The Effect of Sodium Bicarbonate Upon Urinary Citrate Excretion in Calcium Stone Formers

Abstract

To evaluate the effects of oral sodium bicarbonate (NaBic) supplementation upon urinary citrate excretion in calcium stone formers (CSFs). Sixteen adult calcium stone formers with hypocitraturia were enrolled in a randomized, double-blind, crossover protocol using 60 mEq/day of NaBic during 3 days compared to the same period and doses of potassium citrate (KCit) supplementation. Blood and 24-hour urine samples were collected at baseline and during the third day of each alkali salt. NaBic, similarly to KCit supplementation, led to an equivalent and significant increase in urinary citrate and pH. Compared to baseline, NaBic led to a significant increase in sodium excretion without concomitant increases in urinary calcium excretion, whereas KCit induced a significant increase in potassium excretion coupled with a significant reduction in urinary calcium. Although NaBic and KCit both reduced calcium oxalate supersaturation (CaOxSS) significantly vs baseline, KCit reduced calcium oxalate supersaturation significantly further vs NaBic. Both KCit and NaBic significantly reduced urinary phosphate and increased calcium phosphate supersaturation (CaPSS) compared to baseline. Finally, a significantly higher sodium urate supersaturation (NaUrSS) was observed after the use of the 2 drugs. This short-term study suggests that NaBic represents an effective alternative for the treatment of hypocitraturic calcium oxalate stone formers who cannot tolerate or afford the cost of KCit. In view of the increased sodium urate supersaturation, patients with pure uric acid stones and high urate excretion may be less suited for treatment with NaBic.