Uric Acid, Serum
Uric Acid, Serum
    
Number
001057
CPT
84550
Synonyms
UA ; Uric A
Specimen
Serum
Volume
1 mL
Minimum Volume
0.5 mL
Container
Red-top tube or gel-barrier tube
Collection
Separate serum from cells within 45 minutes of collection.
Storage Instructions
Maintain specimen at room temperature.
Patient Preparation
At least 4-hour fast preferred
Causes for Rejection
Improper labeling
Use
An increased uric acid level does not necessarily translate to a diagnosis of gout; about 10% to 15% of instances of hyperuricemia are caused by gout.1,2 The overlap between uric acid levels in those with and without gout is shown in a study in which the lowest level in a gouty subject was 6 mg/dL, while the highest uric acid in a nongouty person was 9.5 mg/dL.3

Elevations of uric acid occur in renal diseases with renal failure4 and prerenal azotemia (eg, dehydration) as well as gout.2 Other drugs causing increased uric acid concentration include diuretics,2,4 pyrazinamide, ethambutol, nicotinic acid, and aspirin in low doses.

Excessive cell destruction: neoplasia, even before as well as following chemotherapy and radiation therapy, especially lymphoma and leukemia; hemolytic anemia, resolving pneumonia and other inflammation; polycythemia,2 myeloma, pernicious anemia, infectious mononucleosis, congestive heart failure, large myocardial infarct.

Endocrine: hypothyroidism, hypoparathyroidism, hyperparathyroidism, pseudohypoparathyroidism; diabetes insipidus of nephrogenic type, Addison disease.

Lead poisoning (saturnine gout) from paint, batteries, and moonshine.5 A causal relationship between plumbism and gout was recognized before 1876. Gout as a common complication of subclinical lead poisoning is described among the Roman aristocracy.6

Acidosis: lactic acidosis, diabetic ketoacidosis, recent alcohol ingestion,1,7 alcoholic ketosis.3 Shock and hypoxia relate to hyperuricemia. Attention has been directed at the cause of hyperuricemia in the intensive care unit; severely increased uric acid levels in acutely ill patients is explained by degradation of ATP with degradation of accumulated nucleotides to purine metabolites, uric acid among them. Such ATP degradation may occur with strenuous exercise and the adult respiratory distress syndrome. With metabolism of ethanol to acetyl CoA, the degradation of ATP explains the hyperuricemia of alcohol use. Hyperuricemia becomes then a marker for cell injury crisis.8

Toxemia of pregnancy, diet, weight loss, fasting or starvation. Decreased urate clearance: cyclosporine-induced hyperuricemia.9

Triglyceride increase bears an association with hyperuricemia, as do diabetes mellitus and obesity.2 Hyperuricemia bears an association with obesity, hypertension2 and statistical association with myocardial infarct.

Hereditary gout: Lesch-Nyhan (X-linked) with deficiency of hypoxanthine-guanine phosphoribosyltransferase. Gout with partial absence HPRT. Increased 5-phosphoribosyl-1-pyrophosphate synthetase. Glycogen storage disease type I.8

Only a minority of individuals with hyperuricemia develop gout.

Three types of kidney disease are caused by precipitation: acute uric acid nephropathy, nephrolithiasis, and chronic urate nephropathy.10

Hyperuricemia in early essential hypertension correlates with renal vascular resistance and inversely with renal blood flow. Increased serum uric acid may indicate renal involvement.11,12

Low uric acid: Drugs: In two-thirds of Ramsdell's and Kelley's series of hypouricemic patients, drugs apparently bearing a relationship to low serum uric acid levels included aspirin (high doses), x-ray contrast agents, glyceryl guaiacolate or allopurinol.13 Corticosteroids and probenecid cause low uric. Massive doses of vitamin C are uricosuric.5

Poor dietary intake of purines and protein; tea, coffee.

Renal tubular defects, Fanconi syndrome, late in Wilson disease, outdated tetracycline,13 cystinosis, galactosemia,5 hypophosphatemia,14 heavy metal poisoning, malignant neoplasms, and hypereosinophilic syndrome.15

Xanthinuria (deficiency of xanthine oxidase).13,16

Hypouricemia is reported with acute intermittent porphyria,13 severe liver disease (especially obstructive biliary disease)13 and as an isolated defect in the tubular transport of uric acid. It has been associated with increased renal clearance of urate, hypercalciuria, and decreased bone density.14

Diabetes.17

With hyponatremia, serum hypo-osmolarity: Beck has described low uric acid with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH): 16 of 17 patients with this syndrome were hypouricemic, with serum urate ≤4.0 mg/dL. All 13 patients with other causes of hyponatremia had serum urate ≥5.0 mg/dL.18 Volume expansion, as with SIADH, causes decreased uric acid. The combination of low uric and low Na+ may also be found in instances of liver disease and was anticipated with ticrynafen.14

Azlocillin is reported to cause decrease of serum uric acid levels.19 Drug effects on uric acid metabolism are published in tabular form.20,21

Idiopathic hypouricemia commonly is transient.14 Familial hypouricemia has been described.

Methodology
Uricase
Additional Information
Drug effects have been summarized.22
Footnotes
  1. Rock RC, Walker WG, and Jennings CD, “Nitrogen Metabolites and Renal Function,” Textbook of Clinical Chemistry, Tietz NW, ed, Philadelphia, PA: WB Saunders Co, 1986, 1254-1316.
  2. Messerli FH, Frohlich ED, Dreslinski GR, et al, “Serum Uric Acid in Essential Hypertension: An Indicator of Renal Vascular Involvement,” Ann Intern Med, 1980, 93(6):817-21.
  3. Seegmiller JE, Laster L, and Howell RR, “Biochemistry of Uric Acid and its Relation to Gout,” N Engl J Med, 1983, 268:712-6.
  4. Langford HG, Blaufox MD, Borhani NO, et al, “Is Thiazide-Produced Uric Acid Elevation Harmful? Analysis of Data From the Hypertension Detection and Follow-Up Program,” Arch Intern Med, 1987, 147(4):645-9.
  5. Cameron JS and Simmonds HA, “Uric Acid, Gout and the Kidney,” J Clin Pathol, 1981, 34(11):1245-54.
  6. Nriagu JO, “Saturnine Gout Among Roman Aristocrats. Did Lead Poisoning Contribute to the Fall of the Empire?” N Engl J Med, 1983, 308(11):660-3.
  7. Faller J and Fox IH, “Ethanol-Induced Hyperuricemia: Evidence for Increased Urate Production by Activation of Adenine Nucleotide Turnover,” N Engl J Med, 1982, 307(26):1598-1602.
  8. Fox IH, Palella TD, and Kelley WN, “Hyperuricemia: A Marker for Cell Energy Crisis,” N Engl J Med, 1987, 317(2):111-2.
  9. Lin HY, Rocker LL, McQuillan MA, et al, “Cyclosporine-Induced Hyperuricemia and Gout,” N Engl J Med, 1989, 321(5):287-92.
  10. Dykman D and Simon EE, “Hyperuricemia and Uric Acid Nephropathy,” Arch Intern Med, 1987, 147(7):1341-5.
  11. Larson AW and Strong CG, “Initial Assessment of the Patient With Hypertension,” Mayo Clin Proc, 1989, 64(12):1533-42.
  12. Nunez BD, Frohlich ED, Garavaglia GE, et al, “Serum Uric Acid in Renovascular Hypertension: Reduction Following Surgical Correction,” Am J Med Sci, 1987, 294(6):419-22.
  13. Ramsdell CM and Kelley WN, “The Clinical Significance of Hypouricemia,” Ann Intern Med, 1973, 78(2):239-42.
  14. Steele TH, “Hypouricemia,” N Engl J Med, 1979, 301(10):549-50 (editorial).
  15. Lugassy G and Michaeli J, “Hypouricemia in the Hypereosinophilic Syndrome. Response to Treatment,” JAMA, 1983, 250(7):937-8.
  16. Pollard A, “Disorders of Purine and Pyrimidine Metabolism,” Applied Biochemistry of Clinical Disorders, Gornall AG, ed, Hagerstown, MD: Harper & Row Publishers, 1980, 335-44.
  17. Shichiri M, Iwamoto H, and Shiigai T, “Diabetic Renal Hypouricemia,” Arch Intern Med, 1987, 147(2):225-8.
  18. Beck LH, “Hypouricemia in the Syndrome of Inappropriate Secretion of Antidiuretic Hormone,” N Engl J Med, 1979, 301(10):528-30.
  19. Ernst JA and Sy ER, “Effect of Azlocillin on Uric Acid Levels in Serum,” Antimicrob Agents Chemother, 1983, 24(4):609-10.
  20. German DC and Holmes EW, “Gout and Hyperuricemia: Diagnosis and Management,” Hosp Pract [Off Ed], 1986, 21(11):119-26, 131-2.
  21. German DC and Holmes EW, “Hyperuricemia and Gout,” Med Clin North Am, 1986, 70(2):419-36 (review).
  22. Zhiri A and Jouanel P, “Urates,” Drug Effects on Laboratory Test Results Analytical Interferences and Pharmacological Effects, Siest G and Galteau MM, eds, Littleton, MA: PSG Publishing Co, Inc, 1988, 423-38

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