Uric acid is an end product of purine catabolism; it is released as DNA and RNA are degraded by dying cells. Most uric acid is synthesized in the liver and intestinal mucosa. Two thirds is excreted by the kidneys, and one third is excreted via the GI tract.
Normal range:
Male: 2.5 " “8.0 mg/dL
Female: 1.9 " “7.5 mg/dL
Use
Monitor treatment of gout
Monitor chemotherapeutic treatment of neoplasms to avoid renal urate deposition with possible renal failure (tumor lysis syndrome)
Interpretation
Increased In
Renal failure (does not correlate with severity of kidney damage; urea and creatinine should be used)
Gout
Twenty-five percent of the relatives of patients with gout
Asymptomatic hyperuricemia (e.g., incidental finding with no evidence of gout; clinical significance is not known but people so afflicted should be rechecked periodically for gout); the higher the level of serum uric acid, the greater the likelihood of an attack of acute gouty arthritis
Increased destruction of nucleoproteins
Leukemia, multiple myeloma
Polycythemia
Lymphoma, especially postirradiation; other disseminated neoplasms
Cancer chemotherapy (e.g., nitrogen mustards, vincristine, mercaptopurine, prednisone)
Hemolytic anemia
Sickle cell anemia
Resolving pneumonia
Toxemia of pregnancy (serial determinations to follow therapeutic response and estimate prognosis)
Psoriasis (one third of patients)
Drugs (examples)
Intoxicants (e.g., barbiturates, methyl alcohol, ammonia, carbon monoxide); some patients with alcoholism
Decreased renal clearance or tubular secretion (e.g., various diuretics [thiazides, furosemide, ethacrynic acid] and all diuretics except spironolactone and ticrynafen)
Nephrotoxic effect (e.g., mitomycin C)
Low-dose salicylates (<4 g/day)
Other effects (e.g., levodopa, phenytoin sodium)
Metabolic acidosis
Diet
High-protein weight reduction diet
Excess nucleoprotein (e.g., sweetbreads, liver) may increase level ≤1 mg/dL
Alcohol consumption
Miscellaneous
von Gierke disease
Chronic lead poisoning
Lesch-Nyhan syndrome
Maple syrup urine disease
Down syndrome
Polycystic kidneys
Calcinosis universalis and circumscripta
Hypoparathyroidism
Primary hyperparathyroidism
Hypothyroidism
Sarcoidosis
Chronic berylliosis
Patients with arteriosclerosis and hypertension (serum uric acid is increased in 80% of patients with elevated serum triglycerides)
Certain population groups (e.g., Blackfoot and Pima Indians, Filipinos, New Zealand Maoris)
Most common causes in hospitalized men are azotemia, metabolic acidosis, diuretics, gout, myelolymphoproliferative disorders, other drugs, unknown causes.
It is difficult to justify therapy in asymptomatic persons with hyperuricemia to prevent gouty arthritis, uric acid stones, urate nephropathy, or risk of cardiovascular disease.
Decreased In
Drugs
ACTH
Uricosuric drugs (e.g., high doses of salicylates, probenecid, cortisone, allopurinol, coumarin)
Various other drugs (radiographic contrast agents, glyceryl guaiacolate, estrogens, phenothiazines, indomethacin)
Healthy adults with isolated defect in tubular transport of uric acid (Dalmatian dog mutation)
Decreased in approximately 5% of hospitalized patients; most common causes are postoperative state (GI surgery, coronary artery bypass), DM, various drugs, and SIADH in association with hyponatremia
A purine-rich diet (liver, kidney, sweetbread) as well as severe exercise, increases uric acid values.
Rapid degradation of uric acid occurs at room temperature in the plasma of patients with tumor lysis syndrome who are treated with rasburicase. Blood should be collected in prechilled tubes containing heparin, immediately immersed in ice water bath, centrifuged in a precooled centrifuge, and the separated plasma maintained in an ice water bath, and it should be analyzed within 4 hours of collection.