Serum Uric Acid to Creatinine Ratio as a Predictor of Coronary Heart Disease: A Research Update
PDF

Keywords

Coronary heart disease
Serum uric acid-to-creatinine ratio
Serum uric acid
Metabolic biomarker

Categories

How to Cite

1.
Wang T, Wang T, Zhang R. Serum Uric Acid to Creatinine Ratio as a Predictor of Coronary Heart Disease: A Research Update. JPHPM. 2026;2(1):1-4. doi:10.64904/fpm2026.01.001

Abstract

Serum uric acid (SUA), the end-product of purine metabolism, functions as an important antioxidant and participates in multiple metabolic pathways. Accumulating evidence has demonstrated that SUA is closely associated with the initiation and progression of cardiovascular events and is considered an independent predictor of various vascular diseases. Elevated SUA can induce vascular endothelial dysfunction, accelerate atherogenesis and ultimately result in coronary heart disease (CHD). However, SUA concentrations are largely influenced by renal function; consequently, impaired renal function frequently increases SUA levels and limits the ability of SUA alone to reflect the true metabolic burden. Recently, the SUA-to-creatinine ratio (SUA/Cr), which normalizes SUA for renal function, has been proposed as a superior indicator of net SUA production. Thus, SUA/Cr provides a more accurate prediction of coronary artery disease severity in patients with CHD.

PDF

References

[1] Yang B, Ma K, Xiang R, et al. Correlation between serum uric acid and Gensini score for evaluating coronary stenosis and its gender difference. BMC Cardiovasc Disord 2023; 23(1): 546.

[2] Chen L. Understanding the middle-age health "killer" – coronary heart disease in 3 minutes. Family Life Guide 2024; 40(1): 87-88.

[3] Pradhan A, Rao S, Sindhu A. Comprehensive evaluation of metabolic biomarkers in atherosclerotic plaque microenvironment: the enigma in its origin and regression. Indian J Vasc Endovasc Surg 2025; 12(1): 3-12.

[4] Ji LL, Yeo D. Oxidative stress: an evolving definition. Fac Rev 2021; 10: 13.

[5] Nazemi SS, Samadi S, Rahsepar S, et al. Systematic review of oxidative stress markers and risk of coronary artery calcification. J Tehran Heart Cent 2024; 19(4): 230-242.

[6] Piani F, Annesi L, Borghi C. New insights into uric acid metabolism in the pathophysiology of ischaemic heart disease. Eur Cardiol 2025; 20: e18.

[7] Prabhakar AP, Lopez-Candales A. Uric acid and cardiovascular diseases: a reappraisal. Postgrad Med 2024; 136(7): 615-623.

[8] Henni Mansour AS, Ragues M, Brevier J, et al. Phenotypic, metabolic and functional characterization of experimental models of foamy macrophages: toward therapeutic research in atherosclerosis. Int J Mol Sci 2024; 25(18): 10146.

[9] Yan L, Hu X, Wu S, et al. Association of platelet-to-high-density lipoprotein cholesterol ratio with hyperuricemia. Sci Rep 2024; 14(1): 15641.

[10] Zeng Y, Chen Y, Li J, et al. Non-linear association between serum uric-acid-to-creatinine ratio and all-cause mortality in hypertensive patients: a ten-year cohort study using NHANES database. Sci Rep 2024; 14(1): 31423.

[11] Yu MA, Sánchez-Lozada LG, Johnson RJ, et al. Oxidative stress with activation of the renin–angiotensin system in human vascular endothelial cells as a novel mechanism of uric acid-induced endothelial dysfunction. J Hypertens 2010; 28(6): 1234-1242.

[12] Gumusdag A, Kalyoncuoglu M, Oguz H, et al. Prognostic role of serum uric-acid-to-creatinine ratio in ST-elevation myocardial infarction patients with multivessel coronary artery disease. Cardiol J 2025; 32(1): 1-9.

[13] Gu W, Zhao J, Xu Y. Hyperuricemia-induced complications: dysfunctional macrophages as a potential bridge. Front Immunol 2025; 16: 1512093.

[14] Yang L, Zhang Y, Chai Z, et al. Regulation of pyroptosis by NF-κB signaling. Front Cell Death 2025; 3: 1503799.

[15] Baeza C, Ribagorda M, Maya-Lopez C, et al. NIK is a mediator of inflammation and intimal hyperplasia in endothelial-denudation-induced vascular injury. Int J Mol Sci 2024; 25(19): 11473.

[16] Wang A, Tian X, Wu S, et al. Metabolic factors mediate the association between serum uric-acid-to-creatinine ratio and cardiovascular disease. J Am Heart Assoc 2021; 10(11): e023054.

[17] Wang J, Li X, Jia L, et al. Correlation between serum uric acid level and thin-cap fibroatheroma of coronary artery. J Clin Cardiol 2019; 35(3): 244-250.

[18] Wang F, Zheng X, Ni X, et al. Increased serum uric-acid-to-creatinine ratio is associated with metabolic dysfunction-associated steatotic liver disease. Sci Rep 2025; 15(1): 26941.

[19] Liu RH, Li J, Sun ZX, et al. Positive correlation between triglyceride glucose-body mass index and presence and severity of early-onset coronary artery disease. Ann Med 2025; 57(1): 2564277.

[20] Petersen MC, Shulman GI. Mechanisms of insulin action and insulin resistance. Physiol Rev 2018; 98(4): 2133-2223.

[21] Dong J, Xu X, Zhang Q, et al. PI3K/AKT pathway promotes fracture healing via crosstalk with Wnt/β-catenin. Exp Cell Res 2020; 394(2): 112137.

[22] Vatseba T, Sokolova L, Pushkarev V. Insulin signaling activation in patients with type 2 diabetes mellitus. TPJ 2025; 6(1): 25-29.

[23] Regan CP, Manro JR, Owens GK. Akt-dependent phosphorylation of myocardin-related transcription factor-A promotes vascular smooth-muscle cell differentiation and inhibits proliferation. Circ Res 2010; 106(6): 1072-1083.

[24] She D, Xu W, Liu J, et al. Serum uric-acid-to-creatinine ratio and risk of metabolic syndrome in overweight/obese patients. Diabetes Metab Syndr Obes 2023; 16: 3007-3017.

[25] Oh M, Cho SH. Serum uric-acid-to-creatinine ratio as predictor of insulin resistance, β-cell function and metabolic syndrome in normal Korean adults: a cross-sectional study. BMC Endocr Disord 2025; 25(1): 18-25.

[26] Rocić B, Vucić-Lovrencić M, Poje N, et al. Uric acid may inhibit glucose-induced insulin secretion via binding to an essential arginine residue in rat pancreatic β-cells. Bioorg Med Chem Lett 2005; 15(4): 1181-1184.

[27] Ghasemi A. Uric acid-induced pancreatic β-cell dysfunction. BMC Endocr Disord 2021; 21(1): 24.

[28] Castro MC, Villagarcía HG, Di Sarli Gutiérrez L, et al. Akt signaling and nitric-oxide synthase as possible mediators of the protective effect of N-acetyl-L-cysteine in sucrose-induced prediabetes. Int J Mol Sci 2024; 25(2): 1215.

[29] Mehta JK, Kaur G, Buttar HS, et al. Role of the renin–angiotensin system in the pathophysiology of coronary heart disease and heart failure: diagnostic biomarkers and therapy with drugs and natural products. Front Physiol 2023; 14: 1034170.

[30] Morat N, Civieri G, Spezia M, et al. Angiotensin II and atherosclerosis: a new cardiovascular risk factor beyond hypertension. Int J Mol Sci 2025; 26(14): 7527.

[31] da Cunha V, Martin-McNulty B, Vincelette J, et al. Angiotensin II induces histomorphologic features of unstable plaque in a murine model of accelerated atherosclerosis. J Vasc Surg 2006; 44(2): 364-371.

[32] Wang XD, Liu J, Zhang YC, et al. Correlation between elevated uric acid levels and circulating renin–angiotensin–aldosterone system activation in atrial fibrillation patients. Cardiovasc Diagn Ther 2021; 11(1): 50-55.

[33] Tang Z, Liu H, Ding Y, et al. Association between serum uric-acid-to-creatinine ratio and cardiovascular and all-cause mortality in adults with hypertension. Sci Rep 2024; 14(1): 18008.

Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 International License.

Copyright (c) 2025 Frontiers in Preventive Medicine