Abstract
Metabolic observations on 5 patients with renal osteodystrophy are presented. The bone lesions varied from slight or moderate osteoporosis with no deformities to marked rarefaction with gross deformities. In 2 cases rachitis-like changes were also present in the epiphyses. Since one of the fundamental defects of renal osteodystrophy is poor intestinal absorption of Ca, therapy was sought to circumvent this difficulty. Vit. D was ineffective; dihydrotachysterol (A. T. 10) promoted Ca absorption and this increased Ca absorption led to increased P absorption and to deposition in the bones of both of these elements. Ferric ammonium citrate facilitated the intestinal excretion of P by the formation of insoluble ferric phosphate. This spared the amt. of Ca necessary for combining with phosphate in excretion of the latter by the intestine. Hyper-phophatemia, an evidence of strain on the kidneys, was usually relieved by the ingestion of Fe. Therefore such therapy is indicated in cases of renal osteodystrophy with marked elevation of serum inorganic P. Occasionally Fe, in large doses, caused diarrhea.