uric acid in 24 hour urine

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[1][2][3][4][5][6][7][8]

Introduction

urine creatinine is also obtained for comparison (ratio)

Indications

Reference interval

Principle

Uric acid is the major product of purine catabolism in man & the anthropoid apes & is formed from xanthine by the action of xanthine oxidase. The average adult has a total body content of about 1.2 g of uric acid, which may be considered to be a miscible pool with high turnover. Uric acid in this pool is derived from three sources: (1) catabolism of ingested nucleoproteins, (2) catabolism of endogenous nucleoproteins, & (3) direct transformation of endogenous purine nucleotides. Approximately 60% of this pool is replaced daily by concomitant formation & excretion. Most uric acid formation occurs in the liver, which has a high activity of xanthine oxidase, as does the intestinal mucosa.

In the ACA methodology, uric acid, which absorbs light at 293 nm, is converted by uricase to allantoin, which is nonabsorbing at 293 nm. The change in absorbance at 293 nm due to the disappearance of uric acid over a 17.07-second measurement period is directly proportional to the concentration of uric acid in the serum.

Clinical significance

Gout: A 40% decrease in urinary uric acid excretion occurs at all serum levels of uric acid in patients with gout.

Renal disease associated with hyperuricemia may take one or more of several forms: (1) gouty nephropathy with urate deposition in renal parenchyma, (2) acute intratubular deposition of urate crystals, & (3) urate nephrolithiasis. Quantitation of urinary uric acid excretion is an aid in selecting appropriate treatment for asymptomatic hyperuricemia. Measurement of both urine pH & uric acid excretion are important in the investigation of uric acid urolithiasis.

Causes of hypouricemia are relatively few. Renal tubular reabsoption defects, either congenital, as in Fanconi syndrome & Wilson's disease, or acquired, particularly through toxic damage, can cause increased urinary loss of urate & low plasma levels. Hypouricemia may be secondary to defective renal tubular reabsoprtion of uric acid.

Increases

Decreases

Specimen

2 mL aliquot of a 24-hour urine collection. Proper 24 hour urine collection procedure should be followed, & collection container should contain 10 mL of 5% NaOH as a preservative. Upon receipt in the work area, it should be well-mixed & measured in a graduated cylinder. The total volume should be recorded. Dilute well mixed urine 1:3 with ACA Purified Water. Multiply results by 3.

More general terms

Additional terms

References

  1. ↑ Teitz, Norbert W., Textbook of Clinical Chemistry, W.B. Saunders, Company, Philadelphis, PA 1986, pp.1284-1287.
  2. ↑ Kaplan, Lawrence A. & Pesce, Amadeo J., Clinical Chemistry: Theory, Analysis, & Correlation, 2nd Edition, The C.V. Mosby Company, St. Louis, MO, 1989, pp. 1024-1026.
  3. ↑ Henry, John Bernard, M.D., Clinical Diagnosis & Management by Laboratory Methods, 18th Edition, W.B. Saunders Company, Philadelphia, PA, 1991, pp. 143-146.
  4. ↑ ACA IV Discrete Clinical Chemistry Analyzer Instrument Manual, Volume 3A, Chapter 6: Test Methodology, URCA 24
  5. ↑ Medline Plus: Uric acid - urine http://www.nlm.nih.gov/medlineplus/ency/article/003616.htm
  6. ↑ Panel of 7 tests Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0020481.jsp
  7. ↑ Panel of 29 tests Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0020805.jsp
  8. ↑ Panel of 13 tests Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0020843.jsp
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