uric acid stones

Uric acid stones account for ~5-10% of kidney stones and form due to low urine pH, low urine volume, and/or hyperuricosuria. Uric acid is a weak acid (pKa 5.35); at low urinary pH, it precipitates as insoluble uric acid crystals rather than the more soluble urate salt. Chronic diarrhea/dehydration (persistently acidic urine from bicarbonate loss), gout, rapid cell turnover states (tumor lysis syndrome, myeloproliferative disorders), and insulin resistance/metabolic syndrome (impaired renal ammoniagenesis leading to low urine pH) are classic risk factors. Unlike calcium oxalate/phosphate stones, uric acid stones are radiolucent on plain X-ray (KUB) but are visible on non-contrast CT and ultrasound—an important distinguishing feature clinically. Diagnosis is supported by urinalysis showing persistently acidic urine and uric acid crystals (rhomboid or rosette-shaped), plus stone analysis. Management centers on increasing urine pH to 6.0-6.5 using potassium citrate or sodium bicarbonate, which increases solubility of uric acid and can dissolve existing stones (chemolysis)—unique among stone types for having a medical dissolution option. Allopurinol or febuxostat may be added if hyperuricosuria persists despite alkalinization, especially in gout patients. Increased fluid intake and dietary purine restriction are also recommended. This topic is high-yield for boards due to the classic radiolucent-on-X-ray-but-visible-on-CT distinction and its association with gout and tumor lysis syndrome.