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Uric acid !

Uric acid is the final product of purines in humans; when it builds up, it forms crystals that cause gout and stones.

Updated 2026-11-01

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Key facts

  • Xanthine oxidase makes it from xanthine; humans have no uricase to break it down.
  • At blood pH it is mostly monosodium urate, which saturates above about 6.8 mg/dL.
  • Two-thirds are excreted by the kidney (filtered and reabsorbed mainly by URAT1) and one-third by the gut.
  • In acidic urine it precipitates as uric acid: radiolucent stones.
Also called
Urate
Formula
C₅H₄N₄O₃
PubChem
CID 1175

Structure

  • A purine with three oxo groups (2,6,8-trioxypurine); its first pKa is about 5.4.
  • It is a major plasma antioxidant.

Clinical notes

  • Hyperuricaemia from overproduction (tumour lysis, HGPRT deficiency) or, more often, from low renal excretion (kidney disease, diuretics, alcohol).
  • It is lowered with xanthine oxidase inhibitors, uricosurics or recombinant uricase, depending on the case.
  • A very low uric acid points to xanthinuria, PNP deficiency or Fanconi syndrome.

Drugs that act here

Pathways

Test yourself

Think of the answer, then tap the question to see it.

Why do uric acid stones form in acidic urine?

At low pH the undissociated form predominates, which is far less soluble than urate.

What is the most common cause of hyperuricaemia?

Low renal urate excretion, rather than overproduction.

What does an almost undetectable uric acid suggest?

A xanthine oxidase defect (xanthinuria), PNP deficiency or renal loss (Fanconi syndrome).

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Molecules are shown in their neutral form, as the databases deposit them; in the cell the acids and phosphates are ionised.

Educational information, not medical advice. For any symptom, see a health professional.

Sources: Uric Acid (CID 1175) (PubChem, NCBI, 2026) · Public domain; Uric acid - blood : MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Purine catabolism (Reactome, 2026).

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Representative model, for educational purposes only.