The healing of renal rickets.

Little has been added to the knowledge of the treatment of renal rickets since the paper by Graham and Oakley (1938), and the reader is referred to their work for a summary of the previous literature of this condition. Whether or not in fact rickets is the principal bony lesion has been questioned by Langmead and Orr (1933). From a morbid anatomical study, they concluded that osteitis fibrosa was the outstanding pathological change in the bones, and attributed this to *osteoclastic activity caused by excessive parathyroid function. They were able to demonstrate the presence of hypertrophy of the parathyroid glands. Their view has received support in America from such authorities as Park and Eliot (1942), and Hamilton (1940) who considers the hyperparathyroidism to be secondary, and called into being in order to rectify the low blood calcium level so often present in chronic nephritis. It is not the purpose of this communication to discuss the underlying pathological process in the bones, although it may be pointed out that so-called renal rickets may occur with a normal blood calcium, as in the cases reported by Karelitz and Kolomoyzeff (1932), but to place on record the history of a boy with chronic nephritis whose bone changes, characteristic of renal rickets, underwent such complete healing during the eight months prior to his death that histological examination of a radius showed neither rickets nor osteitis fibrosa, ossification appearing to be proceeding in an orderly manner.