Mobile Site ›
Print Page Email Page

Interpretive Handbook

‹ Back to index | Back to list | More information

Test 89846:
Uric Acid, Random, Urine

Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test

Uric acid is the end-product of purine metabolism. It is freely filtered by the glomeruli and most is reabsorbed by the tubules. There is also active tubular secretion.

 

Increased levels of uric acid in the urine usually accompany increased plasma uric acid levels unless there is a decreased excretion of uric acid by the kidneys. Urine uric acid levels reflect the amount of dietary purines and also endogenous nucleic acid breakdown.

 

Acute uric acid nephropathy can cause acute renal failure due to uric acid precipitation within tubules. This is most commonly seen in patients with hematologic malignancies (eg, lymphoma, leukemia), often after acute lysis of cells by chemotherapy. Less commonly this may be seen with seizures, treatment of solid tumors, overproduction of uric acid in metabolic disorders such as Lesch-Nyhan syndrome or decreased uric acid reabsorption in the proximal nephron due to tubular disorder (Fanconi syndrome).

Useful For Suggests clinical disorders or settings where the test may be helpful

Differentiation of acute uric acid nephropathy from other causes of acute renal failure

 

Patients who cannot collect a 24-hour specimen, typically small children, a uric acid creatinine ratio can be used to approximate 24-hour excretion

Interpretation Provides information to assist in interpretation of the test results

Uric acid excretion can be either decreased or increased in response to a variety of pharmacologic agents.

 

Urine uric acid levels are elevated in states of uric acid overproduction such as in leukemia and polycythemia and after intake of food rich in nucleoproteins.

 

A uric acid to creatinine ratio (mg/mg) >1.0 is consistent with acute uric acid nephropathy, whereas values <0.75 are consistent with other causes of acute renal failure.(1)

 

A timed 24-hour collection is usually the preferred method for measuring and interpreting this urinary analyte. Random collections normalized to urinary creatinine may be of clinical use in 2 scenarios, however:

-When acute renal failure secondary to uric acid is suspected, a uric acid to creatinine ratio (mg/mg) >1.0 is consistent with acute uric acid nephropathy, whereas values <0.75 are consistent with other causes of acute renal failure.(1)

-In patients who cannot collect a 24-hour specimen, typically small children, a uric acid creatinine ratio can be used to approximate 24-hour excretion.  

              

Pediatric Reference Ranges of Uric Acid/Creatinine (mg/mg)

Age (year)

5th Percentile

95th Percentile

0-0.5

>1.189

<2.378

0.5-1

>1.040

<2.229

1-2

>0.743

<2.080

2-3

>0.698

<1.932

3-5

>0.594

<1.635

5-7

>0.446

<1.189

7-10

>0.386

<0.832

10-14

>0.297

<0.654

14-17

>0.297

<0.594

Matos V, Van Melle G, Werner D et al: Urinary oxalate and urate to creatinine ratios in a healthy pediatric population. Am J Kidney Dis 1999;34:e1

Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances

High levels of bilirubin and ascorbic acid may interfere with measurement.

Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.

No established reference values

Clinical References Provides recommendations for further in-depth reading of a clinical nature

1. Kelton J, Kelley WN Holmes, EW: A rapid method for the diagnosis of acute uric acid nephropathy. Arch Intern Med 1978;138(4):612-615

2. Newman DJ, Price CP: Renal function and nitrogen metabolites. In Textbook of Clinical Chemistry. Edited by NW Tietz. Philadelphia, WB Saunders Company, 1999, pp 1245-1250