Effect of Antihypertensive Drugs on Uric Acid Metabolism in Patients with Hypertension: Cross-Sectional Cohort Study

Abstract

Hypertension is a common complication in patients with gout and/or hyperuricemia. Besides, hyperuricemia is a risk factor of gout as well as ischemic heart disease in hypertensive patients. Moreover, the risk of gout is modified by antihypertensive drugs. However, it remains unclear how antihypertensive agents affect uric acid metabolism. In the present study, we investigated the uric acid metabolism in treated hypertensive patients to find out whether any of them would influence serum levels of uric acid. 751 hypertensive patients (313 men and 438 women) under antihypertensive treatment were selected. Blood pressure (BP), serum uric acid (SUA) and serum creatinine (Scr) were measured and evaluated statistically. In patients treated with diuretics, beta-blockers and/or alpha-1 blockers SUA levels were significantly higher than in patients who were not taking these drugs. Besides, the estimated glomerular filtration rate (eGFR) in patients treated with diuretics, beta-blockers and/or alpha-1 blockers was negatively correlated with SUA level. There were gender differences in the effects of beta-blockers and alpha-1 blockers. Multiple regression analysis indicated that both diuretics and beta-blockers significantly contributed to hyperuricemia in patients with medication for hypertension. Diuretics, beta-blockers and alpha-1 blockers reduced glomerular filtration rate and raised SUA levels. Calcium channel blockers, ACE inhibitors and angiotensin receptor blockers, including losartan, did not increase SUA levels.

What is the role of angiotensin receptor blockers in treatment of hyperuricemia coexisting with arterial hypertension?

“…It is also advised to make urine pH alkaline to prevent formation of kidney stones. The patient should also be interviewed according to the ACR 2012 Checklist for other health problems that increase UA [ 4 , 21 , 22 ].…”

“…In another study conducted by Ueno et al [ 22 ] 751 patients with AH were treated with diuretics, β-blockers or α-1 blockers. The eGFR in patients treated with these drugs was negatively correlated with UA level.…”

“…The drugs reduced eGFR and raised UA levels. Calcium channel blockers, ACE inhibitors and ARBs, including losartan, did not increase serum UA levels [ 22 ].…”

Risk Factors of Gout in MDR-TB Patients in Eritrea: A Case-Control Study

“…Due to the fact that all patients who developed tachycardia while on second-line anti-TB drugs were taking propranolol (40mg once or twice daily for at least three months), incident gout could partially be attributed to the effect of this beta-blocker. This is because beta-blockers like propranolol are known to increase the amount of uric acid in blood [24–26], which is a predisposing factor for the development of gout. However, it is difficult to establish causation between tachycardia (through intake of propranolol) and gout from this study since it is unknown which event developed first.…”

Expert consensus for the diagnosis and treatment of patient with hyperuricemia and high cardiovascular risk

“…Nevertheless, allopurinol may also be considered in hypertensives with asymptomatic HU, particularly those at high CV risk. Among the drugs recommended for the treatment of co-morbidities with HU, great attention should be paid to the key drugs that influence sUA levels (Table 1) [153][154][155][156][157][158][159].…”