In the past, hyperuricemia and hypertension were mostly considered as a concomitant phenomenon.
Nowadays, hyperuricemia is considered to be an independent risk factor for essential hypertension.
The two are closely related. Blood uric acid levels are positively correlated with hypertension.
The prevalence of hyperuricemia in patients with essential hypertension is in the range of 30-35%, and especially in patients with untreated hypertension, the increase in blood uric acid can be as high as about 58%. A 1 mg/dl increase in blood uric acid levels increases the risk of hypertension by 23%, and a 3 mg/dl increase in blood uric acid levels in men increases the likelihood of developing hypertension by 87%. The basal blood uric acid level is the strongest independent predictor of the development of hypertension. A domestic epidemiological study by Fu Wai Hospital of Chinese Academy of Sciences showed that systolic and diastolic blood pressure levels were highly significantly and positively correlated with hyperuric acid, especially elevated diastolic blood pressure was directly correlated with blood uric acid levels.
3.2 Mechanism of hypertension combined with hyperuric acid
3.2.1 Pathogenesis of hyperuric acid in hypertensive patients
(1) Renal hemodynamic disorders: hypertensive patients have increased renal vascular resistance; hypertensive patients are more likely to have microalbuminuria, and the latter is significantly associated with increased blood uric acid; hypertensive patients with severe renal and systemic vascular damage have a more significant increase in blood uric acid; in patients with familial hyperuricemic nephropathy, renal hemodynamic abnormalities precede the appearance of uric acid metabolism disorders.
(2) Microangiopathy: In hypertensive patients, tissue hypoxia due to microangiopathy inhibits the ion exchange transport system, resulting in hyperuricemia due to inhibition of uric acid secretion by the renal tubules.
(3) Inadequate renal perfusion; long-term hypertension can lead to inadequate renal perfusion and promote benign glomerular arteriosclerosis. Increased lactic acid production in this part of the renal tubule due to hypoxia, and lactic acid has a competitive inhibitory effect on uric acid excretion, which reduces uric acid elimination and causes uric acid retention, which in turn causes hyperuricemia.
(4) Insulin resistance: Insulin resistance may exist in long-term hypertension, and secondary hyperinsulinemia occurs. The increased insulin can affect the excretion of uric acid, causing uric acid to rise. In addition, hypertensive patients treated with diuretics, especially with thiazide and tab diuretics, have reduced blood volume and increased uric acid reabsorption.
3.2.2 Mechanisms by which elevated levels of hyperuric acid lead to hypertension
High serum uric acid levels stimulate renin secretion, cause renin-angiotensin activation, inhibit NO synthase 1, and trigger arterial smooth muscle cell proliferation leading to hypertension.
Uric acid also activates increased release of vasoactive substances such as platelet 5-hydroxytryptamine and ADP, and accelerates lipid deposition by damaging vascular endothelial cells, while increased blood uric acid also promotes oxidation of low-density lipoproteins and lipid peroxidation, promotes increased oxygen radical production, and promotes platelet adhesion and aggregation.
The physical solubility of uric acid in blood is very low, and when hyperuricemia occurs, urate microcrystals easily precipitate and deposit in the vessel wall, directly damaging the intima, causing an inflammatory response in the intima and triggering atherosclerosis.
Hyperuric acid increases endothelin in the blood circulation through insulin resistance, which in turn can lead to altered endothelial function and increased peripheral resistance.
Uric acid plays an intermediary role in the reduction of renal units leading to hypertension.
3.3 Dangers of hyperuric acid combined with hypertension
Several studies have confirmed that hypertensive patients with combined hyperuricemia also have an increased risk of cardiovascular events. The risk of cardiovascular events has been reported to be three to five times higher than that of patients with normal uric acid levels. The NHANES III study showed that blood uric acid levels were an independent risk factor for coronary heart disease, and blood uric acid levels ≥417umol/L (7mg/dl) were an independent risk factor for stroke.
In spontaneously hypertensive rats, inhibition of xanthine oxidase significantly reduced microvascular tone and caused a decrease in blood pressure.
4. Management of hyperuricemia
4.1 Lifestyle changes
4.1.2 Diet control
4.1.3 Drink plenty of water
4.1.4 Alkalinization of urine
4.2 Drug treatment
4.2.1 Drugs to promote uric acid excretion: benzbromarone, propofol
4.2.2 Inhibitors of uric acid synthesis: allopurinol
4.3 Treatment of hypertension combined with high uric acid
There is no definite conclusion so far. It has been proposed that in patients with significantly elevated blood uric acid levels >773umol (13mg/dl) in men, women need to add classical uric acid-lowering drugs such as allopurinol.
Care should be taken with the use of diuretics in volume-dependent hypertension. Angiotensin II receptor (AT1-type) antagonists may be used (Cloxacin).
In the Expert Consensus on Recommendations for the Diagnosis and Treatment of Asymptomatic Hyperuricemia Combined with Cardiovascular Disease (Draft), drafted by the Cardiovascular Physicians Branch of the Chinese Medical Association, it is stated that the ideal blood uric acid concentration should be controlled at less than 6 mg/dl. Patients with hyperuricemia combined with cardiovascular risk factors and blood uric acid >471umol/L and patients without comorbidities but with blood uric acid values >530umol/L should be treated with uric acid-lowering drugs.