⚠️ Above the threshold of 6.8 mg/dl (410 µmol/L), the risk of serum uric acid (UA) crystallisation increases significantly → gout, nephrolithiasis, and urate nephropathy.

ℹ️ About

💥 Hyperuricemia = elevated serum urate levels.
UA is poorly soluble → precipitates as crystals in joints (gout) and kidneys (urate stones, nephropathy).

🧬 Aetiology

⬆️ Production: Increased cell turnover (leukaemia, lymphoma, psoriasis, haemolysis).
⬇️ Excretion: CKD, diuretics, lead nephropathy, hyperparathyroidism, pre-eclampsia.
UA precipitation in renal tubules → urate nephropathy.

📏 Normal Values

👨 Men & postmenopausal women: 3.5–7.0 mg/dl (208–416 µmol/L).
👩 Premenopausal women: 2.6–5.7 mg/dl (155–339 µmol/L).

📌 Causes

💧 Renal failure.
💊 Drugs: cytotoxics, thiazides, loop diuretics, pyrazinamide.
🧬 Cell turnover: lymphoma, leukaemia, psoriasis, haemolysis.
⚡ Cell damage: rhabdomyolysis, tumour lysis syndrome.
⬇️ Excretion: CKD, gout, lead nephropathy, hyperparathyroidism.
🧩 Genetic: Lesch–Nyhan syndrome (purine metabolism defect).

👩‍⚕️ Clinical

Underlying condition-specific features (e.g. haematological malignancy, CKD).
⛏️ Renal colic from urate stones.
🦵 Acute gouty arthritis (if urate crystallises in joints).

🔎 Investigations

🧪 U&E: assess renal function, AKI/CKD.
📈 Serum urate: elevated.
🔬 Urine urate crystals possible.

💡 In ITU patients, hyperuricemia is an early marker of severe sepsis, predicting AKI, ARDS, need for ventilation, and mortality.

📖 Management (Guidelines)

🩺 ACR (2012, 2020), 3E (2014), EULAR (2016):

Start acute gout treatment within 24 hrs → colchicine p.o., NSAIDs p.o., or corticosteroids (oral or intra-articular).
Don’t stop ULT (urate-lowering therapy) if already started before a flare.
Initiate ULT (allopurinol, febuxostat, probenecid; pegloticase second-line) only after acute phase resolves unless already on it.
Start allopurinol low, titrate to minimum effective dose.
🎯 Treat to target: maintain UA < 6 mg/dl (360 µmol/L) lifelong.
Consider colchicine/NSAID prophylaxis when starting ULT.
Screen for comorbidities (HTN, CKD, diabetes, obesity, CAD).

🧪 Tumour lysis / chemotherapy: Prevent hyperuricemia with allopurinol or rasburicase.
💧 Urate-induced AKI: IV fluids ± IV furosemide to achieve good diuresis. If oliguria → haemodialysis.
💎 Renal urate stones: ~10% radiolucent, common in hot climates. Risk: acidic urine, chronic diarrhoea, ileostomy, obesity, DM, dehydration, chemo. • Hydration. • Potassium citrate/bicarbonate to raise urine pH > 6.7 → dissolves stones. • Allopurinol if recurrent.

📚 References

Pathophysiology of hyperuricemia and its clinical significance – Narrative Review

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Hyperuricaemia