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Biomarkers

Uric acid

DEHarnsäure

Uric acid is the end product of breaking down purines in your body. Your liver makes it (via an enzyme, xanthine oxidase), and you clear it mostly through your kidneys (~70%), with the rest through the gut. When uric acid gets too high (hyperuricemia), it can crystallize. The usual threshold is above 6.8 mg/dL (404 µmol/L), the point where urate crystals can form. (Some guidelines use sex-specific cutoffs: above 6 in women, above 7 in men. And for established gout, the urate-lowering target is below 6 mg/dL / 360 µmol/L, per ACR 2020 and EULAR 2016.) Those crystals cause gout (painful joint inflammation) and urate kidney damage. Beyond gout, persistently high uric acid is linked to high blood pressure, insulin resistance, metabolic syndrome, chronic kidney disease, and heart events. Whether it causes those or just travels with them is debated; genetic (Mendelian randomization) results have been mixed. Your levels are pushed up by dietary purines (red meat, organ meat, beer, fructose) and some drugs (thiazides, low-dose aspirin, cyclosporine). And in most studies, lower uric acid goes with better metabolic health.

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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). Hyperuricemia and coronary heart disease: a systematic review and meta-analysis. *Arthritis Care & Research*doi:10.1002/acr.20065