THE MOST common form of rickets in the United States at present is probably the entity variously known as primary hypophosphatemic vitamin D resistant rickets, familial hypophosphatemia, or hereditary hypophosphatemia.1 Hereditary hypophosphatemia may be a preferable name since familial incidence is not always present and rickets can be minimal or absent. The major biochemical manifestation is marked hypophosphatemia which is not restored to normal by large doses of vitamin D (unless the vitamin D is pushed to toxicity with reduction of glomerular filtration rate) nor by large intake of inorganic phosphate. An important consequence of hereditary hypophosphatemia is stunting of growth. Even with high intake of both vitamin D and phosphate, which causes healing of the rickets and permits fairly normal mineralization of bone as indicated by the roentgenogram, linear growth remains slow. The possibility that the low concentration of inorganic phosphate in extracellular fluid may be responsible for