Vit C was once thought to be one of the main causative factor
for oxalate stones in the kidneys, because it's metabolism or
breakdown produces oxalic acid which in turn gets excreted in the
urine and can be measured for it's quantity. Higher intake gives
rise to raised oxaluria, but later randomized clinical trial showed
that this was not significant enough to show the formation of
kidney stones. In fact, it has been shown to reduce the chances of
stone formation. However, there remains a strong debate on it, so I
dare not comment further...
STUDY
[Vitamin C and stone risk. Review of the literature]
[Article in French]
Traxer O, Pearle MS, Gattegno B, Thibault P.
Service d'Urologie, Hopital Tenon, Paris, France.
[email protected]
The popularity of vitamin C can be attributed to Linus Pauling who,
in the 1970s, recommended the use of vitamin C for the prevention
of influenza. Vitamin C has subsequently been used extensively in a
wide range of diseases. Ascorbic acid (vitamin C) has been
incriminated as a possible risk factor for calcium oxalate stones
due to its enzymatic conversion into oxalate. However, this
lithogenic role has never been clearly established. Studies
evaluating the effect of ascorbic acid on lithogenesis have
reported contradictory results. Ascorbic acid has also been
extensively used as an urine acidifier for the treatment of chronic
or recurrent urinary tract infection. Once again, the data of the
literature are contradictory. The purpose of this article was to
review the effects of ascorbic acid on lithogenesis and urinary pH
based on a review of the literature.
CONTRADICTORY STUDY
Ascorbate increases human oxaluria and kidney stone risk.
Massey LK, Liebman M, Kynast-Gales SA.
Department of Food Science and Human Nutrition, Washington State
University, Spokane, WA, USA. [email protected]
Currently, the recommended upper limit for ascorbic acid (AA)
intake is 2000 mg/d. However, because AA is endogenously converted
to oxalate and appears to increase the absorption of dietary
oxalate, supplementation may increase the risk of kidney stones.
The effect of AA supplementation on urinary oxalate was studied in
a randomized, crossover, controlled design in which subjects
consumed a controlled diet in a university metabolic unit.
Stoneformers (n = 29; SF) and age- and gender-matched
non-stoneformers (n = 19; NSF) consumed 1000 mg AA twice each day
with each morning and evening meal for 6 d (treatment A), and no AA
for 6 d (treatment N) in random order. After 5 d of adaptation to a
low-oxalate diet, participants lived for 24 h in a metabolic unit,
during which they were given 136 mg oxalate, including 18 mg 13C2
oxalic acid, 2 h before breakfast; they then consumed a controlled
very low-oxalate diet for 24 h. Of the 48 participants, 19 (12
stoneformers, 7 non-stoneformers) were identified as responders,
defined by an increase in 24-h total oxalate excretion > 10%
after treatment A compared with N. Responders had a greater 24-h
Tiselius Risk Index (TRI) with AA supplementation (1.10 +/- 0.66
treatment A vs. 0.76 +/- 0.42 treatment N) because of a 31%
increase in the percentage of oxalate absorption (10.5 +/- 3.2%
treatment A vs. 8.0 +/- 2.4% treatment N) and a 39% increase in
endogenous oxalate synthesis with treatment A than during treatment
N (544 +/- 131 A vs. 391 +/- 71 micromol/d N). The 1000 mg AA twice
each day increased urinary oxalate and TRI for calcium oxalate
kidney stones in 40% of participants, both stoneformers and
non-stoneformers.
