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Published in: BMC Nephrology 1/2022

Open Access 01-12-2022 | Research

The association of urinary prostaglandins with uric acid in hyperuricemia patients

Authors: Huagang Lin, Ying Xu, Yuqi Zheng, Deping Wu, Zhibin Ye, Jing Xiao

Published in: BMC Nephrology | Issue 1/2022

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Abstract

Purpose

To explore the association between uric acid and urinary prostaglandins in male patients with hyperuricemia.

Methods

A total of 38 male patients with hyperuricemia in outpatients of Huadong Hospital from July 2018 to January 2020 were recruited. Serum uric acid (SUA), 24 h urinary uric acid excretion and other indicators were detected respectively. 10 ml urine was taken to determine prostaglandin prostaglandin D (PGD), prostaglandin E1 (PGE1), prostaglandin E2 (PGE2), 6-keto-PGF1α, thromboxane A2 (TXA2) and thromboxane B2 (TXB2). Fraction of uric acid excretion (FEua) and uric acid clearance rate (Cua) were calculated. According to the mean value of FEua and Cua, patients were divided into two groups, respectively. The independent-samples t test and the Mann–Whitney U test were applied for normally and non-normally distributed data, respectively.

Results

After adjusting confounding factors (age, BMI, eGFR, TG, TC, HDL and LDL), SUA was negatively correlated with urinary PGE1(r = -0.615, P = 0.009) and PGE2(r = -0.824, P < 0.001). Compared with SUA1 group (SUA < 482.6 mg/dl), SUA2 (SUA \(\ge\) 482.6 mg/dl) had lower urinary PGE1(P = 0.022) and PGE2(P = 0.019) levels. Cua was positively correlated with PGE2 (r = 0.436, P = 0.01). The correlation persisted after adjustment for age, BMI, eGFR, TG, TC, HDL and LDL by multiple linear regression analysis. In the Cua1 group (Cua < 4.869 mL /min/1.73 m2), PGE2 were lower than that in Cua2 (Cua \(\ge\) 4.869 mL /min/1.73 m2) group (P = 0.011).

Conclusions

In male patients with hyperuricemia, SUA was negatively correlated with urinary PGE2, Cua was positively correlated with urinary PGE2. Urinary PGE2 were significantly different between different SUA and Cua groups.
Literature
1.
go back to reference Maiuolo J, Oppedisano F, Gratteri S, Muscoli C, Mollace V. Regulation of uric acid metabolism and excretion. Int J Cardiol. 2016;213:8–14.CrossRef Maiuolo J, Oppedisano F, Gratteri S, Muscoli C, Mollace V. Regulation of uric acid metabolism and excretion. Int J Cardiol. 2016;213:8–14.CrossRef
2.
go back to reference Gustafsson D, Unwin R. The pathophysiology of hyperuricaemia and its possible relationship to cardiovascular disease, morbidity and mortality. BMC Nephrol. 2013;14:164.CrossRef Gustafsson D, Unwin R. The pathophysiology of hyperuricaemia and its possible relationship to cardiovascular disease, morbidity and mortality. BMC Nephrol. 2013;14:164.CrossRef
3.
go back to reference He H, Pan L, Ren X, et al. The Effect of Body Weight and Alcohol Consumption on Hyperuricemia and Their Population Attributable Fractions: A National Health Survey in China. Obes Facts. 2022;15(2):216–27.CrossRef He H, Pan L, Ren X, et al. The Effect of Body Weight and Alcohol Consumption on Hyperuricemia and Their Population Attributable Fractions: A National Health Survey in China. Obes Facts. 2022;15(2):216–27.CrossRef
4.
go back to reference Yang L, Chang B, Guo Y, Wu X, Liu L. The role of oxidative stress-mediated apoptosis in the pathogenesis of uric acid nephropathy. Ren Fail. 2019;41(1):616–22.CrossRef Yang L, Chang B, Guo Y, Wu X, Liu L. The role of oxidative stress-mediated apoptosis in the pathogenesis of uric acid nephropathy. Ren Fail. 2019;41(1):616–22.CrossRef
5.
go back to reference Liu S, Yuan Y, Zhou Y, et al. Phloretin attenuates hyperuricemia-induced endothelial dysfunction through co-inhibiting inflammation and GLUT9-mediated uric acid uptake. J Cell Mol Med. 2017;21(10):2553–62.CrossRef Liu S, Yuan Y, Zhou Y, et al. Phloretin attenuates hyperuricemia-induced endothelial dysfunction through co-inhibiting inflammation and GLUT9-mediated uric acid uptake. J Cell Mol Med. 2017;21(10):2553–62.CrossRef
6.
go back to reference Xiao J, Zhang XL, Fu C, et al. Soluble uric acid increases NALP3 inflammasome and interleukin-1β expression in human primary renal proximal tubule epithelial cells through the Toll-like receptor 4-mediated pathway. Int J Mol Med. 2015;35(5):1347–54.CrossRef Xiao J, Zhang XL, Fu C, et al. Soluble uric acid increases NALP3 inflammasome and interleukin-1β expression in human primary renal proximal tubule epithelial cells through the Toll-like receptor 4-mediated pathway. Int J Mol Med. 2015;35(5):1347–54.CrossRef
7.
go back to reference Li Y, Xia W, Zhao F, et al. Prostaglandins in the pathogenesis of kidney diseases. Oncotarget. 2018;9(41):26586–602.CrossRef Li Y, Xia W, Zhao F, et al. Prostaglandins in the pathogenesis of kidney diseases. Oncotarget. 2018;9(41):26586–602.CrossRef
8.
go back to reference Hao C, Breyer M. Physiological regulation of prostaglandins in the kidney. Annu Rev Physiol. 2008;70:357–77.CrossRef Hao C, Breyer M. Physiological regulation of prostaglandins in the kidney. Annu Rev Physiol. 2008;70:357–77.CrossRef
9.
go back to reference Nørregaard R, Kwon T, Frøkiær J. Physiology and pathophysiology of cyclooxygenase-2 and prostaglandin E2 in the kidney. Kidney Res Clin Pract. 2015;34(4):194–200.CrossRef Nørregaard R, Kwon T, Frøkiær J. Physiology and pathophysiology of cyclooxygenase-2 and prostaglandin E2 in the kidney. Kidney Res Clin Pract. 2015;34(4):194–200.CrossRef
10.
go back to reference Breyer M, Harris R. Cyclooxygenase 2 and the kidney. Curr Opin Nephrol Hypertens. 2001;10(1):89–98.CrossRef Breyer M, Harris R. Cyclooxygenase 2 and the kidney. Curr Opin Nephrol Hypertens. 2001;10(1):89–98.CrossRef
11.
go back to reference Lu H, Yao H, Zou R, Chen X, Xu H. Galangin Suppresses Renal Inflammation via the Inhibition of NF-κB, PI3K/AKT and NLRP3 in Uric Acid Treated NRK-52E Tubular Epithelial Cells. Biomed Res Int. 2019;2019:3018357.PubMedPubMedCentral Lu H, Yao H, Zou R, Chen X, Xu H. Galangin Suppresses Renal Inflammation via the Inhibition of NF-κB, PI3K/AKT and NLRP3 in Uric Acid Treated NRK-52E Tubular Epithelial Cells. Biomed Res Int. 2019;2019:3018357.PubMedPubMedCentral
12.
go back to reference Bardin T, Richette P. Definition of hyperuricemia and gouty conditions. Curr Opin Rheumatol. 2014;26(2):186–91.CrossRef Bardin T, Richette P. Definition of hyperuricemia and gouty conditions. Curr Opin Rheumatol. 2014;26(2):186–91.CrossRef
13.
go back to reference Ekambaram P, Lambiv W, Cazzolli R, Ashton A, Honn K. The thromboxane synthase and receptor signaling pathway in cancer: an emerging paradigm in cancer progression and metastasis. Cancer Metastasis Rev. 2011;30:397–408.CrossRef Ekambaram P, Lambiv W, Cazzolli R, Ashton A, Honn K. The thromboxane synthase and receptor signaling pathway in cancer: an emerging paradigm in cancer progression and metastasis. Cancer Metastasis Rev. 2011;30:397–408.CrossRef
14.
go back to reference Wang N, Vendrov K, Simmons B, Schuck R, Stouffer G, Lee C. Urinary 11-dehydro-thromboxane B2 levels are associated with vascular inflammation and prognosis in atherosclerotic cardiovascular disease. Prostaglandins Other Lipid Mediat. 2018;134:24–31.CrossRef Wang N, Vendrov K, Simmons B, Schuck R, Stouffer G, Lee C. Urinary 11-dehydro-thromboxane B2 levels are associated with vascular inflammation and prognosis in atherosclerotic cardiovascular disease. Prostaglandins Other Lipid Mediat. 2018;134:24–31.CrossRef
15.
go back to reference Stevens P, Levin A. Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline. Ann Intern Med. 2013;158(11):825–30.CrossRef Stevens P, Levin A. Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline. Ann Intern Med. 2013;158(11):825–30.CrossRef
16.
go back to reference Lannoy M, Valluru M, Chang L, et al. The positive effect of selective prostaglandin E2 receptor EP2 and EP4 blockade on cystogenesis in vitro is counteracted by increased kidney inflammation in vivo. Kidney Int. 2020;98(2):404–19.CrossRef Lannoy M, Valluru M, Chang L, et al. The positive effect of selective prostaglandin E2 receptor EP2 and EP4 blockade on cystogenesis in vitro is counteracted by increased kidney inflammation in vivo. Kidney Int. 2020;98(2):404–19.CrossRef
18.
go back to reference Knepper M, Kwon T, Nielsen S. Molecular physiology of water balance. N Engl J Med. 2015;372(14):1349–58.CrossRef Knepper M, Kwon T, Nielsen S. Molecular physiology of water balance. N Engl J Med. 2015;372(14):1349–58.CrossRef
19.
go back to reference Kömhoff M, Wang J, Cheng H, et al. Cyclooxygenase-2-selective inhibitors impair glomerulogenesis and renal cortical development. Kidney Int. 2000;57(2):414–22.CrossRef Kömhoff M, Wang J, Cheng H, et al. Cyclooxygenase-2-selective inhibitors impair glomerulogenesis and renal cortical development. Kidney Int. 2000;57(2):414–22.CrossRef
20.
go back to reference Cheng H, Wang J, Zhang M, Wang S, McKanna J, Harris R. Genetic deletion of COX-2 prevents increased renin expression in response to ACE inhibition. Am J Physiol Renal Physiol. 2001;280(3):F449-456.CrossRef Cheng H, Wang J, Zhang M, Wang S, McKanna J, Harris R. Genetic deletion of COX-2 prevents increased renin expression in response to ACE inhibition. Am J Physiol Renal Physiol. 2001;280(3):F449-456.CrossRef
21.
go back to reference Nasrallah R, Zimpelmann J, Eckert D, et al. PGE2 EP1 receptor inhibits vasopressin-dependent water reabsorption and sodium transport in mouse collecting duct. Lab Invest. 2018;98(3):360–70.CrossRef Nasrallah R, Zimpelmann J, Eckert D, et al. PGE2 EP1 receptor inhibits vasopressin-dependent water reabsorption and sodium transport in mouse collecting duct. Lab Invest. 2018;98(3):360–70.CrossRef
22.
go back to reference Chen L, Lan Z, Zhou Y, et al. Astilbin attenuates hyperuricemia and ameliorates nephropathy in fructose-induced hyperuricemic rats. Planta Med. 2011;77(16):1769–73.CrossRef Chen L, Lan Z, Zhou Y, et al. Astilbin attenuates hyperuricemia and ameliorates nephropathy in fructose-induced hyperuricemic rats. Planta Med. 2011;77(16):1769–73.CrossRef
23.
go back to reference Sánchez-Lozada L, Tapia E, Avila-Casado C, et al. Mild hyperuricemia induces glomerular hypertension in normal rats. Am J Physiol Renal Physiol. 2002;283(5):F1105-1110.CrossRef Sánchez-Lozada L, Tapia E, Avila-Casado C, et al. Mild hyperuricemia induces glomerular hypertension in normal rats. Am J Physiol Renal Physiol. 2002;283(5):F1105-1110.CrossRef
24.
go back to reference Sánchez-Lozada L, Tapia E, Santamaría J, et al. Mild hyperuricemia induces vasoconstriction and maintains glomerular hypertension in normal and remnant kidney rats. Kidney Int. 2005;67(1):237–47.CrossRef Sánchez-Lozada L, Tapia E, Santamaría J, et al. Mild hyperuricemia induces vasoconstriction and maintains glomerular hypertension in normal and remnant kidney rats. Kidney Int. 2005;67(1):237–47.CrossRef
25.
go back to reference Persson A, Hahne B, Selén G. The effect of tubular perfusion with PGE2, PGF2 alpha, and PGI2 on the tubuloglomerular feedback control in the rat. Can J Physiol Pharmacol. 1983;61(11):1317–23.CrossRef Persson A, Hahne B, Selén G. The effect of tubular perfusion with PGE2, PGF2 alpha, and PGI2 on the tubuloglomerular feedback control in the rat. Can J Physiol Pharmacol. 1983;61(11):1317–23.CrossRef
26.
go back to reference Wang Y, Hu J, Qu P, et al. Association between urinary sodium excretion and uric acid, and its interaction on the risk of prehypertension among Chinese young adults. Sci Rep. 2018;8(1):7749.CrossRef Wang Y, Hu J, Qu P, et al. Association between urinary sodium excretion and uric acid, and its interaction on the risk of prehypertension among Chinese young adults. Sci Rep. 2018;8(1):7749.CrossRef
27.
go back to reference Li F, Guo H, Zou J, et al. The Association of Urinary Sodium and Potassium with Renal Uric Acid Excretion in Patients with Chronic Kidney Disease. Kidney Blood Press Res. 2018;43(4):1310–21.CrossRef Li F, Guo H, Zou J, et al. The Association of Urinary Sodium and Potassium with Renal Uric Acid Excretion in Patients with Chronic Kidney Disease. Kidney Blood Press Res. 2018;43(4):1310–21.CrossRef
28.
go back to reference Serebruany VL, Herzog WR, Gurbel PA. Serial changes of the plasma prostanoids during myocardial ischemia-reperfusion in swine. Effects of magnesium, diltiazem, and a novel Mac-1 inhibitor. Prostaglandins Leukot Essent Fatty Acids. 1997;56(2):135–42.CrossRef Serebruany VL, Herzog WR, Gurbel PA. Serial changes of the plasma prostanoids during myocardial ischemia-reperfusion in swine. Effects of magnesium, diltiazem, and a novel Mac-1 inhibitor. Prostaglandins Leukot Essent Fatty Acids. 1997;56(2):135–42.CrossRef
29.
go back to reference Ding X, Murray P. Cellular mechanisms of thromboxane A2-mediated contraction in pulmonary veins. Am J Physiol Lung Cell Mol Physiol. 2005;289(5):L825-833.CrossRef Ding X, Murray P. Cellular mechanisms of thromboxane A2-mediated contraction in pulmonary veins. Am J Physiol Lung Cell Mol Physiol. 2005;289(5):L825-833.CrossRef
30.
go back to reference Smyth E. Thromboxane and the thromboxane receptor in cardiovascular disease. Clinical lipidology. 2010;5(2):209–19.CrossRef Smyth E. Thromboxane and the thromboxane receptor in cardiovascular disease. Clinical lipidology. 2010;5(2):209–19.CrossRef
31.
go back to reference Chien C, Fan S, Lin S, et al. Glucagon-like peptide-1 receptor agonist activation ameliorates venous thrombosis-induced arteriovenous fistula failure in chronic kidney disease. Thromb Haemost. 2014;112(5):1051–64.CrossRef Chien C, Fan S, Lin S, et al. Glucagon-like peptide-1 receptor agonist activation ameliorates venous thrombosis-induced arteriovenous fistula failure in chronic kidney disease. Thromb Haemost. 2014;112(5):1051–64.CrossRef
32.
go back to reference Welch W. Effects of isoprostane on tubuloglomerular feedback: roles of TP receptors, NOS, and salt intake. Am J Physiol Renal Physiol. 2005;288(4):F757-762.CrossRef Welch W. Effects of isoprostane on tubuloglomerular feedback: roles of TP receptors, NOS, and salt intake. Am J Physiol Renal Physiol. 2005;288(4):F757-762.CrossRef
33.
go back to reference Boini K, Xia M, Li C, et al. Acid sphingomyelinase gene deficiency ameliorates the hyperhomocysteinemia-induced glomerular injury in mice. Am J Pathol. 2011;179(5):2210–9.CrossRef Boini K, Xia M, Li C, et al. Acid sphingomyelinase gene deficiency ameliorates the hyperhomocysteinemia-induced glomerular injury in mice. Am J Pathol. 2011;179(5):2210–9.CrossRef
34.
go back to reference Smith A, Visioli F, Frei B, Hagen T. Age-related changes in endothelial nitric oxide synthase phosphorylation and nitric oxide dependent vasodilation: evidence for a novel mechanism involving sphingomyelinase and ceramide-activated phosphatase 2A. Aging Cell. 2006;5(5):391–400.CrossRef Smith A, Visioli F, Frei B, Hagen T. Age-related changes in endothelial nitric oxide synthase phosphorylation and nitric oxide dependent vasodilation: evidence for a novel mechanism involving sphingomyelinase and ceramide-activated phosphatase 2A. Aging Cell. 2006;5(5):391–400.CrossRef
35.
go back to reference Bautista-Pérez R, del Valle-Mondragón L, Cano-Martínez A, Pérez-Méndez O, Escalante B, Franco M. Involvement of neutral sphingomyelinase in the angiotensin II signaling pathway. Am J Physiol Renal Physiol. 2015;308(10):F1178-1187.CrossRef Bautista-Pérez R, del Valle-Mondragón L, Cano-Martínez A, Pérez-Méndez O, Escalante B, Franco M. Involvement of neutral sphingomyelinase in the angiotensin II signaling pathway. Am J Physiol Renal Physiol. 2015;308(10):F1178-1187.CrossRef
36.
go back to reference Mandal AK, Mount DB. The molecular physiology of uric acid homeostasis. Annu Rev Physiol. 2015;77:323–45.CrossRef Mandal AK, Mount DB. The molecular physiology of uric acid homeostasis. Annu Rev Physiol. 2015;77:323–45.CrossRef
37.
go back to reference Yang B, Li S, Zhu J, et al. miR-214 Protects Against Uric Acid-Induced Endothelial Cell Apoptosis. Front Med (Lausanne). 2020;7:411.CrossRef Yang B, Li S, Zhu J, et al. miR-214 Protects Against Uric Acid-Induced Endothelial Cell Apoptosis. Front Med (Lausanne). 2020;7:411.CrossRef
38.
go back to reference Convento MS, Pessoa E, Dalboni MA, Borges FT, Schor N. Pro-inflammatory and oxidative effects of noncrystalline uric acid in human mesangial cells: contribution to hyperuricemic glomerular damage. Urol Res. 2011;39(1):21–7.CrossRef Convento MS, Pessoa E, Dalboni MA, Borges FT, Schor N. Pro-inflammatory and oxidative effects of noncrystalline uric acid in human mesangial cells: contribution to hyperuricemic glomerular damage. Urol Res. 2011;39(1):21–7.CrossRef
39.
go back to reference Theo Schermuly R, Ardeschir Ghofrani H, Weissmann N. Prostanoids and phosphodiesterase inhibitors in experimental pulmonary hypertension. Curr Top Dev Biol. 2005;67:251–84.CrossRef Theo Schermuly R, Ardeschir Ghofrani H, Weissmann N. Prostanoids and phosphodiesterase inhibitors in experimental pulmonary hypertension. Curr Top Dev Biol. 2005;67:251–84.CrossRef
Metadata
Title
The association of urinary prostaglandins with uric acid in hyperuricemia patients
Authors
Huagang Lin
Ying Xu
Yuqi Zheng
Deping Wu
Zhibin Ye
Jing Xiao
Publication date
01-12-2022
Publisher
BioMed Central
Published in
BMC Nephrology / Issue 1/2022
Electronic ISSN: 1471-2369
DOI
https://doi.org/10.1186/s12882-022-02928-y

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