“…Since this improvement of renal osteodystrophy was achieved without acceleration of renal failure, these studies are quite interesting. One should, however, remember that 1.25(OH)2D3 does not only correct malabsorption of calcium but also that of phosphate [7] and that in patients with more advanced renal failure such treatment may lead to marked hyper phosphatemia which when combined with hypercal cemia accelerates the decline of renal function, as pre viously reported [8,9]. Furthermore, such an increase in plasma phosphate limits the beneficial effect of l,25(OH)2D3 on bone resorption [10], Finally, one should keep in mind that in experimental uremia la-OH vitamin D 3 given at doses keeping plasma calcium an phosphate in the normal range may increase the calcium content of the aorta [11] and that in man la-OH vitamin D3 increases plasma aluminum in uremic patients taking Al(OH)3 [12], Therefore, we ask ourself whether another approach for the prevention of hyperparthyroidism in early, as well as more advanced renal failure, would not simply be the use of oral calcium carbonate at the highest doses not inducing hypercalcemia greater than 10.4 mg/dl.…”