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Introduction ⬇

Uric acid is formed from the breakdown of nucleonic acids and is an end product of purine metabolism. Uric acid is transported by the plasma from the liver to the kidney, where it is filtered and where about 70% is excreted. The remainder of uric acid is excreted into the GI tract and degraded. A lack of the enzyme uricase allows this poorly soluble substance to accumulate in body fluids.

The basis for this test is that an overproduction of uric acids occurs when there is excessive cell breakdown and catabolism of nucleonic acids (as in gout), excessive production and destruction of cells (as in leukemia), or an inability to excrete the substance produced (as in kidney disease). Measurement of uric acid is used most commonly in the evaluation of kidney disease, gout, and leukemia. In hospitalized patients, acute kidney injury is the most common cause of elevated uric acid levels, and gout is the least common cause.

Normal Findings ⬆ ⬇

Men: 3.4–7.0 mg/dL or 202–416 μmol/L

Women: 2.4–6.0 mg/dL or 143–357 μmol/L

Children: 2.0–5.5 mg/dL or 119–327 μmol/L

Procedure ⬆ ⬇

  1. Obtain a 5-mL venous blood sample. Serum is preferred; heparinized blood is acceptable. Label the specimen with the patient’s name, date and time of collection, and test(s) ordered. Place the specimen in a biohazard bag.

  2. Observe standard precautions.

Clinical Implications ⬆ ⬇

  1. Elevated uric acid levels (hyperuricemia) occur in the following conditions:

    1. Gout (the amount of increase is not directly related to the severity of the disease)

    2. Kidney diseases and acute kidney injury, prerenal azotemia

    3. Alcoholism (ethanol consumption)

    4. Down syndrome

    5. Lead poisoning

    6. Leukemia, multiple myeloma, lymphoma

    7. Lesch–Nyhan syndrome (hereditary gout)

    8. Starvation, weight loss diets

    9. Metabolic acidosis, diabetic ketoacidosis

    10. Toxemia of pregnancy (serial determination to follow therapy)

    11. Liver disease

    12. Hyperlipidemia, obesity

    13. Hypoparathyroidism, hypothyroidism

    14. Hemolytic anemia, sickle cell anemia

    15. Following excessive cell destruction, as in chemotherapy and radiation treatment (acute elevation sometimes follows treatment)

    16. Psoriasis

    17. Glycogen storage disease (G-6-PD deficiency)

  2. Decreased levels of uric acid occur in the following conditions:

    1. Fanconi syndrome (disease of the proximal renal tubules)

    2. Wilson disease (autosomal recessive disorder resulting in the accumulation of copper in tissues)

    3. SIADH

    4. Some malignancies (e.g., Hodgkin disease, multiple myeloma)

    5. Xanthinuria (deficiency of xanthine oxidase)

Interventions ⬆ ⬇

Pretest Patient Care

  1. Advise the patient of test purpose and blood-drawing procedure; fasting is preferred.

  2. Promote relaxation; avoid strenuous exercise.

  3. Follow guidelines in Chapter 1 for safe, effective, informed pretest care.

Posttest Patient Care

  1. Have the patient resume normal activities.

  2. Review test results and monitor appropriately for renal failure, gout, or leukemia. Uric acid level should fall in patients who are treated with uricosuric drugs such as allopurinol, probenecid, and sulfinpyrazone. Modify the nursing care plan as needed.

  3. Follow guidelines in Chapter 1 for safe, effective, informed posttest care.

Clinical Alert

  1. Monitor uric acid levels during treatment of leukemia.

  2. Acute, dangerous levels may occur following administration of cytotoxic drugs.

Interfering Factors ⬆

  1. Stress and strenuous exercise will falsely elevate uric acid.

  2. Many drugs cause increase or decrease of uric acid (see Appendix E).

  3. Purine-rich diet (e.g., liver, kidney, sweetbreads) increases uric acid levels.

  4. High levels of aspirin decrease uric acid levels.

  5. Low purine intake, coffee, and tea decrease uric acid levels.