Abstract
Citrate is a tricarboxylic acid and an intermediate metabolite of Krebs cycle. It contributes to oxidative metabolism of both kidney and liver. Alkaline sodium or potassium salts have the potential to increase alkaline reserve. In the kidney citrate is completely filtered at the glomerulus, undergoing to 10-40% tubular resorption. Renal insufficiency, even early, metabolic acidosis, potassium depletion induce hypocitraturia. Its importance in nephrolithiasis stems from its ability to form soluble complexes with calcium and to interfere with crystal formation, thus exerting a dual inhibition, thermodynamic and kinetic. Moreover, its alkalizing property has shown benefits of bone mineralization. The alkalizing effect is also useful in uric acid and cystine stone disease. Hypocitraturia has a significant incidence in the course of calcium nephrolithiasis, either secondary to aforementioned causes, or in idiopathic and/or familial forms. Citrate is used in the prevention of stone recurrences and given as tripotassic or potassium-magnesium salt, 0.1 mmol/kg/day in 2-3 dosages. In uric acid disease, in addition to prevention, it can induce dissolution of renal stones, provided urine pH is maintained at higher than 6.5 values. As concerns its effects on bone, it was shown to induce both decreases in marker of bone resorption and increases in bone mineral density.
Key words: citrate, potassium citrate, hypocitraturia, calcium nephrolithiasis