Uric Acid

Serum (preferred) or plasma

1 mL

0.7 mL (Note: This volume does not allow for repeat testing.)

Red-top tube, gel-barrier tube, or green-top (lithium heparin) tube. Do not use oxalate, EDTA, or citrate plasma.

Uric acid measurements are useful in the diagnosis and treatment of gout, renal failure, and a variety of other disorders including leukemia, psoriasis, starvation, and other wasting conditions. Patients receiving cytotoxic drugs may be monitored with uric acid measurements. Only a minority of individuals with hyperuricemia develop gout. An increased uric acid level does not necessarily translate to a diagnosis of gout.³ The therapeutic goal for uric acid-lowering therapy is to promote crystal dissolution and prevent crystal formation. This is achieved by maintaining a uric acid level <6 mg/dL.²

Elevated uric acid: Elevations of uric acid occur with increased purine synthesis, inherited metabolic disorders, excess dietary purine intake, increased nucleic acid turnover, malignancy, cytotoxic drugs, decreased excretion due to chronic renal failure, and increased renal reabsorption.

Drugs: Drugs causing increased uric acid concentration include diuretics, pyrazinamide, ethambutol, and nicotinic acid.³

Endocrine: Hypothyroidism, hypoparathyroidism, hyperparathyroidism, pseudohypoparathyroidism, diabetes insipidus of nephrogenic type, and Addison disease can cause uric acid elevation. Lead poisoning from paint, batteries, and moonshine can cause elevated uric acid.⁴ Toxemia of pregnancy, diet, weight loss, fasting, or starvation can elevate uric acid levels.⁵

Decreased uric acid: Drugs bearing a relationship to low serum uric acid levels include aspirin (high doses), x-ray contrast agents, glyceryl guaiacolate, allopurinol corticosteroids, and probenecid.⁶ Massive doses of vitamin C increase urine uric acid secretion, lowering serum uric acid.⁴ Poor dietary intake of purines and protein can decrease serum uric acid. Diabetes, Fanconi syndrome, Wilson's disease, cystinosis, galactosemia, hypophosphatemia, heavy metal poisoning, malignant neoplasms, hypereosinophilic syndrome, and Xanthinuria (deficiency of xanthine oxidase) can lower serum uric acid.^4,6,7 Hypouricemia is reported with acute intermittent porphyria and severe liver disease (especially obstructive biliary disease).⁸ Isolated defects in the tubular transport of uric acid have been associated with increased renal clearance of urate, hypouricemia, hypercalciuria, and decreased bone density.⁹

Uricase

• Male:¹

− 0 to 30 days: 3.9−7.8 mg/dL

− 1 to 6 months: 1.9−8.1 mg/dL

− 7 to 11 months: 2.0−6.5 mg/dL

− 1 to 11 years: 2.2−5.5 mg/dL

− 12 years: 2.9−7.0 mg/dL

– 13 to 17 years: 3.9–7.7 mg/dL

– 18 years and older: 3.8–8.4 mg/dL

• Female:

− 0 to 30 days: 2.7−6.5 mg/dL

− 1 to 6 months: 2.0−6.6 mg/dL

− 7 to 11 months: 2.1−5.7 mg/dL

− 1 to 5 years: 2.0−5.0 mg/dL

− 6 to 11 years: 2.4−5.6 mg/dL

– 12 to 17 years: 2.9–6.1 mg/dL

– 18 to 50 years: 2.6–6.2 mg/dL

– 51 to 70 years: 3.0–7.2 mg/dL

– 71 years and older: 3.1–7.9 mg/dL

Therapeutic target for gout patients: <6.0²

Drug effects have been summarized.¹⁰