Synonyms: uricaemia (in serum); uricosuria (in urine)
Related tests: Creatinine, Urea, eGFR, Creatinine clearance, albuminuria, urinalysis
Clinical significance
Uric acid is the end product of the breakdown of purine nucleotides, namely adenylic acid (AMP) and guanylic acid (GMP). Nucleotides are the building blocks of nucleic acids (DNA and RNA) but also play an important role in our metabolism in free form. Uric acid is poorly soluble in water, and a rise in its blood concentration can lead to it being deposited in the joint tissues (gouty tophi) or in the urinary tract (kidney stones). A rise in blood uric acid comes from an imbalance between its production and its elimination (2/3 in the urine and 1/3 in the bile). Increased production can be due to excessive endogenous production from increased breakdown or to a diet particularly rich in nucleic acids (meat, especially liver and kidneys), while reduced elimination is due to impaired kidney function.
Raised serum uric acid can be due to primary gout, kidney failure, leukaemia, multiple myeloma, polycythaemia or psoriasis; increased daily excretion of uric acid can be due to leukaemia, Wilson’s disease or gout.
Reduced serum uric acid can be due to Wilson’s disease, viral hepatitis or low-purine diets; reduced daily excretion of uric acid can be due to folic acid deficiency, lead poisoning or fasting
Clinical indications
Suspected gout, monitoring of drug treatment for hyperuricaemia, monitoring of the catabolic effects of chemotherapy.
Sample type
The patient must have a blood sample taken.
If requested, the patient must collect all urine passed over 24 hours.
Preparation
You must fast for at least 8 hours; a small amount of water is allowed. You must have been standing or sitting upright for at least 30 minutes.
Notes
A true rise in serum uric acid can be caused by beta blockers, chemotherapy drugs, furosemide, ethanol, nicotinic acid and salicylates.
A true fall in serum uric acid can be caused by allopurinol, azathioprine, clofibrates and furosemide.