Background. Nephrolithiasis is a frequent disorder affecting 10 to 15% of t
he population in Europe and the United States. More than 80% of renal stone
s are made of calcium oxalate and calcium phosphate. The main identified ri
sks for calcium renal stone formation are hypercalciuria and urinary satura
tion. A urine phosphate (Pi) loss is often associated with hypercalciuria;
furthermore, hyperphosphaturia increases urinary saturation.
Methods. To determine whether urinary phosphate loss is associated with cal
cium urolithiasis. we measured renal Pi threshold (TmPi) in 207 stent: form
ers with normal parathyroid hormone (PTH) serum concentration and in 105 co
ntrol subjects.
Results. The TmPi followed a normal distribution in both groups. The mean T
mPi was significantly lower in stone formers versus controls (0.72 +/- 0.13
vs. 0.87 +/- 0.18 mmol/L, P < 0.0001) because of a shift to the left of th
e TmPi distribution curve in the stone former population, with no evidence
for bimodal distribution. Five percent of the controls had a TmPi < 0.63 ve
rsus 19% of the stone formers. Daily urinary calcium excretion was signific
antly higher in stone formers than in controls. Calcium excretion was also
significantly higher in stone formers with TmPi < 0.63 mmol/L compared with
those with TmPi greater than or equal to0.63. Serum PTH and ionized calciu
m concentrations were not different in stone formers and in control subject
s, whatever the TmPi value.
Conclusions. A low TmPi is more frequently encountered in stone formers wit
h a normal PTH concentration than in control subjects and is associated wit
h a high urinary Ca excretion. The hypophosphatemia induced by a renal phos
phate leak may predispose the subject to calcium stone formation by increas
ing the serum calcitriol level, calcium excretion, and urinary saturation.