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Interpretive Handbook

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Test 8440:
Uric Acid, Serum

Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test

Uric acid is the final product of purine metabolism in humans. Purines, compounds that are vital components of nucleic acids and coenzymes, may be synthesized in the body or they may be obtained by ingesting foods rich in nucleic material (eg, liver, sweetbreads, etc.). Approximately 75% of the uric acid excreted is lost in the urine; most of the remainder is secreted into the gastrointestinal tract, where it is degraded to allantoin and other compounds by bacterial enzymes.

 

Asymptomatic hyperuricemia is frequently detected through biochemical screening.  The major causes of hyperuricemia are increased purine synthesis, inherited metabolic disorder, excess dietary purine intake, increased nucleic acid turnover, malignancy, cytotoxic drugs, and decreased excretion due to chronic renal failure or increased renal reabsorption. Long-term follow-up of these patients is undertaken because many are at risk of renal disease that may develop; few of these patients ever develop the clinical syndrome of gout.

 

Hypouricemia, often defined as serum urate less than 2.0 mg/dL, is much less common than hyperuricemia. It may be secondary to severe hepatocellular disease with reduced purine synthesis; defective renal tubular reabsorption; overtreatment of hyperuricemia with allopurinol and well as some cancer therapies (eg, 6-mercaptopurine).

 

Useful For Suggests clinical disorders or settings where the test may be helpful

Uric acid measurements are used in the diagnosis and treatment of renal failure and monitoring patients receiving cytotoxic drugs and a variety of other disorders, including gout, leukemia, psoriasis, starvation and other wasting conditions.

Interpretation Provides information to assist in interpretation of the test results

Hyperuricemia is most commonly defined by serum or plasma uric acid concentrations >8.0 mg/dL in males or >6.1 mg/dL in females.

Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances

The following drugs cause interference (falsely decreased levels) at the therapeutic concentrations: a-methyldopa, desferoxamine and calcimdobesilate.

Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.

Males

1-10 years: 2.4-5.4 mg/dL

11 years: 2.7-5.9 mg/dL

12 years: 3.1-6.4 mg/dL

13 years: 3.4-6.9 mg/dL

14 years: 3.7-7.4 mg/dL

15 years: 4.0-7.8 mg/dL

> or =16 years: 3.7-8.0 mg/dL

Reference values have not been established for patients that are less than 12 months of age.

Females

1 year: 2.1-4.9 mg/dL

2 years: 2.1-5.0 mg/dL

3 years: 2.2-5.1 mg/dL

4 years: 2.3-5.2 mg/dL

5 years: 2.3-5.3 mg/dL

6 years: 2.3-5.4 mg/dL

7-8 years: 2.3-5.5 mg/dL

9-10 years: 2.3-5.7 mg/dL

11 years: 2.3-5.8 mg/dL

12 years: 2.3-5.9 mg/dL

> or =13 years:  2.7-6.1 mg/dL

Reference values have not been established for patients that are less than 12 months of age.

Clinical References Provides recommendations for further in-depth reading of a clinical nature

Tietz Textbook of Clinical Chemistry. 4th edition, Edited by CA Burtis, ER Ashwood, WS Bruns. W.B. Saunders Company, Philadelphia, 2006;24:803-807