ReviewFrontiers in endocrinology2022
Excess Uric Acid Induces Gouty Nephropathy Through Crystal Formation: A Review of Recent Insights.
Review in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 108 citations in OpenAlex.
- Titanium Dioxide Exacerbates Calcium Phosphate and Urate-Induced Oxidative Stress, Injury and Inflammatory Response in Human Kidney-2 Cells.Journal of biochemical and molecular toxicology · 2026Article
- Multi-target effects of Limosilactobacillus reuteri RE225 on hyperuricemia through xanthine oxidase inhibition, nucleoside degradation, gut microbiota modulation, and renal TLR4-NF-κB suppression.Journal of the science of food and agriculture · 2026Article
- Exploring Risks of Adverse Drug Events From Single Drug to Three-Drug Combination.Clinical and translational science · 2026Article
- Uric Acid Extremes and Lipid Dysregulation: Evidence from a Large Population-Based Study.Metabolites · 2026Article
- Oxidative Stress-Driven Mechanisms and Biomarkers of Drug-Induced Nephrotoxicity: Translational Insights and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2026Review
- Non-linear association between preoperative uric acid levels and female thyroid cancer risk.Discover oncology · 2026Article
- Therapeutic Effects of Tea Polyphenols on Renal Damage Induced by High Uric Acid.Current medicinal chemistry · 2026Article
- LncSLED1 inhibits monosodium urate-induced macrophage inflammation by promoting Cosmc methylation to upregulate CA72-4.Central-European journal of immunology · 2026Article
- The role of gut microbiota dysbiosis in the pathogenesis of hyperuricemic nephropathy.Frontiers in molecular biosciences · 2026Review
- Study on the pro-inflammatory injury of neutrophil extracellular traps in gouty nephropathy.Frontiers in immunology · 2026Review
- Innovative Insights into Interleukin-Mediated Macrophage Polarization: Metabolic Reprogramming and Inflammatory Pathway Crosstalk in Chronic Kidney Disease and Therapeutic Implications-A Narrative Review.International journal of general medicine · 2026Review
- Case Report: A case of acute kidney injury due to star fruit-infused liquor.Frontiers in medicine · 2026Article
- Serum Uric Acid as a Mediator of Insulin Resistance: Molecular Mechanisms and Metabolic Pathways.Endocrinology, diabetes & metabolism · 2026Review
- Multidimensional mechanisms of natural products in modulating metabolic dysfunction-associated kidney disease: recent advances and future perspectives.Frontiers in pharmacology · 2026Review
- Programmed cell death in gouty nephropathy: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Lipid-Derived Cardiometabolic Indices in Normouricemic and Hyperuricemic Adults: A Retrospective Cross-Sectional Association Study.Healthcare (Basel, Switzerland) · 2025Article
- Hyperuricemia-induced kidney injury: a narrative review of mechanisms and therapeutic advances.BMC nephrology · 2025Review
- The Pathogenesis of Chronic Kidney Disease (CKD) and the Preventive and Therapeutic Effects of Natural Products.Current issues in molecular biology · 2025Review
- Body Mass Index as a Potential Mediator of the Association Between Gout and Hypertension Among Chinese Older Adults: A Mediation Analysis in a Cross-Sectional Study.Aging medicine (Milton (N.S.W)) · 2025Article
- Effect of Allopurinol Use on Kidney Function Among Patients with Gout and Chronic Kidney Disease.Gout, urate, and crystal deposition disease · 2025Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uric acid (UA) is the final product of purine metabolism in the human body, and impaired purine metabolism can increase the uric acid in serum, finally resulting in hyperuricemia (HUA). Current evidences suggest that urates might have antioxidant properties under certain circumstances, but most evidences suggest that urates promote inflammation. Hyperuricemia leads to the formation of urate crystals, which might be recognized as a red flag by the immune system. Such a response stimulates macrophage activation, leads to the activation of NOD-like receptor protein 3 (NLRP3) inflammasome vesicles, and ultimately the production and liberation of interleukin-1b (IL-1b) and interleukin-18 (IL-18), which can mediate inflammation, apoptosis and necroinflammation and cause an inflammatory cascade response. The kidney is one of the most commonly affected organs in HUA, which promotes the development of chronic kidney disease (CKD) by damaging endothelial cells, activating the renin-angiotensin system (RAS), and promoting inflammatory responses. Pharmacological interventions and lifestyle modifications are the primary means for controlling gout and lowering UA. The febuxostat is safe for CKD patients in the UA lowering therapy. Although dialysis can reduce UA levels, the application of drug is also necessary for dialysis patients. This article reviews the synthesis and metabolism of UA, etiology of HUA, the relationship between HUA and kidney disease, the treatment of gout and gouty nephropathy (GN).
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.