Magnesium, citrate, magnesium citrate and magnesium-alkali citrate as modulators of calcium oxalate crystallization in urine: observations in patients with recurrent idiopathic calcium urolithiasis

The effects of magnesium (Mg) and citrate on the metastable limit of calciu m oxalate (CaOx) solubility (synonym: tolerable oxalate TO) were examined i n artificial urine and in postprandial urine of male patients with idiopath ic calcium urolithiasis (ICU). In artificial urine increasing pH, Mg and ci trate elevate TO, decrease CaOx supersaturation only marginally, but elevat e considerably free citrate; the effect of Mg alone was small in comparison with citrate alone, and the effects of both substances appeared additive. In ICU patients, matched for sex, age and CaOx supersaturation to non-stone -forming controls, TO was decreased (mean values 0.33 vs. 0.52 mM/l in cont rols, P < 0.05). Additional significant (P < 0.05) differences were found b etween ICU and controls: the former exhibited increased CaOx crystal growth , decreased crystal agglomeration time, a more acidic urinary pH, increased concentrations of free calcium and free Mg, and decreased free oxalate and free citrate. After ingestion of a urine-acidifying test meal, or this mea l supplemented with either neutral Mg citrate or Mg-alkali citrate, by thre e groups of male ICU patients, matched for age and CaOx supersaturation, on ly the last-named preparation evoked an increase in TO and a decrease in cr ystal diameter, while the normally occurring pH decline from fasting urine was virtually abolished, and the ratios urinary Mg/citrate and calcium/citr ate tended towards low values. In contrast, Mg citrate increased crystal ag glomeration time, while changes in the other parameters were only insignifi cant. The crystals formed in urine were CaOx di- and monohydrate (by electr on microscopy), and energy dispersive X-ray analysis showed calcium peaks e xclusively. However, chemical analysis of crystals verified the presence no t only of oxalate and calcium, but also of Mg, phosphate, citrate, and urat e; moreover, these crystal constituents seemed to be influenced by Mg citra te and Mg-alkali citrate in different ways. It was concluded that (1) Mg an d citrate are effecters of TO in artificial and natural urine; (2) in ICU, low TO and other disturbed CaOx crystallization parameters appear related t o the prevailing low urinary pH and low free citrate; (3) Mg-alkali citrate inhibits CaOx crystallization, probably via actions of the citrate, but no t the Mg. Because of the eminent role of Mg in human health and ICU, furthe r studies on crystallization after oral intake of Mg in the form of citrate are warranted.