Rheumatology

Uric Acid: Gout, Kidney Stones & Metabolic Risk

Uric acid is the end product of purine metabolism. Normally your kidneys clear it efficiently, but when levels rise above the saturation point, needle-shaped crystals can form in joints, kidneys, and soft tissue — causing gout, kidney stones, and cardiovascular damage. Hyperuricaemia affects roughly 7% of adult Australians.

What Is Uric Acid?

Purines are nitrogen-containing compounds found in every cell of your body and in many foods. When cells turn over or you digest purine-rich foods, the liver converts those purines into uric acid as the final waste product. In most mammals an enzyme called uricase breaks uric acid down further, but humans lost this enzyme millions of years ago — so we rely entirely on renal excretion to keep levels in check.

About 70% of uric acid is excreted by the kidneys and 30% via the gut. Problems begin when production exceeds excretion: uric acid concentration rises above the supersaturation point of approximately 0.42 mmol/L (7.0 mg/dL), and monosodium urate (MSU) crystals begin to form. These microscopic, needle-shaped crystals trigger an intense inflammatory response — the excruciating pain of a gout attack.

Importantly, crystal deposition can occur silently for years before the first attack. Studies using dual-energy CT show that many people with elevated uric acid have crystal deposits in joints and tendons long before symptoms appear, which is why regular monitoring matters.

Uric Acid Reference Ranges (RCPA)

Australian pathology laboratories report uric acid in mmol/L. The table below includes US mg/dL equivalents and treatment targets recommended by the Australian Rheumatology Association.

Marker	Men	Women	Unit	US Equivalent
Uric Acid (Serum)	0.20 – 0.42	0.14 – 0.36	mmol/L	Men 3.4–7.0 mg/dL, Women 2.4–6.0 mg/dL
Gout Treatment Target	< 0.36	< 0.36	mmol/L	< 6.0 mg/dL
Severe Tophaceous Gout Target	< 0.30	< 0.30	mmol/L	< 5.0 mg/dL
Urine Uric Acid (24hr)	1.5 – 4.5	1.5 – 4.5	mmol/day	250–750 mg/day

Note: Helps classify overproducers (>4.5) vs underexcretors (<1.5). Guides treatment choice.

Related Markers to Request

eGFR / Creatinine

Kidney function determines uric acid excretion. Impaired eGFR raises levels.

CRP / ESR

Inflammation markers confirm acute gout vs chronic hyperuricaemia.

Fasting Glucose / HbA1c

Insulin resistance and metabolic syndrome correlate strongly with hyperuricaemia.

Electrolytes

Diuretics affecting sodium and potassium also raise uric acid levels.

Understanding Your Uric Acid Level

Risk depends on how far above the supersaturation threshold your level sits, and whether you have symptoms. The colour-coded guide below helps you interpret your result.

Normal

< 0.36 mmol/L (women) / < 0.42 mmol/L (men)

Below the supersaturation threshold. Low risk of monosodium urate crystal formation. No treatment required.

Elevated — Asymptomatic

0.42 – 0.54 mmol/L

Asymptomatic hyperuricaemia. No joint symptoms yet, but cardiovascular risk is increasing. Lifestyle changes recommended: reduce purine-rich foods, increase hydration, limit alcohol (especially beer).

Gout Range

0.54 – 0.70 mmol/L

High risk of crystal deposition and acute gout attacks. Urate-lowering therapy (allopurinol, febuxostat) is usually indicated, especially with prior attacks. Target < 0.36 mmol/L.

Severe

> 0.70 mmol/L

Very high risk of tophi formation, recurrent acute gout, urate kidney stones, and urate nephropathy. Urgent urate-lowering therapy and renal assessment needed.

Gout: More Than Just a Sore Toe

An acute gout attack is one of the most painful conditions in medicine. It typically strikes without warning — often overnight — with sudden, severe swelling, redness, warmth, and exquisite tenderness in a single joint. The first metatarsophalangeal joint (big toe) is affected in over 50% of first attacks, a presentation called podagra.

Acute Gout Attack

Sudden onset over 6–12 hours, often waking you at night
Joint is red, hot, swollen, and incredibly tender to touch
Even the weight of a bedsheet can be unbearable
Peaks in 24–48 hours, resolves within 1–2 weeks untreated
Counterintuitively, uric acid may be NORMAL during an acute attack
Diagnosis confirmed by joint aspiration showing MSU crystals

Chronic Tophaceous Gout

Develops after years of poorly controlled hyperuricaemia
Tophi: visible chalky lumps of urate crystals under skin
Common sites: ears, fingers, elbows, Achilles tendon
Progressive joint erosion and deformity if untreated
Tophi can ulcerate and discharge white chalky material
Reversible with sustained urate-lowering therapy (target < 0.30)

Important: Uric acid levels often drop during an acute gout attack because inflammation increases renal excretion. A normal result during a flare does not rule out gout. Recheck levels 2–4 weeks after the attack resolves for a true baseline reading.

Beyond Gout: Why Uric Acid Matters

Elevated uric acid is far more than a joint problem. Research increasingly shows it as an independent risk factor for several serious conditions.

Cardiovascular Disease

Independent predictor of heart attack and stroke
Each 0.06 mmol/L increase raises CV mortality by 12%
Promotes endothelial dysfunction and arterial stiffness
Linked to hypertension — uric acid reduces nitric oxide

Kidney Disease

Urate nephropathy: crystals deposit in kidney tubules
Uric acid kidney stones (5–10% of all stones)
Accelerates CKD progression independently of other factors
Acidic urine (pH < 5.5) dramatically increases stone risk

Metabolic Syndrome

Strong correlation with insulin resistance and type 2 diabetes
Hyperuricaemia present in 70% of metabolic syndrome patients
Fructose intake raises both uric acid and triglycerides
Pre-eclampsia risk increases with elevated maternal uric acid

High-Purine vs Low-Purine Foods

Dietary modification alone can lower uric acid by 0.06–0.10 mmol/L. While this is modest, combining diet with adequate hydration, weight management, and medication when needed achieves the best outcomes.

High Purine — Limit or Avoid

Organ meats
Liver, kidney, sweetbreads — extremely high purine content
Shellfish
Prawns, mussels, scallops, crab — moderate to high purines
Red meat
Beef, lamb, pork — limit to 1–2 serves per week
Beer and spirits
Beer is worst (contains guanosine). Spirits also raise levels.
Sugary drinks
Fructose increases uric acid production directly via purine metabolism
Anchovies and sardines
Very high purine — avoid during active gout
Game meats
Venison, rabbit, duck — high purine content

Low Purine — Encourage

Vegetables
Even high-purine vegetables (spinach, asparagus) do NOT increase gout risk
Low-fat dairy
Protective effect — milk proteins (casein, lactalbumin) increase urate excretion
Cherries and berries
Anthocyanins may reduce attacks by 35% (studies show 2–3 serves/day)
Water (2–3L daily)
Dilutes urine, reduces crystal formation and stone risk
Coffee
Protective — 4+ cups/day associated with 40% lower gout risk (xanthine effect)
Vitamin C
500mg/day may lower uric acid by ~0.02 mmol/L via increased renal excretion
Whole grains and eggs
Low purine, good protein alternatives to red meat

Who Should Be Tested?

Uric acid is not routinely included in standard blood panels. Ask your GP specifically if any of the following apply to you.

Acute joint swelling, redness, and pain (especially the big toe)
Recurrent joint pain or a history of diagnosed gout
Family history of gout or kidney stones
Chronic kidney disease or declining eGFR
Metabolic syndrome (obesity, hypertension, dyslipidaemia, insulin resistance)
Starting thiazide diuretics or other medications that raise uric acid
Before chemotherapy or radiation therapy (tumour lysis syndrome risk)
Recurrent calcium oxalate or urate kidney stones

Medications That Affect Uric Acid

Several common medications can significantly raise or lower uric acid levels. Always tell your doctor about all medications before interpreting results.

Medication	Effect	Mechanism
Thiazide diuretics	↑ Uric acid	Reduce renal urate excretion by competing for tubular secretion.
Low-dose aspirin (≤ 2g/day)	↑ Uric acid	Inhibits urate secretion in the proximal tubule at low doses.
Cyclosporine	↑ Uric acid	Reduces glomerular filtration and impairs tubular urate handling.
Allopurinol	↓ Uric acid	Xanthine oxidase inhibitor — blocks purine-to-uric acid conversion. First-line ULT.
Febuxostat	↓ Uric acid	Selective xanthine oxidase inhibitor. Used when allopurinol is contraindicated or not tolerated.
Probenecid	↑ Excretion	Uricosuric agent — increases renal uric acid excretion. Requires adequate kidney function.
Losartan	Mild ↓	Unique among ARBs — has mild uricosuric effect. Useful in hypertensive gout patients.

Related Blood Test Guides

Kidney Function Tests

eGFR, creatinine, urea — renal health and uric acid excretion

Inflammation Markers

CRP and ESR — confirming acute gout inflammation

Glucose & Insulin

Metabolic syndrome and insulin resistance links

Electrolytes

Diuretic effects and electrolyte imbalance connections

Joint Pain Blood Tests

Comprehensive panel for diagnosing joint conditions

Heart Health Markers

Cardiovascular risk and hyperuricaemia

When to See a Doctor

Sudden hot, swollen, red joint — especially the big toe or ankle

Recurrent joint pain episodes, even if mild or self-resolving

Visible lumps near joints or on ears (possible tophi)

Severe flank pain, blood in urine, or difficulty passing urine (kidney stone symptoms)

Uric acid above 0.60 mmol/L with existing chronic kidney disease

Starting new medications known to raise uric acid (diuretics, chemotherapy)

Track Your Uric Acid Over Time

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This page is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional for diagnosis and treatment decisions.