Successful management of uric acid nephrolithiasis with potassium citrate

Abstract

Eighteen patients with uric acid nephrolithiasis (six with uric acid stones alone and 12 with both uric acid and calcium stones) underwent long-term treatment (1 to 5.33 years, mean of 2.78 years) with potassium citrate (30 to 80 mEq/day, usually 60 mEq/day). Urinary pH increased from low (5.30 +/- 0.31 SD) to normal (6.19 to 6.46) during treatment. Urinary content of undissociated uric acid, which was high to begin with at 204 +/- 82 mg/day, decreased to the normal range (64 to 108 mg/day) following treatment. Urinary citrate rose from 503 +/- 225 mg/day to 852 to 998 mg/day. Urinary saturation of calcium oxalate significantly declined with potassium citrate treatment. New stone formation rate declined from 1.20 +/- 1.68 stones/year to 0.01 +/- 0.04 stones/year (P less than 0.001 by chi square). Remission was experienced in 94.4% of patients, and the group stone formation rate declined by 99.2%. Detailed case reports were obtained in five patients showing different responses between sodium alkali and potassium alkali treatment. All five patients had persistently low urinary pH (typically less than 5.5) and normouricosuria, and four had hyperuricemia. Before treatment, they had stones surgically removed or spontaneously passed, which were pure uric acid in composition. When sodium alkali was give (as bicarbonate or citrate, 60 to 118 mEq/day), new stone formation continued in four patients, and a radiolucent (uric acid) calculus become "calcified" in the remaining patient. The stone analysis disclosed calcium oxalate in five patients and calcium phosphate in three patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparative Value of Orange Juice versus Lemonade in Reducing Stone-Forming Risk

“…Citrate retards the crystallization of stone-forming salts through two mechanisms. First, it forms a soluble complex with calcium and reduces ionized calcium concentration, thereby reducing calcium oxalate and calcium phosphate supersaturation (6). The second mechanism is the direct inhibitory effect of citrate on spontaneous nucleation, crystal growth, and crystal agglomeration of preformed calcium oxalate crystals (19).…”

“…The increase in urinary citrate retards spontaneous nucleation and agglomeration of calcium oxalate crystals (5). Moreover, by increasing urinary pH and decreasing urinary content of undissociated uric acid, this treatment is useful in preventing uric acid stones (6).…”

Dysregulation of the Glutamine Transporter Slc38a3 (SNAT3) and Ammoniagenic Enzymes in Obese, Glucose-Intolerant Mice

“…UAN is highly associated with low urinary pH and urine volume, hyper- or normouricosuria, and the increased incidence of diabetes or insulin resistance [6,7,8,9,10]. Pharmacological treatment with potassium or sodium citrate has been proven to increase urinary pH and inhibit UA stone formation, providing further evidence that UAN is linked to low urinary pH [11,12,13,14]. Patients with diabetes and UAN not only have low urinary pH values, but also exhibit decreased renal ammonium excretion.…”

Urinary Citrate Levels Do Not Correlate with Urinary pH in Patients with Urinary Stone Formation

“…The absolute difference in pH, 0.28, was not as great as that (0.55 to 0.85) observed by Pak and Peterson 18 when treating patients with hyperuricosuric calcium stone formation. Pak et al 19 also observed a much greater increase in pH (0.9) with citrate therapy when treating patients with uric acid stone formation.…”