Why we measure it

Elevated uric acid — hyperuricaemia — is best known as the cause of gout, where uric acid crystals deposit in joints, causing intensely painful inflammatory arthritis. But gout is the most visible manifestation of hyperuricaemia, not its only consequence. Beyond joints, uric acid has direct vascular and metabolic effects. At elevated concentrations, it inhibits nitric oxide production by endothelial cells, impairing vascular relaxation and driving hypertension. It activates the renin-angiotensin system, stimulates the NLRP3 inflammasome, promotes oxidative stress, and drives low-grade systemic inflammation. A prospective analysis by Fang and Alderman in JAMA (2000), following 5,926 adults from NHANES I over 16.4 years, found that elevated serum uric acid was associated with significantly increased cardiovascular mortality, independent of other risk factors. Uric acid is also closely intertwined with metabolic syndrome. Hyperuricaemia is associated with insulin resistance, visceral adiposity, dyslipidaemia, and hypertension — the components of metabolic syndrome. Fructose metabolism is a particularly direct driver: unlike glucose, fructose is metabolised in a pathway that rapidly generates uric acid. The epidemic rise in dietary fructose — particularly from high-fructose corn syrup — has been proposed as a contributor to the parallel rise in hyperuricaemia, hypertension, and metabolic syndrome over the past several decades. Kidney function is both a cause and a consequence of elevated uric acid. Impaired renal excretion raises serum urate; elevated urate reciprocally damages the kidneys, creating a self-reinforcing cycle. The cystatin-C and uACR readings in the same Pulse draw provide context for interpreting uric acid trends.

Why every 3 months

Uric acid is responsive to diet, alcohol intake, hydration status, and kidney function on a timescale of days to weeks. Fructose intake is the fastest dietary driver — a single high-fructose meal can acutely elevate uric acid within hours. Quarterly tracking allows you to see how sustained dietary patterns, body composition changes, and hydration habits are affecting uric acid over time, rather than capturing a single dietary moment. In individuals with a known tendency toward elevated uric acid, quarterly monitoring is particularly valuable because the conditions that drive it — metabolic syndrome, fructose intake, poor kidney function — are themselves tracked in the Pulse draw.

What movement means

The American College of Rheumatology defines hyperuricaemia as serum urate above 6.8 mg/dL — the crystallisation threshold at which urate becomes supersaturated in physiological fluids and begins to precipitate as monosodium urate crystals. Below this threshold, crystallisation is chemically unlikely. For individuals with gout, the ACR Guideline for the Management of Gout recommends a treat-to-target serum urate below 6.0 mg/dL to dissolve existing crystal deposits over time. These thresholds are defined by the ACR — not by Nexuses.

In the protocol