Uric acid kidney stones

Why uric acid stones form

Uric acid is a waste product of purine breakdown. Stones form when the urine is persistently acidic (pH usually below 5.5) - in acidic urine, uric acid precipitates into crystals even at normal blood levels.¹

The dominant risk factor is low urinary pH, which is strongly associated with:

• The metabolic syndrome - obesity, type 2 diabetes, insulin resistance.
• High dietary animal protein.
• Gout and other causes of high serum uric acid.
• Chronic diarrhoea and bicarbonate losses.
• A naturally acidic urine pH in some individuals.

How to recognise a uric acid stone

Uric acid stones have a very distinctive fingerprint:

• Radiolucent on plain x-ray - they do not show up on a KUB film.
• Low density on CT - typically 200-500 HU, much lower than calcium stones.
• Urine pH consistently under 5.5.
• Often found in patients with gout, obesity, or diabetes.

A stone with these features on a non-contrast CT, in a patient with a persistently acid urine, is almost certainly a uric acid stone - and the diagnosis matters because it changes the treatment plan.

Treatment - dissolution therapy

Uric acid stones are the only common stone that can be dissolved with medical treatment. The principle is simple: raise the urinary pH into the 6.5-7.0 range and uric acid goes back into solution.¹

• Potassium citrate is the first-line alkalinising agent, taken as tablets or liquid typically two to three times a day.
• Urine pH is monitored with cheap dipstick strips at home to confirm that the target range has been reached.
• Allopurinol may be added, particularly if serum uric acid is high.
• Stones over 2 cm rarely dissolve completely, and obstructing ureteric stones usually still need urgent ureteroscopy regardless of composition.

For stones that do not dissolve, or that are causing obstruction or infection, the usual surgical options apply - ESWL, ureteroscopy with Holmium laser, or PCNL for large stones. See the treatments hub.

Prevention

• High fluid intake - a urine output of at least 2.5 L/day.
• Urinary alkalinisation to a pH of 6.5-7.0 with potassium citrate (monitored by dipstick).
• Reduce dietary purines - red meat, offal, shellfish, anchovies, sardines.
• Weight reduction in patients with metabolic syndrome.
• Allopurinol for patients with true hyperuricaemia or gout.

Related pages

Reference

1. Skolarikos A, et al. EAU Guidelines on Urolithiasis. European Association of Urology; 2025.