Lab Test: Uric Acid (Serum) Level
- Measurement of uric acid in serum for the evaluation of nucleoprotein metabolism or kidney disease
- Adult males: 2.5-8 mg/dL (150-480 micromol/L)
- Adult females: 1.5-6 mg/dL (90-360 micromol/L) *(PDR)
- Male: 4.0-8.5 mg/dL (0.24-0.51 mmol/L)
- Female: 2.7-7.3 mg/dL (0.16-0.43 mmol/L)
- Elderly: Values may be slightly increased
- Child: 2.5-5.5 mg/dL (0.12-0.32 mmol/L)
- Newborn: 2.0-6.2 mg/dL
- Physiologic saturation threshold: >6 mg/dL (>0.357 mmol/L)
- Therapeutic target for gout: <6 mg/dL (<0.357 mmol/L)
- Critical Values: >12 mg/dL
- Tumor lysis syndrome - cell breakdown is the major source of increased uric acid levels. Increased uric acid levels may also result from increased production or decreased excretion of uric acid, or both.
- Diagnosis and monitoring of tumor lysis syndrome - hyperuricemia results from the release of purine nucleic acids that metabolize into uric acid after spontaneous or cytotoxic therapy-induced lysis. This causes rapid increases in plasma and renal tubular concentrations. Uric acid nephropathy should be suspected when the uric acid:creatinine ratio is >1.
- In TLS, a uric acid level >9 mg/dL is treated with hydration, allopurinol and alkalinization of the urine. Dialysis should be considered for a uric acid level >10 mg/dL.
- Gout related to suspected hyperuricemia - hyperuricemia does not establish the diagnosis of gout; however, as uric acid levels rise above 600 micromol/L, the risk for developing gout also rises. Approximately 80% to 90% of persons with a serum uric acid level >9 mg/dL (uricase method) develop gout, although the degree of elevation does not necessarily correlate with disease severity. Hyperuricemia in gout patients increases the risk of kidney stones.
- In patients with hyperuricemia a 24-hour uric acid excretion of >800 mg indicates overproduction; a 24-hour uric acid excretion of <600 mg indicates hypoexcretion, possibly due to renal tubular defect. In the presence of hyperuricemia, even normal uric acid excretion is evidence of hypoexcretion of the increased urate load, which is filtered at the glomerulus.
- Kidney stone related to suspected hyperuricemia - most patients with increased serum uric acid levels are asymptomatic and do not have renal calculi; however, hyperuricemia increases the risk of developing kidney stones, often in association with gouty arthritis. Increased serum uric acid levels are seen in some patients with nephrolithiasis. Increased serum uric acid levels can be caused by increased dietary intake of purines, increase in uric acid production, or decrease in excretion.
- Leukemia - aggressive hematologic malignancies, including leukemia, may be associated with increased uric acid production resulting in hyperuricemia (values >7 mg/dL).
- Suspected heat stroke - hyperuricemia is common in heat stroke and may contribute to renal dysfunction.
- Suspected hyponatremia - uric acid levels may be useful in the differential diagnosis of hyponatremia. An increased serum uric acid level (> 0.3 mmol/L) may be suggestive of hypovolemic hyponatremia.
- Decreased uric acid levels (<0.24 mmol/L) are commonly seen in patients with SIADH.
- Suspected or known hypertensive disorder - hyperuricemia is typically defined as serum uric acid levels (SUA) >6.5 mg/dL or >7 mg/dL in men and >6 mg/dL in women.
- An SUA level >5.5 mg/dL in an adolescent with otherwise unexplained hypertension and normal renal function strongly suggests primary hypertension and tends to rule out white-coat hypertension or secondary hypertension.
- Although the SUA level is likely to increase, gout is uncommon in patients receiving ≤50 mg/day of hydrochlorothiazide or ≤25 mg/day of chlorthalidone.
- Methods to reduce high SUA levels include decreasing or eliminating the diuretic dose, or adding losartan (an angiotensin receptor blocker) because it attenuates the diuretic-induced increase in SUA levels compared with a beta-blocker.
- Suspected pregnancy-induced hypertension - in women with chronic hypertension, increased uric acid levels may be helpful in identifying those with increased likelihood of developing superimposed preeclampsia, and may precede the signs and symptoms of the disease.
- Increased uric acid level precedes the onset of heavy proteinuria (>5 g/24 hours) in pregnancies complicated by preeclampsia.
- Hyperuricemia reflects renal retention of urate and correlates with renal histologic changes; however, this finding in itself does not constitute an indication for delivery.
- Suspected rhabdomyolysis - skeletal muscle injury leads to an overproduction of uric acid with subsequent hyperuricemia, especially in the patient with exertional rhabdomyolysis.
- Kidney failure - can cause hyperuricemia due to decreased excretion of uric acid.
- Catabolic enzyme deficiency - results in overproduction of uric acid due to the stimulation of purine metabolism.
- Increased levels (hyperuricemia) may indicate:
- Increased production of uric acid:
- Increased ingestion of purines, genetic inborn error in purine metabolism, metastatic cancer, multiple myeloma, leukemia, lymphoma, cancer chemotherapy, hemolysis, or rhabdomyolysis (e.g., heavy exercise, burns, crush injury, epileptic seizure, myocardial infarction)
- Decreased excretion of uric acid:
- Idiopathic, chronic renal disease, acidosis (ketotic [diabetic or starvation] or lactic), hypothyroidism, toxemia of pregnancy, hyperlipoproteinemia, alcoholism, or shock or chronic blood volume depletion states
- Decreased levels may indicate:
- Wilson disease, Fanconi syndrome, lead poisoning, or yellow atrophy of liver
- Uric acid, urine - used in the evaluation of patients with nephrolithiasis
- Arthritis panel
- Bone and joint panel
- General health panel
- Prenatal screening panel
- Stress may cause increased uric acid levels.
- X-ray contrast agents increase uric acid excretion and may cause decreased levels.
- High-protein infusion (especially glycine), as in total parental nutrition, may cause increased uric acid, which is a breakdown product of glycine.
- Drugs that may cause increased levels include: alcohol ascorbic acid, aspirin (low dose), caffeine, cisplatin, diazoxide, epinephrine, ethambutol, levodopa, methyldopa (Aldomet), nicotinic acid, phenothiazines, and theophylline.
- Drugs hat may cause decreased levels include: allopurinol, aspirin (high dose), azathioprine (Imuran), clofibrate, corticosteroids, diuretics, estrogens, glucose infusions, guaifenesin, mannitol, probenecid, and warfarin.
- Follow the institution's requirements regarding fasting. (Some recommend that the patient fast.)
- Collect a venous blood sample.
- Apply pressure or a pressure dressing to the venipuncture site and assess the site for bleeding.
Uric acid is a nitrogenous compound that is a product of purine (a deoxyribonucleic acid [DNS] building block) catabolism. Uric acid is excreted to a large degree by the kidney and to a smaller degree by intestinal tract. When uric acid levels are elevated (hyperuricemia), the patient may have gout. Gout is a common metabolic disorder characterized by chronic hyperuricemia, defined as serum urate >6.8 mg/dL (>0.360 mmol/L). At this level, uric acid concentrations exceed the physiologic saturation threshold and monosodium urate crystals may be deposited in the joints and soft tissues. Gout may be managed through urate-lowering therapy with the goal of treatment being uric acid <6 mg/dL (<0.357 mmol/L).
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