25-OH-Vitamin D Metabolism in Calcium Stone Formers
In addition to hypercalciuria, calcium stone formers demonstrate hypophosphatemia (serum Pi 1.03 ± 0.16 SD mM, N = 111) in comparison to normal subjects (Pi 1.22 ± 0.18 mM, N = 83; p < 0.001). Phosphate deprivation in animals increases urinary Ca excretion and accelerates renal formation of 1,25-(OH)2-D3. Phosphate deprivation in humans accelerates turnover of the plasma 25-OH-D pool determined from measurement of the serum 25-OH-D level, plasma volume taken as 5 percent of body weight and the rate of disappearance of injected 3H-25-OH-D3 or 14C-25-OH-D3. This accelerated turnover of the plasma 25-OH-D pool is associated with increased intestinal Ca absorption, the classical expression of Vitamin D activity, as well as, hypercalciuria and provides inferential evidence that in humans, as in animals, P04-deprivation accelerates renal production of 1, 25-(OH)2-D3. We have similarly evaluated turnover of the plasma 25-OH-D pool in Ca stone formers in an attempt to discover whether Vitamin D metabolism may be altered in this disease(s). We studied a small group of 8 stone formers among whom mean serum Pi averaged 1.28 ± 0.11 mM, a value somewhat, but not significantly, lower than in 11 healthy adults (Pi 1.36 ± 0.16 mM). Among the stone formers, turnover of the plasma 25-OH-D pool averaged 5.8 ± 1.7 nanomoles/day, a value not different from that of 5.7 ± 1.2 nanomoles/day in the 11 normals.