Blood Tests for Gout
Serum urate, the critical timing rule, treatment targets, and how to interpret your results — in plain English.
The Quick Answer
Gout is the most common inflammatory arthritis in Australian adults, affecting an estimated 3-4% of people, predominantly men over 40. It is caused by deposition of monosodium urate crystals in joints and soft tissues when blood urate (uric acid) levels are persistently too high.
The key diagnostic blood test is serum urate, but there is a critical caveat: do not test during an acute flare — the result is often falsely normal and will mislead you and your doctor. Wait at least 4 weeks after the attack resolves.
High Urate Does NOT Equal Gout
Hyperuricaemia (elevated serum urate) is common — affecting around 20% of the general population — but only a minority ever experience a gout attack. Most people with a high urate level will never get gout. The crystal deposition that causes the excruciating pain of a gout attack requires a combination of high urate, local joint temperature changes, dehydration, and often a triggering event.
Conversely, urate can be normal during a gout flare (in up to 40% of cases), because inflammation temporarily drives urate from blood into the joint space. A normal urate level during a painful joint episode does NOT rule out gout. This is one of the most common sources of diagnostic confusion in primary care.
The Blood Tests — What Each One Shows
A complete gout workup is not just serum urate — it includes kidney function, metabolic markers, and a full blood count to guide treatment and exclude other conditions.
Serum Urate (Uric Acid)
Do NOT measure during an acute flare — often falsely low. Measure at least 4 weeks after the flare resolves. Above 0.40 mmol/L: crystal precipitation risk. Treatment target on allopurinol: < 0.36 mmol/L.
eGFR (Estimated Glomerular Filtration Rate)
CKD reduces uric acid excretion (kidneys handle ~70% of urate excretion). Allopurinol dose MUST be reduced in CKD. eGFR < 30: specialist input recommended before starting allopurinol.
Creatinine
Dehydration concentrates urate and is a common gout trigger — especially after illness, surgery, or a hot summer day without adequate fluid intake.
Fasting Lipid Profile
Hypertriglyceridaemia and gout are both driven by insulin resistance. Fructose (from soft drinks and fruit juice) raises both triglycerides and urate. Treating dyslipidaemia reduces overall cardiovascular risk, which is substantially elevated in gout.
Fasting Glucose and HbA1c
Insulin reduces renal urate excretion — so insulin resistance directly raises serum urate. Over 50% of people with gout have metabolic syndrome. Pre-diabetes and type 2 diabetes should be actively screened for.
Full Blood Count (FBC)
A very high white cell count during an acute flare might suggest septic arthritis (infected joint) rather than gout — which is a surgical emergency. The two can be impossible to distinguish clinically without joint aspiration.
CRP (C-Reactive Protein)
CRP is markedly elevated (often 50-200 mg/L) during a gout flare. A high CRP confirms significant inflammation but cannot differentiate gout from septic arthritis. Joint aspiration and Gram stain remain essential when septic arthritis is possible.
Joint Fluid Analysis (Synovial Fluid)
Polarised light microscopy identifies negatively birefringent needle-shaped monosodium urate crystals — pathognomonic for gout. Also excludes septic arthritis (Gram stain, culture). Joint aspiration is performed by a GP or specialist using a needle and local anaesthetic.
Interpreting Your Serum Urate Result
< 0.36 mmol/L
If on allopurinol, this is the treatment goal. If not on treatment, risk of gout is low but not zero — one single attack may still occur.
0.36–0.42 mmol/L
Above the urate solubility threshold. Gout risk increases. Lifestyle modification recommended. Urate-lowering therapy indicated after 2+ attacks or if CKD/tophi present.
0.42–0.60 mmol/L
Significant hyperuricaemia. High gout flare risk. After any confirmed gout attack, urate-lowering therapy is recommended.
> 0.60 mmol/L
Very high crystal deposition risk. Urate-lowering therapy indicated after even a single attack. Tophi and renal stones are more likely at this level.
Red Flags — When to Seek Urgent Assessment
Hot, swollen, intensely tender single joint with fever
Septic arthritis (joint infection) must be excluded — it is a medical emergency requiring joint aspiration and IV antibiotics. Gout and septic arthritis can occur simultaneously. Go to an emergency department, do not wait.
Gout in a joint other than the big toe in a young person
Unusual gout distribution (wrist, knee, multiple joints at once) in people under 30 should prompt investigation for underlying causes: myeloproliferative disorders, psoriasis, enzyme defects (Lesch-Nyhan), or medications.
Rapidly progressing tophi with worsening kidney function
Tophaceous gout with declining eGFR suggests the need for urgent rheumatology and nephrology review. Urate deposition in the kidneys can accelerate CKD.
Allopurinol rash or skin blistering
Allopurinol hypersensitivity syndrome (AHS) is a rare but potentially fatal drug reaction — blistering rash, organ failure. Stop allopurinol immediately and seek emergency care. HLA-B*5801 testing (highest risk in people of Han Chinese, Thai, or Korean descent) is recommended before starting allopurinol in these populations.
Serum urate > 0.60 mmol/L on two occasions
Very high urate significantly increases crystal deposition risk in joints, kidneys, and soft tissues. Urate-lowering therapy is indicated after even a single gout attack at this level.
The Australian Gout Management Pathway
Confirm the clinical picture
Classic gout presents as an intensely painful, red, swollen single joint (most often the first metatarsophalangeal joint — the big toe) that peaks within 24 hours and resolves within 7-10 days. Podagra (big toe gout) is so characteristic that a clinical diagnosis is often made on history and examination alone.
Measure serum urate — at the right time
Do NOT check serum urate during an acute flare — results are often falsely low. Wait at least 4 weeks after the flare has fully resolved for an accurate baseline. Ask your GP to organise the full metabolic workup (eGFR, creatinine, FBC, lipids, glucose/HbA1c) at the same time.
Consider joint aspiration for diagnostic certainty
If the diagnosis is in doubt — atypical joints, young patient, or concurrent fever — joint aspiration with polarised light microscopy is the gold standard. Most Australian GPs can perform aspiration of accessible joints (knee, ankle) or refer to a rheumatologist.
Identify and treat comorbidities
Screen for and manage metabolic syndrome components: fasting glucose/HbA1c for diabetes, lipid profile for dyslipidaemia, blood pressure, and kidney function. Review all medications for urate-raising effects (thiazide and loop diuretics, low-dose aspirin, ciclosporin, tacrolimus, pyrazinamide).
Decide on urate-lowering therapy
Australian guidelines recommend starting allopurinol for: ≥ 2 gout attacks per year, any attack with tophi, renal stones, or CKD, or serum urate > 0.60 mmol/L. Start only once the acute flare has fully resolved. Begin at 50-100 mg/day and titrate upward every 4-6 weeks.
Monitor to the urate target
Check serum urate 4-6 weeks after each allopurinol dose change. Titrate until urate is consistently below 0.36 mmol/L (below 0.30 mmol/L for tophaceous gout). Once the target is stable, annual monitoring is sufficient. Warn patients that flares may paradoxically increase in the first 6-12 months after starting allopurinol (urate mobilisation from joints) — prophylactic colchicine or low-dose NSAID during this period reduces this risk.
Lifestyle modification
Reduce dietary purines (organ meats, red meat, shellfish, beer, spirits), replace sugary drinks and fruit juice with water, limit alcohol (especially beer and spirits), and aim for a healthy body weight. Low-fat dairy products modestly lower urate. Dietary changes alone rarely achieve the urate target but improve overall metabolic health.
Treatment — Medications and Targets
Treating an acute flare
Acute gout flares are treated with anti-inflammatory medications to reduce pain and swelling: colchicine (first-line — 1.5 mg initial dose then 0.5 mg after 1 hour), NSAIDs such as naproxen or indomethacin (avoid in CKD and peptic ulcer disease), or prednisolone for those who cannot tolerate colchicine or NSAIDs. Do not start or change allopurinol during a flare — this can prolong or worsen the attack.
Allopurinol — the mainstay of prevention
Allopurinol inhibits xanthine oxidase, reducing urate production. It is PBS-subsidised in Australia. Starting dose is 50-100 mg/day (lower with CKD), titrated upward every 4-6 weeks until serum urate is below 0.36 mmol/L. Most patients require 300-600 mg/day. Many people with gout are undertreated on insufficient doses — the dose should be titrated to the target, not left at the initial starting dose.
Febuxostat — an alternative
Febuxostat (40-80 mg daily) is an alternative urate-lowering agent for patients who cannot tolerate allopurinol. It is PBS-listed for patients with allopurinol intolerance and gout. It may be slightly more effective at achieving the urate target, but there are some concerns about cardiovascular events in high-risk patients — discuss with your GP or rheumatologist.
Costs and Medicare in Australia
Gout management in Australia is well-supported by Medicare and the PBS:
Serum urate, renal function, FBC
Fully Medicare-rebatable with GP referralBulk-billed at most collection centres
Fasting lipids, glucose, HbA1c
Fully Medicare-rebatable with GP referralStandard metabolic screen, no additional cost
Allopurinol (100 mg, 300 mg)
PBS-subsidised (low co-payment)Extremely affordable long-term treatment
Colchicine (acute flares)
PBS-subsidisedRequires prescription from GP
Rheumatologist referral
Specialist consultation rebate via MedicareGP referral required; out-of-pocket gap may apply
Related Reading
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This page provides general educational information about gout and the blood tests used to investigate and monitor it. It is not a substitute for professional medical advice, diagnosis, or treatment. Always consult your GP or rheumatologist about gout management. SmarterBlood does not provide medical care.