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Biomarkers

Uric acid

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Uric acid is the final catabolic product of purine metabolism in humans, produced mainly in the liver by xanthine oxidase and excreted predominantly by the kidney (~70%) with the remainder through the gut. Hyperuricemia (typically defined as serum uric acid >6.8 mg/dL or >404 µmol/L — the saturation threshold above which monosodium urate crystals can form; some guidelines use sex-specific cut-offs of >6 mg/dL in women and >7 mg/dL in men, while 6 mg/dL / 360 µmol/L is the urate-lowering treatment target in established gout) is the prerequisite for monosodium urate crystal deposition, which causes gout arthritis and urate nephropathy. Beyond gout, persistently elevated uric acid is epidemiologically associated with hypertension, insulin resistance, metabolic syndrome, chronic kidney disease, and cardiovascular events; whether these associations are causal or confounded is debated, as Mendelian randomization results have been inconsistent. Uricosuria and renal tubular handling are strongly influenced by dietary purines (red meat, organ meat, beer, fructose) and medications (thiazides, low-dose aspirin, cyclosporine), and lower serum levels are associated with better metabolic health in most population studies.

Sources

  1. Alderman MH, Cohen H, Madhavan S, Kivlighn S. (1999). Serum uric acid and cardiovascular events in successfully treated hypertensive patients. *Hypertension*doi:10.1161/01.HYP.34.1.144
  2. Kim SY, Guevara JP, Kim KM, Choi HK, Heitjan DF, Albert DA. (2010). Uric acid and cardiovascular risk: a systematic review and meta-analysis of prospective studies. *Arthritis & Rheumatism*doi:10.1002/art.27592