The Relationship Between Ambulatory Blood Pressure Monitoring and Uric Acid Level in Hypertensive Patients

Year 2024, Volume: 11 Issue: 3, 434 - 441, 30.09.2024

Musa İlker Durak

https://doi.org/10.34087/cbusbed.1487249

Abstract

Abstract
Giriş: Serum uric acid (SUA) pürin metabolizmasının son ürünüdür. Aşırı üretimi veya böbrek atılımının azalması hiperürisemiye sebep olur. SUA yüksekliğinin kardiyovasküler hastalıklar için risk faktörü olduğu bilinmektedir. Ürik asit yüksekliği olan hastalarda kan basıncının (KB) daha yüksek olduğu ve ürik asit düşürücü ilaç kullanımı sonrası KB düşüşünün görüldüğü bildirilmiştir.
Metod: Hastanemize hipertansiyon (HT) sebebiyle başvuran ve ambulatuar kan basıncı monitorizasyonu (AKBM) yapılan hastalarda SUA düzeyi ile ilişkisine bakıldı. Çalışmaya 310 hasta dahil edildi. SUA düzeyi enzimatik kolorimetrik otoanalizorde belirlendi. AKBM, noninvazif multitasking KB kayıt cihazları (TM2425; A&D, Tokyo, Japonya) kullanılarak gerçekleştirildi.
Sonuçlar: Hastaların %49.6’sında hiperürisemi tespit edildi. Hiperürisemi olan hastalarda gündüz, gece ve 24 saatlik diastolik kan basıncı (DKB) anlamlı düzeyde daha yüksekti (p=0.021, p=0.029 p=0.005). Hiperürisemi olan hastalarda ortalama arter basıncı (OAB) ve OAB gece değerleri daha yüksekti (p=0.022, p=0.003). Hiperürisemi olan hastalarda dipper HT olanların oranı, hiperürisemi olmayanlara göre daha az olduğu görüldü (p=0.041). Hiperürisemi olan hastalarda reverse dipper HT olma oranı, hiperürisemi olmayanlara göre daha yüksek olarak saptanmıştır (p=0.022).
Conclusion: Ürik asit yüksekliği ile DKB, reverse HT ve OAB ile ilişki saptandı. SUA'nın ölçümü kardiyovasküler riskin değerlendirilmesi ve azaltılması için değerli bir araç olabilir. Ürik asit düşürülmesinin gece kan basıncının ve DKB azaltılmasına etkisini gösteren ileri çalışmalara ihtiyaç vardır.

Keywords

Ambulatuvar kan basıncı monitorizasyonu, Ürik asit, dipper-hipertansiyon, non-dipperhipertansiyon, reverse dipper hipertansiyon

Ethical Statement

Ankara Bilkent Şehir Hastanesi Etik Kurulundan E1-20-1355 onamı vardır.

Supporting Institution

Yok

The Relationship Between Ambulatory Blood Pressure Monitoring and Uric Acid Level in Hypertensive Patients

Abstract

Abstract
Introduction: Serum uric acid (SUA) is the end product of purine metabolism. Excessive SUA production or decreased renal excretion causes hyperuricemia. Elevated SUA is known to be a risk factor for cardiovascular diseases. It was reported that blood pressure (BP) was higher in patients with elevated uric acid and a decrease in BP was observed after the administration of uric acid-lowering drugs.
Methods: We examined the relationship between SUA levels and hypertension in patients admitted to our hospital with hypertension (HT) and undergoing ambulatory blood pressure monitoring (ABPM). A total of 310 patients were included in the study. SUA levels were determined using an enzymatic colorimetric autoanalyzer. ABPM was performed using noninvasive multitasking CR recorders (TM2425; A&D, Tokyo, Japan).
Results: Hyperuricemia was observed in 49.6% of the patients. Daytime, nocturnal, and 24-hour diastolic blood pressure (DBP) were significantly higher in patients with hyperuricemia (p=0.021, p=0.029, and p=0.005, respectively). Mean arterial pressure (MAP) and nocturnal MAP values were higher in patients with hyperuricemia (p=0.022 and p=0.003, respectively). The rate of patients with dipper HT was lower in patients with hyperuricemia than those without hyperuricemia (p=0.041). The rate of reverse-dipper HT was found to be higher in patients with hyperuricemia compared to those without hyperuricemia (p=0.022).
Conclusion: Elevated uric acid was correlated with DBP, reverse HT, and MAP. Measurement of SUA could provide a valuable aid for the assessment and reduction of cardiovascular risk. Further studies are required to assess the effect of lowering uric acid on the reduction of nocturnal BP and DBP.
Key words: Ambulatory blood pressure monitoring, uric acid, dipper hypertension, non-dipper hypertension, reverse-dipper hypertension

Keywords

Ambulatory blood pressure monitoring, uric acid, dipper hypertension, non-dipper hypertension, reverse-dipper hypertension

References

• 1. Maiuolo J, Oppedisano F, Gratteri S, Muscoli C, Mollace V. Regulation of uric acid metabolism and excretion. Int J Cardiol. 2016;213:8–14
• 2. Choi HK. A prescription for lifestyle change in patients with hyperuricemia and gout. Curr Opin Rheumatol 2010; 22: 165–172.
• 3. Gois PH, Souza ER. Pharmacotherapy for hyperuricemia in hypertensive patients. Cochrane Database Syst Rev 2013; 1: CD008652
• 4. Borghi C. Agabiti-Rosei E. Johnson R.J. et al. Hyperuricaemia and gout in cardiovascular, metabolic and kidney disease. Eur J Intern Med. 2020; 80: 1-11https://doi.org/10.1016/j.ejim.2020.07.006
• 5. Miyabayashi I, Mori S, Satoh A, Kawazoe M, Funakoshi S, Ishida S, et al. Uric acid and prevalence of hypertension in a general population of Japanese: ISSA-CKD Study. J Clin Med Res. 2020;12:431–5
• 6. Williams B, Mancia G, Spiering W, Agabiti-Rosei E, Azizi M, Burnier M, et al. 2018 European Society of Cardiology/European Society of Hypertension guidelines for the management of arterial hypertension. Eur Heart J. 2018;39:3021-194. The latest European guidelines document for the diagnosis and treatment of essential hypertension.
• 7. Soletsky B, Feig DI. Uric acid reduction rectifies prehypertension in obese adolescents. Hypertension 2012; 60: 1148–1156.
• 8. Mancia G, Facchetti R, Seravalle G, Cuspidi C, Grassi G. Adding home and/or ambulatory blood pressure to ofce blood pressure 34 Current Hypertension Reports (2022) 24:29–35 1 3 for cardiovascular risk prediction. Hypertension. 2021;77:640- 49. Evidence that out-of-ofce blood pressure, when added to ofce blood pressure, may signifcantly improve cardiovascular risk prediction.
• 9. Hermida RC, Ayala DE, Fernández JR, Portaluppi F, Fabbian F, Smolensky MH. Circadian rhythms in blood pressure regulation and optimization of hypertension treatment with ACE inhibitor and ARB medications. Am J Hypertens. 2011 Apr;24(4):383-91. doi: 10.1038/ajh.2010.217. Epub 2010 Oct 7. PMID: 20930708.
• 10. Yu T, Song S, Chen X, et al. Diabetic Kidney Disease versus Primary Glomerular Disease: A Propensity Score-Matched Analysis of Association between Ambulatory Blood-Pressure Monitoring and Target-Organ Damage.J Clin Med. 2022;12(1):167. Published 2022 Dec 25. doi:10.3390/jcm12010167
• 11. Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study Group. Ann Intern Med 1999; 130: 461-70
• 12. Zhu Y, Pandya BJ, Choi HK. Prevalence of gout and hyperuricemia in the US general population: The National Health and Nutrition Examination Survey 2007-2008. Arthritis Rheum 2011;63:3136-41
• 13. Jones, D. P., Richey, P. A., Alpert, B. S., & Li, R. (2008). Serum uric acid and ambulatory blood pressure in children with primary hypertension. Pediatric research, 64(5), 556–561. https://doi.org/10.1203/PDR.0b013e318183fd7c
• 14. Castro-Torres, Y., Khan, N. Y., & Carmona-Puerta, R. (2017). Levels of uric acid and increased diastolic blood pressure: Risk factors for atrial fibrillation in patients older than 60 years. Revista da Associacao Medica Brasileira (1992), 63(7), 600–605. https://doi.org/10.1590/1806-9282.63.07.600
• 15. Sun GZ, Guo L, Wang J, Ye N, Wang XZ, Sun YX. Association between hyperuricemia and atrial fibrillation in rural China: a cross-sectional study. BMC Cardiovasc Disord. 2015; 15:98.
• 16. de la Sierra A, Redon J, Banegas JR, et al. Prevalence and factors associated with circadian blood pressure patterns in hypertensive patients. Hypertension. 2009;53:466–472.
• 17. Mann S, Altman DG, Raftery EB, Bannister R. Circadian variation of blood pressure in autonomic failure. Circulation. 1983;68:477– 483
• 18. Wang J, Wang Y, Zhao D, et al. Association between serum uric acid and mortality in a Chinese population of hypertensive patients. Ren Fail 2015;37:73–6.
• 19. Turak, O., Ozcan, F., Tok, D., Işleyen, A., Sökmen, E., Taşoğlu, I., Aydoğdu, S., Sen, N., McFann, K., Johnson, R. J., & Kanbay, M. (2013). Serum uric acid, inflammation, and nondipping circadian pattern in essential hypertension. Journal of clinical hypertension (Greenwich, Conn.), 15(1), 7–13. https://doi.org/10.1111/jch.12026
• 20. Giallauria F, Predotti P, Casciello A, Grieco A, Russo A, Viggiano A, Citro R, Ravera A, Ciardo M, Guglielmi M, Maggio M, Vigorito C. Serum uric acid is associated with non-dipping circadian pattern in young patients (30–40 years old) with newly diagnosed essential hypertension. Clin Exp Hypertens 2016; 38:233–237
• 21. Zhang, S., Wang, Y., Cheng, J., Huangfu, N., Zhao, R., Xu, Z., Zhang, F., Zheng, W., & Zhang, D. (2019). Hyperuricemia and Cardiovascular Disease. Current pharmaceutical design, 25(6), 700–709. https://doi.org/10.2174/1381612825666190408122557
• 22. Forman JP, Choi H, Curhan GC. Plasma uric acid level and risk for incident hypertension among men. J Am Soc Nephrol. 2007; 18(1):287-92.
• 23. Acevedo A, Benavides J, Chowdhury M, Lopez M, Pena L, Montenegro A, et al. Hyperuricemia and cardiovascular disease in patients with hypertension. Conn Med 2016; 80(2):85-90.
• 24. Sanchez-Lozada, L. G., Rodriguez-Iturbe, B., Kelley, E. E., Nakagawa, T., Madero, M., Feig, D. I., Borghi, C., Piani, F., Cara-Fuentes, G., Bjornstad, P., Lanaspa, M. A., & Johnson, R. J. (2020). Uric Acid and Hypertension: An Update With Recommendations. American journal of hypertension, 33(7), 583–594. https://doi.org/10.1093/ajh/hpaa044
• 25. Mazzali M, Hughes J, Kim YG, Jefferson JA, Kang DH, Gordon KL, et al. Elevated uric acid increases blood pressure in the rat by a novel crystal-independent mechanism. Hypertension 2001; 38: 1101– 1106.
• 26. Watanabe S, Kang DH, Feng L, Nakagawa T, Kanellis J, Lan H, Mazzali M, Johnson RJ. Uric acid, hominoid evolution, and the pathogenesis of salt-sensitivity. Hypertension 2002; 40:355–360.
• 27. Edwin K, Garrison JC. Renina y angiotensina. In: Goodman & Gilman, editors. Las bases farmacológicas de la terapéutica médica. McGraw-Hill. México DF; 1996. v.2, p. 791-3
• 28. Cannon, P. J., Stason, W. B., Demartini, F. E., Sommers, S. C., & Laragh, J. H. (1966). Hyperuricemia in primary and renal hypertension. The New England journal of medicine, 275(9), 457–464. https://doi.org/10.1056/NEJM196609012750902
• 29. Kang DH, Han L, Ouyang X, Kahn AM, Kanellis J, Li P, et al. Uric acid causes vascular smooth muscle cell proliferation by entering cells via a functional urate transporter. Am J Nephrol 2005; 25: 425– 433.
• 30. Mazzali M, Kanellis J, Han L, Feng L, Xia YY, Chen Q, et al. Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure-independent mechanism. Am J Physiol Renal Physiol 2002; 282: F991–F997.