Acute oral alkali citrate load in healthy humans--response of blood and urinary citrate, mineral metabolism, and factors related to stone formation.

In ten healthy volunteers (male/female = 5/5) the effects of two doses (2.5 and 5.0 g) of orally ingested alkali citrate (AC) on serum citrate, variables of mineral metabolism in serum, the urinary excretion of citrate, sodium and minerals were studied and compared with the effects of an oral vehicle load. Also, phosphate crystalluria and the supersaturation of several stone forming phases in urine were evaluated under all loads. The data allow to conclude that 1) the rise in serum citrate may result from citrate absorbed intestinally under AC; 2) systemic metabolic alkalosis is not detectable with the chosen AC doses but may be reflected by the more alkaline urinary pH and a higher citrate excretion; 3) mineral metabolism, serum ionized calcium, parathormone, calcitonin and urinary cyclic AMP included, are more or less stable under acute loads of AC; 4) postprandial phosphate crystalluria is more pronounced with increasing AC, but despite this the direct correlation with the supersaturation of hydroxyapatite is progressively weakened with both doses AC suggesting that the inhibitory effects of this drug may dominate over its effects upon initiation of precipitation.