Citrate and mineral metabolism kidney stones and bone disease

Abstract

Citrate is a weak acid that is formed in the tricarboxylic acid cycle or that may be introduced with diet. In the present paper all the mechanisms involved in intestinal absorption, renal handling and modulation of citrate will be reviewed. The evaluation of plasma citric acid is scarcely used in the diagnosis of human diseases. On the contrary urinary citrate excretion is a common tool in the differential diagnosis of kidney stones, renal tubular acidosis and it plays also a role in bone diseases. Therefore the importance of hypocitraturia will be reviewed with regard to bone mass, urine crystallization and urolithiasis. Finally particular attention will be paid to the incidence of hypocitraturia and to the therapy with citrate salts, both in kidney stone disease and in osteopenia.

Vanishing hypercalciuric kidney stones after treating underlying acromegaly

“…(2) reviewed the mechanism of kidney stones with respect to acromegaly. They found hypercalciuria, hyperoxaluria and hypercitraturia and explained the low incidence of urolithiasis by the presence of hypercitraturia, which prevents the formation of urolithiasis (18) (19) (20). In the patient described here, urinary citrate concentration also decreased after controlling his acromegaly, which supports the mechanism observed by Auriemma et al .…”

Calcium-deficiency assessment and biomarker identification by an integrated urinary metabonomics analysis

“…Citrate has an important role in bone metabolism and bone diseases [48-50], and it can be considered a biomarker of calcium deficiency. Citric acid (citrate) can be formed in the Krebs cycle.…”

Prevention of renal crystal deposition by an extract of Ammi visnaga L. and its constituents khellin and visnagin in hyperoxaluric rats

“…It has been shown in literature that urinary citrate plays an important role in reducing recurrences of calcium oxalate stones [19]. Its inhibitory effect on calcium oxalate crystallization is generally recognized, the mechanism of action being a reduction of calcium oxalate supersaturation by formation of complexes with calcium and direct inhibition of crystal growth with aggregation and increasing urinary pH [3, 4, 24]. There are several factors that increase urinary citrate including a decrease of dietary protein intake, administration of alkali such as potassium citrate, and an increase of hormone modulation turnover such as estrogen leading to an increase of citrate excretion [7, 25].…”