Ascorbic acid in idiopathic recurrent calcium urolithiasis in humans - does it have an abettor role in oxalate, and calcium oxalate crystallization?

The role of ascorbic acid (ASC) in the pathophysiology of renal calcium sto nes is not clear. We evaluated ASC in blood and urine of fasting male patie nts with idiopathic calcium urolithiasis (ICU) and healthy volunteers. Usin g smaller subgroups, we also evaluated their response to exogenous ASC [eit her intravenous or oral ASC (5 mg/kg bodyweight)] administered together wit h an oxalate-free test meal. The influence of ASC on calcium oxalate crysta llization, the morphology of crystals at urinary pH 5, 6 and 7, and the eff ect of increasing duration of urine incubation on urinary oxalate at these pHs, without and with addition of ASC, were studied too. In normo- and hype rcalciuric ICU, blood and urinary ASC from fasting patients remained unchan ged, but the slope of the regression line of urinary ASC versus urinary oxa late was steeper than in the controls; the plasma ASC half-life did not dif fer between controls, normo- and hypercalciuric ICU; the ASC-supplemented m eal caused an increase in the integrated plasma oxalate in the normocalciur ic subgroup versus controls. In normo- and hypercalciuric ICU urinary oxala te, the oxalate/glycolate ratio, and calcium oxalate supersaturation were i ncreased, but urinary glycolate was unchanged. In the controls, oral ASC di d not affect calcium oxalate crystallization, while in ICU, ASC inhibited c rystal growth. In control urine calcium oxalate dihydrate and calcium oxala te monohydrate develops, while in ICU urine only the former crystal type de velops. In vitro oxalate neoformation from ASC did not occur. It was conclu ded that (1) under normal conditions an abettor role of ASC for renal stone s is not recognizable, (2) in ICU, urinary oxalate excess unrelated to degr adation of exogenous ASC is exhibited, and that this is most likely unrelat ed to an initial increase in oxalate biosynthesis, and (3) ASC appears to m odulate directly calcium oxalate crystallization in ICU, although the true mode of action is still not known.