L, Danish H, Alamoudi D, Alshamrani G, et al.. Impact of lifestyle factors and dietary patterns on serum uric acid levels and disease activity in gout: a systematic review. . 2025. PMID 40605100 · DOI · PMC12225473
- Ali N. Serum Uric Acid as a Mediator of Insulin Resistance: Molecular Mechanisms and Metabolic Pathways. . 2026. PMID 41521685 · DOI · PMC12793067
- Nie S, Zhou S, Chen R, Li L, Sun Y, Liu J, et al.. Urate-lowering therapy and kidney outcomes in patients with chronic kidney disease and hyperuricemia. . 2025. PMID 41361176 · DOI · PMC12686408
- Du L, Zong Y, Li H, Wang Q, Xie L, Yang B, et al.. Hyperuricemia and its related diseases: mechanisms and advances in therapy. Signal Transduct Target Ther. 2024. PMID 39191722 · DOI · PMC11350024
- Borghi C, Rosei EA, Bardin T, Dawson J, Dominiczak A, Kielstein JT, et al.. Serum uric acid and the risk of cardiovascular and renal disease. J Hypertens. 2015. PMID 26136207 · DOI
- Ndrepepa G. Uric acid and cardiovascular disease. Clin Chim Acta. 2018. PMID 29803897 · DOI
- Huang H, Huang B, Li Y, Huang Y, Li J, Yao H, et al.. Uric acid and risk of heart failure: a systematic review and meta-analysis. Eur J Heart Fail. 2014. PMID 23933579 · DOI
- Kimura Y, Tsukui D, Kono H. Uric Acid in Inflammation and the Pathogenesis of Atherosclerosis. Int J Mol Sci. 2021. PMID 34830282 · DOI · PMC8624633
- Yuan H, Yu C, Li X, Sun L, Zhu X, Zhao C, et al.. Serum Uric Acid Levels and Risk of Metabolic Syndrome: A Dose-Response Meta-Analysis of Prospective Studies. J Clin Endocrinol Metab. 2015. PMID 26308292 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.