Gout and high blood pressure are closely linked, and the connection runs deeper than shared risk factors. About 64% of people with gout also have hypertension, and genetic evidence now points to a direct causal relationship: the excess uric acid that causes gout also drives up blood pressure through several distinct pathways in your blood vessels and kidneys.
How Uric Acid Raises Blood Pressure
Gout develops when uric acid levels in the blood stay elevated long enough for crystals to form in joints. But those high uric acid levels do more than cause joint pain. They trigger a cascade of changes in your cardiovascular system that push blood pressure upward.
The first mechanism involves a hormonal system your body uses to regulate blood pressure, called the renin-angiotensin system. When uric acid levels are high, this system becomes overactive. Lab studies on human blood vessel cells show that exposing them to elevated uric acid directly increases the production of angiotensin II, a hormone that constricts blood vessels. In animal studies, raising uric acid levels activated this system and increased systolic blood pressure, and the effect could be reversed with uric acid-lowering medication.
The second mechanism targets nitric oxide, a molecule your blood vessels produce to stay relaxed and flexible. High uric acid interferes with the enzyme responsible for making nitric oxide, not by destroying the enzyme but by disrupting its ability to bind with a key activating protein called calmodulin. The result is less nitric oxide, stiffer arteries, and higher blood pressure.
Researchers have proposed a two-step model for how this plays out over time. Initially, elevated uric acid causes reversible blood vessel constriction through these hormonal and chemical changes. If uric acid stays high, the damage becomes permanent: small blood vessels develop structural changes (arteriosclerosis) that lead to chronic, salt-sensitive hypertension.
Genetic Evidence for a Causal Link
For years, scientists debated whether uric acid truly caused high blood pressure or whether the two conditions simply shared common causes like obesity and kidney problems. A 2025 Mendelian randomization study put this question to rest with a powerful approach: instead of tracking lifestyle habits, researchers used genetic variants that naturally raise uric acid levels to test whether those variants also predicted higher blood pressure.
They found a clear, one-directional relationship. People genetically predisposed to higher uric acid had significantly higher systolic and diastolic blood pressure. Critically, the reverse was not true: genetic variants associated with high blood pressure did not raise uric acid. This confirms that elevated uric acid drives hypertension, not the other way around.
Kidney Damage Adds a Third Pathway
Your kidneys play a central role in blood pressure regulation, and uric acid damages them in ways that compound the problem. Studies of kidney tissue from hypertensive patients show that uric acid levels correlate with glomerulosclerosis, a form of scarring in the kidney’s filtering units. Higher uric acid is also associated with worsening damage to the small arteries within the kidneys. As these tiny blood vessels stiffen and the kidney’s filtering capacity declines, the body retains more sodium and fluid, further elevating blood pressure.
Blood Pressure Medications That Make Gout Worse
If you have both gout and high blood pressure, the type of blood pressure medication you take matters significantly. Thiazide diuretics, one of the most commonly prescribed classes of blood pressure drugs, actively raise uric acid levels by increasing urate reabsorption in the kidneys. In one study, 24.5% of people taking thiazides had elevated uric acid compared to 15.3% of those on other medications. The longer you take them, the worse it gets: the Systolic Hypertension in the Elderly Program found that thiazide users saw uric acid levels climb 0.90 mg/dL higher than the placebo group over three years.
The Framingham Heart Study, spanning over 53 years of data, concluded that diuretic use is an independent risk factor for gout, with a 3.4 times higher relative risk in men and 2.4 times in women. Combining loop diuretics with thiazides raises the odds of developing gout by 4.6 times.
This creates a frustrating cycle: gout raises blood pressure, and one of the most common blood pressure treatments worsens gout.
Smarter Medication Choices
The American College of Rheumatology’s gout management guidelines address this problem directly. For anyone with gout, regardless of whether they’re having active flares, the guidelines recommend switching off hydrochlorothiazide (a thiazide diuretic) to an alternative blood pressure medication when possible. They also recommend choosing losartan as the preferred blood pressure drug.
Losartan stands out because it does double duty. Beyond lowering blood pressure, it has a uricosuric effect, meaning it helps your kidneys excrete more uric acid. It does this by blocking a transporter called URAT1 in the kidney’s tubules, the same transporter that thiazides exploit to increase uric acid reabsorption. In every study reviewed in a comprehensive analysis, losartan produced statistically significant reductions in uric acid levels. No other drug in its class (angiotensin II receptor blockers) consistently matched this benefit.
Lowering Uric Acid Can Lower Blood Pressure
Treating the root cause of gout, elevated uric acid, also helps with blood pressure. A meta-analysis of 10 clinical trials involving 738 participants found that allopurinol, the most commonly prescribed uric acid-lowering drug, reduced systolic blood pressure by an average of 3.3 mmHg and diastolic by 1.3 mmHg. These numbers held up when the analysis was restricted to only high-quality randomized controlled trials.
A 3.3 mmHg drop might sound modest, but at a population level, reductions of this size meaningfully lower the risk of stroke and heart attack. For someone whose blood pressure is borderline or mildly elevated, it could be the difference between needing additional medication and staying in a healthy range.
Diet Changes That Target Both Conditions
The DASH diet (Dietary Approaches to Stop Hypertension) is one of the most effective dietary interventions for lowering blood pressure, and it happens to address many of the dietary factors linked to high uric acid as well. The diet emphasizes fruits, vegetables, low-fat dairy, whole grains, poultry, fish, and nuts while reducing red meat, saturated fat, and sugar-sweetened beverages.
Several of these components directly affect uric acid. Lower red meat intake means fewer purines, the compounds your body breaks down into uric acid. Higher low-fat dairy consumption is independently associated with lower uric acid levels. The increased fruit and vegetable intake provides more vitamin C, which helps the kidneys excrete uric acid, and alkalinizes urine, which further promotes uric acid elimination. For someone managing both gout and hypertension, the DASH diet addresses both problems through a single set of changes.