Uric Acid

Order Code

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2233

Preferred Specimen

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Volume: 2 mL of serum

Collection Instructions:

• Collect in a Serum Separator Tube (SST).
• Allow sample to clot upright for at least 30 minutes.
• Centrifuge within 2 hours of collection.
• Store refrigerated.

ContainerType

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Serum separator tube

Alternate Specimen Requirements

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Volume: 2 mL of serum

Collection Instructions:

• Use a plain red top tube (no gel).
• Allow sample to clot upright for at least 60 minutes.
• Centrifuge and transfer serum to a plastic transport tube within 2 hours.
• Clearly label as: “Serum from plain red top tube.”
• Store refrigerated.

Minimum Volume

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Adult: 1 mL serum
Pediatric: 0.2 mL serum (does not allow for repeat or
additional testing).

Transport Temperature

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Refrigerated

Specimen Stability

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5 days room temperature; 1 week refrigerated; 6 months frozen

Methodology

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Roche COBAS enzymatic colorimetric (uricase) Note: STAT or regional laboratory testing may use different methodology and/or manufacturer

Rejection Criteria

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• Gross hemolysis

Overview

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Uric acid is an organic acid produced primarily in the liver as the end product of purine metabolism, which derives from both endogenous nucleic acid breakdown and dietary sources. Approximately:

• 75% is excreted via the kidneys
• 25% is metabolized by gut bacteria

Serum uric acid levels are influenced by:

1. Rate of hepatic production (purine degradation)
2. Renal excretion efficiency
3. Combined metabolic and renal factors

When levels exceed the solubility limit (~6.8 mg/dL), uric acid may precipitate and form crystals, leading to:

• Acute or chronic urate nephropathy
• Gout
• Nephrolithiasis (kidney stones)

Clinical Significance

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• Evaluation and monitoring of gout, especially with monoarticular joint pain (often first MTP joint)
• Assessment of renal stones
• Aid in diagnosis and monitoring of renal failure or chronic kidney disease
• Monitor patients undergoing chemotherapy or radiation (tumor lysis syndrome)
• Evaluate disorders with high nucleic acid turnover (e.g., leukemia, lymphoma, polycythemia vera)

Additional Information

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• Hyperuricemia is strongly linked with:
  • Hypertension
  • Metabolic syndrome
  • Type 2 diabetes
  • Increased cardiovascular risk, including stroke and myocardial infarction (MI)
• Asymptomatic hyperuricemia is common and may not always require treatment, but may still indicate elevated risk for chronic conditions.

Renal Manifestations of Hyperuricemia:

1. Uric Acid Nephrolithiasis:
   • 5–10% of all U.S. kidney stones
   • Triggered by low urine pH (<5–5.5)
2. Acute Uric Acid Nephropathy (UAN):
   • Rapid renal failure from urate crystal deposition
   • Often follows chemotherapy or tumor lysis
3. Chronic Urate Nephropathy:
   • Progressive renal failure
   • Requires biopsy for definitive diagnosis

Interpretative Information

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Increased Uric Acid (Hyperuricemia)

Due to Decreased Excretion (85–90% of cases)

• Chronic kidney disease
• Pre-eclampsia, eclampsia
• Lead toxicity (saturnine gout)
• Dehydration (prerenal azotemia)
• Genetic disorders (e.g., familial juvenile gouty nephropathy)
• Acidosis (lactic, diabetic, alcoholic, starvation)
• Hypothyroidism
• Hypertension
• Metabolic syndrome

Due to Increased Production

• High dietary purine intake
• Increased purine synthesis (inherited or idiopathic)
• Hematologic malignancies (e.g., leukemia, lymphoma)
• Cytotoxic therapy
• Genetic conditions:
  • Lesch-Nyhan syndrome
  • Kelley-Seegmiller syndrome
• Hemolytic and myeloproliferative disorders

Combined Mechanisms

• Alcohol use
• Excessive exercise
• High-fructose intake (especially soft drinks)
• Inherited metabolic disorders (e.g., aldolase B deficiency, G6Pase deficiency)

Drug-Induced Elevation

Numerous medications can elevate serum uric acid via metabolic or renal mechanisms. These include but are not limited to:

• Diuretics: furosemide, thiazides
• Cytotoxic agents: methotrexate, mercaptopurine
• Low-dose aspirin
• Immunosuppressants: cyclosporine
• Antibiotics: ethambutol
• Others: niacin, levodopa, propranolol, etc.

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Decreased Uric Acid (Hypouricemia)

Due to Decreased Production

• Xanthine oxidase deficiency (congenital or allopurinol-induced)
• PNP deficiency (Purine nucleoside phosphorylase)
• Liver failure
• Poor dietary intake (low purine/protein)

Due to Increased Excretion

• Genetic defects (e.g., familial renal hypouricemia)
• Fanconi syndrome
• SIADH or cerebral salt-wasting
• Hodgkin lymphoma

Drug-Induced Decrease

Numerous agents can reduce serum uric acid by increasing renal excretion or reducing production:

• Allopurinol
• High-dose aspirin
• Vitamin C (high doses)
• Probenecid
• Steroids
• Cefotaxime
• Methotrexate
• Verapamil, spironolactone, and many others

References

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Test Setup Days

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Monday through Friday PM shift

CPT

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84550 LOINC: 3084-1

CPT

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MALE:
AGE 0-10 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
>=16 YEARS: 3.7-8.0 MG/DL
FEMALE:
AGE 0-1 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
>=13 YEARS: 2.7-6.1 MG/DL