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Uric Acid 

  • Author: Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP; Chief Editor: Eric B Staros, MD  more...
 
Updated: Jan 16, 2014
 

Reference Range

The final breakdown product of purine catabolism in humans is uric acid. The liver and intestinal mucosa produce most of the uric acid. The kidneys eliminate two thirds of the uric acid, with the GI tract excreting the other one third. Uric has a pKa of 5.75 and 10.3 and thus is a weak acid. The ionized forms of uric acid, urates, are present in synovial fluid and in plasma; approximately 98% exists as monosodium urate, with a pH of 7.4.[1]

The reference ranges for uric acid are as follows:

  • Men: 2.5-8 mg/dL
  • Women: 1.9–7.5 mg/dL [2]

Serum urate concentrations in most children range from 3-4 mg/dL. During male puberty, levels begin to rise. Female levels remain low until menopause. Adult men have mean serum urate values of 6.8 mg/dL, and premenopausal women have mean serum urate values of 6 mg/dL. Values for women increase after menopause and approximate those of men. Throughout adulthood, concentrations rise steadily and can vary with height, blood pressure, body weight, renal function, and alcohol intake.[3]

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Interpretation

Elevated uric acid levels can be seen in the following:

  • Destruction of massive amounts of nucleoproteins (leukemia, anemia, chemotherapy, toxemia of pregnancy, psoriasis, sickle cell anemia, hemolytic anemia, polycythemia, resulting pneumonia)
  • Drugs (especially diuretics, barbiturates)
  • Chronic kidney disease
  • Parathyroid diseases
  • Low-dose salicylates
  • Metabolic acidosis
  • Diet (high-protein weight-reducing diet, alcohol, liver, and sweetbread)
  • Chronic lead poisoning
  • Polycystic kidney disease
  • Lesch-Nyhan syndrome
  • von Gierke disease
  • Chronic berylliosis [2]

Decreased uric acid levels can be seen in the following:

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Collection and Panels

Tiger top or Red-Top tube

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Background

Description

The final breakdown product of purine catabolism in humans is uric acid. The liver and intestinal mucosa produce most of the uric acid. The kidneys eliminate two thirds of the uric acid, with the GI tract excreting the other one third. Uric has a pKa of 5.75 and 10.3 and thus is a weak acid. The ionized forms of uric acid, urates, are present in synovial fluid and in plasma; approximately 98% exists as monosodium urate, with a pH of 7.4.[1]

In hospitalized patients, the most common causes of uric acid elevation are azotemia, metabolic acidosis, gout, diuretic use, and myelolymphoproliferative diseases.

Approximately 80% of patients with elevated serum triglyceride levels also have increased serum uric acid levels. Various ethnic groups, such as Pima Indians, Blackfoot Indians, New Zealand Maoris, and Filipinos, have increased serum uric acid levels.

About 5% of hospitalized patients have decreased serum uric acid levels, with a postoperative state, diabetes mellitus, drugs, and SIADH being the most common causes.[2]

Indications

Indications are as follows:

  • To monitor gout treatment
  • To monitor chemotherapeutic treatment of neoplasms to avoid renal urate deposition and possible renal failure [2]

Considerations

One end product of nucleoprotein metabolism is uric acid, which is excreted in the urine. Hyperuricemia (plasma urate concentration >6.8 mg/dL) can result from decreased elimination or uric acid, increased formation of uric acid, or a combination of these processes. In general, hyperuricemia is present in 2-13.2% of ambulatory adults and is even more common in hospitalized patients.

Urate levels correlate with the risk developing gouty arthritis or urolithiasis. Chronically elevated urine uric acid levels predispose some individuals to develop urolithiasis, gouty arthritis, and renal dysfunction. Because pure uric acid urinary stones typically are radiolucent, they may not be detected with plain abdominal radiography but can be detected with noncontrast CT scanning.

Uric acid levels are affected by age, sex, and renal function.

Of note, one study found that serum uric acid values are a poor predictor of maternal and fetal complications in women with preeclampsia.[4]

Factors that partly account for an increased prevalence of gout and hyperuricemia in African and Asian countries include alcohol consumption, obesity, and hypertension; however, prevalence is also influenced by genetic factors.[5]

One mechanism by which alcohol is associated with hyperuricemia is that it increases adenine nucleotide breakdown and increases lactate levels in the blood.

With regard to plasma uric acid levels, purines also contribute to an increase in plasma uric acid in beer drinkers. Further, dehydration and alcoholic ketoacidosis lead to increases in serum uric acid levels. By accelerating adenine nucleotide breakdown and possibly weakly inhibiting xanthine dehydrogenase activity, ethanol also raises plasma concentrations and urinary excretion of hypoxanthine and xanthine.[6]

Experimental evidence in rats has shown that hyperuricemia can increase systemic blood pressure, renal dysfunction, progressive renal scarring, proteinuria, and vascular disease. Evidence supports the idea that hyperuricemia may be a key mechanism for activation of the renin-angiotensin and cyclooxygenase-2 (COX-2) systems in progressive renal disease.[7]

Whether uric acid acts as an independent risk factor for heart disease is controversial. However, data have elucidated important information on the complex relationships between hyperuricemia, gout, and comorbid conditions, particularly the association of serum urate levels with cardiovascular morbidity and mortality.[8]

Limitations

Limitations of uric acid testing are as follows:

  • Methodological interference and in cases of vitamin C, levodopa, and alpha-methyldopa
  • Early purine-rich diet (eg, liver, kidney, sweetbread)
  • Severe exercise increases uric acid level
  • Rapid degradation of uric acid, which occurs at room temperature in the plasma of patients with tumor lysis syndrome treated with rasburicase (Blood should be collected in prechilled tubes containing heparin, and it should be immediately immersed in an ice-water bath and centrifuged in a precooled centrifuge. The separated plasma should then be maintained in an ice-water bath and analyzed within 4 hours of collection.)
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Contributor Information and Disclosures
Author

Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP Associate Professor of Medicine, St Louis University School of Medicine

Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP is a member of the following medical societies: American College of Physicians, American Medical Informatics Association, Royal College of Physicians and Surgeons of Glasgow, Royal College of Surgeons of Edinburgh, Healthcare Information and Management Systems Society

Disclosure: Nothing to disclose.

Chief Editor

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

References
  1. Gomella L, Haist S. Laboratory Diagnosis: Chemistry, Immunology, Serology. Clinician's Pocket Reference: The Scut Monkey. 11th ed. New York, NY: McGraw-Hill; 2007.

  2. Williamson MA, Snyder LM, Wallach JB. Wallach's Interpretation of Diagnostic Tests. 9th ed. Philadelphia, Pa: Wolters Kluwer/Lippincott Williams & Wilkins Health; 2011.

  3. Burns CM, Wortman RL. Disorders of Purine and Pyrimidine Metabolism. Longo D, Fauci A, Kasper D, Hauser S, Jameson J, Loscalzo J, eds. Harrison's Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. Chapter 359.

  4. Thangaratinam S, Ismail KM, Sharp S, Coomarasamy A, Khan KS. Accuracy of serum uric acid in predicting complications of pre-eclampsia: a systematic review. BJOG. 2006 Apr. 113(4):369-78. [Medline].

  5. Wortmann RL. Gout and hyperuricemia. Curr Opin Rheumatol. 2002 May. 14(3):281-6. [Medline].

  6. Yamamoto T, Moriwaki Y, Takahashi S. Effect of ethanol on metabolism of purine bases (hypoxanthine, xanthine, and uric acid). Clin Chim Acta. 2005 Jun. 356(1-2):35-57. [Medline].

  7. Kang DH, Nakagawa T. Uric acid and chronic renal disease: possible implication of hyperuricemia on progression of renal disease. Semin Nephrol. 2005 Jan. 25(1):43-9. [Medline].

  8. Mikuls TR, Saag KG. New insights into gout epidemiology. Curr Opin Rheumatol. 2006 Mar. 18(2):199-203. [Medline].

 
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