by Dr. Valerie Milne

Gout and chronic kidney diseases create a vicious cycle: gout can damage the kidneys, while kidney disease makes gout worse. Early screening, lifestyle changes, and careful medication management are essential to preventing complications.

Gout occurs when high levels of uric acid in the blood form crystals in the joints, causing painful flare-ups. However, these crystals don’t just affect the joints. They can also accumulate in the kidneys, contributing to kidney stones and long-term kidney damage.

At the same time, chronic kidney disease reduces the kidneys’ ability to remove uric acid from the body, leading to higher levels of uric acid in the blood and an increased risk of gout attacks. Research shows that people with gout are significantly more likely to develop chronic kidney disease, likely due to chronic inflammation and uric acid buildup.

Managing both conditions together presents challenges, especially when it comes to medication. Many common gout treatments, such as NSAIDs and colchicine, can be harmful to weakened kidneys, requiring careful medical supervision. However, urate-lowering therapy (ULT) with medications like allopurinol or febuxostat may help slow chronic kidney disease progression, though research on this is still ongoing.

Risk factors for gout and kidney disease

Genetic factors underlie hyperuricemia (high uric acid levels) that lead to gout. Uric acid is produced when proteins called purines are metabolised from food, and most of it usually passes out of the body in the urine. As well as gout, high uric acid levels can also lead to chronic kidney disease and kidney stones. While genetic factors underlie high uric acid levels, there are some manageable risk factors that also contribute to this condition. Manageable risk factors include reducing the consumption of high-protein and high-sodium diets, as well as sugary drinks. Reducing high sugar levels in the blood and hypertension (high blood pressure) can also improve a person’s chances of reducing gout flares and some kidney conditions.

Dietary considerations

The relationship between diet and gout is well-documented. Some foods have been found to increase uric acid levels, while others may reduce the risk of high uric acid levels and gout flares.

Foods that can increase uric acid levels:

• Seafood high in purines
• Organ meats
• Sugary soft drinks and processed foods
• Alcohol, particularly beer

Foods that may reduce uric acid levels:

• Low-fat dairy
• Non-citrus fruits, carrots, mushrooms, and eggs
• Peanuts, whole grains, and soy products
• Coffee and black tea
• Vitamin C (in moderate amounts) may help lower uric acid, though excessive doses could increase kidney stone risk
• Drinking more water (6 to 8 cups a day) is important to lower uric acid levels

Gout and kidney stones

Kidney stones are composed of different materials, including calcium, struvite (caused by bacteria), cystine (from amino acids), and uric acid. Individuals with gout are more likely to develop uric acid kidney stones due to consistently high uric acid levels and acidic urine. Researchers who look at the connections between gout and kidney disease have calculated that people with gout are nearly twice as likely as people without gout to develop uric acid kidney stones.

Medications and impact on gout

Treating gout in people with chronic kidney disease and/or with other conditions requires careful management. Some medications used to treat conditions other than gout trigger or exacerbate gout by increasing uric acid levels and/or reducing the excretion of uric acid. These types of medicines include:

• Diuretics for treating hypertension
• Antiretroviral drugs
• Beta-blockers, ACE inhibitors, and other medications for heart health
• Immunosuppressants

Urate-lowering therapy and chronic kidney disease progression

Studies suggest nearly 25% of adults with chronic kidney disease at stage 3 or higher also have gout, and the management of gout in patients with chronic kidney disease presents some challenges because nonsteroidal anti-inflammatory drugs (NSAIDs) and colchicine should be used cautiously, and lower doses of ULT such as allopurinol may be required. The effect of glucocorticoids, used for gout flares, on kidney function is unclear.

Despite the concerns about ULT worsening kidney function, a recent study involving 14,792 patients with gout and chronic kidney disease (stage 3) found that achieving urate levels low enough to prevent gout flares using ULT was not linked to an increased risk of severe kidney disease progression. Instead, patients who achieved this target had a slightly lower risk of developing end-stage kidney disease. Therefore, using ULT medications, such as allopurinol, to reduce urate levels appears to be helpful for managing gout in chronic kidney disease patients. Download the Change your life gout booklet for more information about how ULT works.

Gout and kidney transplantation

Kidney transplant recipients are at a higher risk of high uric acid levels, and new-onset gout than people who have not had a kidney transplant, and gout is often more severe and harder to manage in transplant patients. Cyclosporine, a commonly used immunosuppressant, significantly increases the risk of high uric acid levels.

To summarise, gout and kidney disease share complex interconnections, with each condition impacting on the other. Individuals with gout are at higher risk for kidney stones and chronic kidney disease, making early screening essential. Dietary modifications, careful medication management, and appropriate urate-lowering therapy can help reduce the risk of complications. Lowering ULT levels can also reduce the risk of kidney stones. Further research is needed to establish standardised guidelines for managing gout in chronic kidney disease patients, particularly regarding medication safety and long-term outcomes.