Uric acid stones

Uric acid (UA) stones are typically red-orange and often appear as sand/ gravel though they may be large. They are totally radiolucent. They account for about 10% of all kidney stones in most countries, and up to 20% in some populations. It is twice as frequent in males, prevalence increases with age, and it is two to three times higher in patients with type 2 diabetes or with features of the metabolic syndrome. Factors that induce the formation of UA stones are a low urine volume, hyperuricosuria, and, more importantly, a permanently low urine pH (< 5). Indeed, below its pKa of 5.35 at 37°C, UA is in non-dissociated form, whose solubility is at best 100 mg/L, whereas urinary UA excretion normally exceeds 600 mg/day and may exceed 1g/day.Because UA solubility increases up to approximately 500 mg/L at urine pH > 6, urine alkalinization, with a target pH of 6.5–7, is the cornerstone of medical treatment. This most often allows dissolution of existing stones and prevention of recurrent stone formation so that urological intervention is infrequently needed. The preferred agent for alkalinization is potassium citrate (30–60 mEq/day in divided doses), because potassium urate is twice more soluble than sodium urate. However, in patients with poor gastric tolerance to potassium citrate or contraindication to potassium supplements, sodium bicarbonate is an acceptable alternative. Limitation of animal proteins, purine-rich foods (including beer), alcoholic drinks and acidified beverages (sodas) are useful measures, together with large fluid intake (> 2–2.5 L/day). Allopurinol may be indicated in cases of symptomatic hyperuricaemia. Regular observance of alkalinisation, with periodic controls of urine pH by the patient, is needed to prevent the rapid formation of UA stones. Patients affected by UANL, especially if overweight, should be evaluated for type 2 diabetes or glucose intolerance and managed accordingly.