Hyperuricemia (high uric acid)

What is hyperuricaemia?

Hyperuricaemia occurs when the level of urate in the blood is persistently elevated. Uric acid is produced when the body breaks down purines, which come from normal cell turnover and certain foods and drinks. Most urate is removed from the body through the kidneys, with the remainder excreted through the gut. Hyperuricaemia can result from reduced renal excretion, increased production, or a combination of both.

While many people experience no symptoms at all, chronic buildup can cause significant issues over time:

• Asymptomatic hyperuricaemia: high uric acid with no outward symptoms. While most people in this group never get gout, it is an independent risk factor for heart disease, high blood sugar, and kidney strain.

• Gout: the most common complication, where sharp crystals settle inside joints to trigger sudden, agonizing attacks of painful inflammation.

• Kidney stones: excess uric acid crystallizes in the urinary tract, causing painful stones that block urine flow.

• Chronic kidney damage: crystals can become embedded directly inside kidney tissues, slowly reducing your organs' filtering power over time.

• Tophi (tophaceous gout): in long-term untreated cases, large, chalky lumps of crystals pile up beneath the skin around your ears, fingers, or joints, leading to permanent joint damage.

Symptoms of hyperuricaemia

Hyperuricaemia itself usually causes no symptoms. When symptoms occur, they are generally related to complications such as gout or uric acid kidney stones:

• Sudden, severe joint pain, warmth, redness, and swelling, typically monoarticular and affecting the big toe (podagra), ankle, knee, or wrist, during an acute gout attack

• Episodes typically peak within 24 hours and resolve spontaneously over days to weeks without treatment

• Recurrent attacks affecting multiple joints over time if untreated

• Flank pain, haematuria, and renal colic from uric acid kidney stones

• Progressive joint deformity and reduced mobility from tophaceous gout in chronic untreated disease

• Reduced kidney function from chronic urate nephropathy in longstanding severe hyperuricaemia

What causes hyperuricaemia?

Hyperuricaemia results from overproduction of uric acid, underexcretion by the kidneys, or both. Contributing causes include:

• Dietary factors high intake of purine-rich foods, particularly organ meats and some types of meat and seafood, can increase urate levels. Fructose, especially from sugar-sweetened drinks, can also increase urate production.

• Alcohol beer and spirits can increase urate levels by increasing production and reducing renal excretion. Higher alcohol intake is associated with a greater risk of hyperuricaemia and gout.

• Obesity and metabolic syndrome insulin resistance reduces renal uric acid excretion through competition at the proximal tubule. Hyperuricaemia is strongly associated with obesity, hypertension, dyslipidaemia, and type 2 diabetes.

• Medications diuretics, particularly thiazides and loop diuretics, reduce renal uric acid excretion significantly. Aspirin at low doses, ciclosporin, tacrolimus, and pyrazinamide also raise uric acid levels.

• Chronic kidney disease impairs uric acid excretion as nephron mass is lost, creating a bidirectional relationship where hyperuricaemia worsens kidney function and kidney disease worsens hyperuricaemia.

• Increased cell turnover from haematological malignancies, haemolytic anaemia, psoriasis, and chemotherapy increases purine load and uric acid production.

• Genetic factors familial hyperuricaemia and gout have a strong genetic component, with variants in uric acid transporter genes (URAT1, ABCG2) determining individual excretory capacity.

• Dehydration concentrates uric acid in the blood and reduces renal excretion.

How is hyperuricaemia detected?

Hyperuricaemia is directly and definitively detected through a blood test measuring serum uric acid, with supporting markers identifying the metabolic conditions most commonly associated with its development and consequences.

Blood tests Elfcare's panel includes uric acid alongside the key related markers:

• Serum uric acid the primary marker, directly measuring circulating urate levels and confirming hyperuricaemia when persistently elevated above sex-specific thresholds

• Creatinine, cystatin C, and eGFR assess kidney function, both as a cause of reduced uric acid excretion and as a consequence of chronic urate nephropathy

• HbA1c and glucose assess insulin resistance and diabetes, closely associated with hyperuricaemia through reduced renal uric acid excretion

• Total cholesterol, LDL, HDL, and triglycerides dyslipidaemia is strongly associated with hyperuricaemia as part of metabolic syndrome

• CRP reflects systemic inflammation, elevated during acute gout attacks and relevant to the chronic inflammatory state of longstanding hyperuricaemia

• Full blood count identifies haematological conditions causing increased cell turnover and uric acid overproduction

• ALT, AST, and GGT assess liver function and alcohol-related damage, both relevant to purine metabolism and uric acid production

Abdominal MRI While CT remains the standard, most sensitive tool for detecting kidney stones directly, Elfcare's full body MRI images the kidneys as part of routine imaging and can assess renal parenchymal changes from chronic urate nephropathy and overall kidney structure, which are useful complementary findings alongside dedicated stone imaging. Joint MRI, available as a targeted regional examination, can identify urate crystal deposits in affected joints and tophi in soft tissues, providing structural confirmation of gout.

Why early detection matters

Early identification of hyperuricaemia matters because elevated urate can remain unnoticed for years before symptoms appear. Detecting it early provides an opportunity to understand your risk of gout, uric acid kidney stones, and reduced kidney function, while also identifying related health factors such as obesity, hypertension, insulin resistance, and chronic kidney disease. Higher and persistent urate levels increase the likelihood of urate crystal formation, so recognising the pattern early can support timely monitoring and informed action before recurrent attacks or complications develop.

Management depends on the clinical context. For people with gout, recurrent uric acid kidney stones, very high urate levels, or other relevant risk factors, early assessment can help guide appropriate urate-lowering treatment and lifestyle changes, including reducing excessive alcohol intake, maintaining a healthy weight, and making appropriate dietary adjustments. Even when there are no symptoms, knowing your urate level can provide valuable insight into your wider metabolic and kidney health, helping you and your clinician decide whether monitoring, further investigation, or treatment is appropriate.

How Elfcare can help

Elfcare's blood panel includes serum uric acid as standard alongside a comprehensive metabolic profile covering kidney function, HbA1c, lipids, CRP, and liver markers. This provides both the direct measurement of hyperuricaemia and the complete metabolic context in which it develops, identifying the conditions most commonly driving elevated uric acid and the organ consequences most closely associated with its persistence.

Our abdominal MRI images the kidneys directly, identifying structural consequences of chronic hyperuricaemia including kidney stones and parenchymal changes.

If our blood tests or MRI identify hyperuricaemia or related findings, we take care of further diagnostics or refer you to the appropriate specialist.