We have previously shown that an oral glucose load increased both calc
iuria and oxaluria while the ingestion of fructose induced a rise in c
alciuria and a decrease in oxaluria. This latter effect remains unclea
r and might be linked to the reduced intestinal oxalate absorption sub
sequent to digestive intolerance in some subjects. Such a hypothesis c
ould be enlightened by the study of a parenteral fructose load. Theref
ore in 7 healthy subjects, we compared the effects of fructose infusio
n (F) (15 min iv infusion at 0.185 mmol/kg BW/min) to a control glucos
e infusion (G) on urinary calcium and oxalate. In this study, glycemia
and insulinemia increased less after (F) than after (G) (respectively
+ 21 % vs + 216 %, p < 0.001 and + 230 % vs + 402 %, p < 0.05) and ph
osphatemia decreased less after (F) than after (G) (-7 % vs 14%, p < 0
.05). Urinary calcium and oxalate increased only after (F) (respective
ly + 64 %, p < 0.01 and + 60 %, p < 0.05). Urinary uric acid, another
urolithiasis factor, increased after both (F) and (G) (respectively 45 %; p < 0.01 and + 42 %; p < 0.01) but uricemia increased only after
(F) (+ 25 %: p < 0.01). Our results suggest an additional reason to a
void the use of fructose in parenteral nutrition, particularly in indi
viduals with a known history of either calcium oxalate or urate urolit
hiasis.