Uremic hyperphosphatemia still represents a considerable challenge to physicians treating patients with advanced kidney insufficiency. Phosphatebinding agents containing aluminium were the therapy of choice for many years, although, as we now 45know, at the price of serious organ damage such as osteopathy, anemia and encephalopathy (1-3). Since dietetic intervention is practicable in only a few cases, therapeutic strategies not involving aluminium were sought intensively. The use of calcium carbonate, today a preferred treatment for uremic hyperphosphatemia, goes back to the investigations of Clarkson et al. (4), who reported as early as 1966 that high-dose calcium carbonate therapy (20 g of calcium carbonate per day) could succeed in lowering serum phosphate levels in nondialysis patients with kidney insufficiency. In carefully administered balance tests, the same authors demonstrated that calcium carbonate binds phosphate primarily in the intestine. It was, however, also shown that a considerable percentage of the administered calcium is simultaneously absorbed by the intestine. Recent studies by Ramirez et al. ( 5 ) confirmed these results and showed that, while the administration of calcium carbonate does result in considerable intestinal binding of phosphate, 28% of the calcium carbonate taken is absorbed. Sheikh et al. (6) recently published similar results on calcium absorption following administration of calcium carbonate. Their in vivo investigations showed that, of a dosage of 2.5 g of calcium carbonate (1 . O g of calcium), about 250 mg of calcium were absorbed. Since most published therapeutic studies involve dosages of approximately 8.1 st 4.9 g of this substance (7), the amount of calcium absorbed by the body could, at least theoretically, be over 800 mg per day, or just under 300 g per year.It is well known that the pathogenesis of uremic osteopathy is not solely a result of phosphate retention. Insufficient 1,25 dihydroxy-vitamin D3 (1,25 (OH)*D3) formation is, of course, a major pathogenetic mechanism and administering 1,25 (OH)2D3 to patients with advanced or dialytically treated kidney insufficiency is appropriate. Simultaneous administration of 1,25 (OH)zD3 with calcium carbon-