To the Editor.
—I read with great interest the article by Drs Weinstein and Hudson, in the Archives (1980;140:410-411), on parathyroid hormone (PTH) and serum 25-hydroxycholecalciferol (25-OHD) levels in hypercalcemia of acute renal failure. There is one point in that article on which I would like to comment.Their data make me conclude that there was less possibility of secondary hyperparathyroidism and some possibilty of muscle injury as the cause of the hypercalcemia in that situation. However, the measurement of serum 25-OHD levels only cannot satisfactorily rule out the possibility that vitamin D metabolism participated in that hypercalcemia.The low values of serum 25-OHD may suggest that serum 25-OHD has been metabolized to the more polar derivatives, 1,25(OH)2D3 or 24,25 (OH)2D3. If serum levels of 1,25 (OH)2D3 or 24,25 (OH)2D3 are high, the hypercalcemia can be explained by