This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Administration of potassium citrate is now considered an effective treatment for recurrent urolithiasis. It has been shown to decrease stone formation rate in patients with idiopathic hypocitraturic calcium nephrolithiasis by as much as 72% in a placebo-controlled trial. Other studies have demonstrated that potassium citrate therapy can effectively reduce the rate of stone formation in hypocitraturic, hyperuricosuric, as well as in thiazide-unresponsive patients. The effect of potassium citrate is believed to be exerted through its citraturic and alkalinizing actions. Both potassium and citrate are nearly completely absorbed from the gastrointestinal tract. Citrate is nearly completely oxidized in vivo, but absorbed potassium is not metabolized. Thus, a 'cation excess' is created, producing an alkali load. The alkali load enhances urinary citrate excretion by reducing renal tubular reabsorption of citrate. A small fraction of the absorbed citrate escapes oxidation in vivo and is excreted in the urine, contributing to the citraturic action of potassium citrate. The object of this study is to compare the urinary alkalinizing and citraturic effects of potassium-rich citrus fruit product (orange juice) with those of potassium-poor product (lemonade) under controlled metabolic conditions in both normal subjects and stone former.s
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