RT Journal
T1 BOne-cell metabolism in uremia
JF JAMA
JO JAMA
YR 1969
FD November 17
VO 210
IS 7
SP 1274
OP 1275
DO 10.1001/jama.1969.03160330074016
UL http://dx.doi.org/10.1001/jama.1969.03160330074016
AB Although skeletal disease has long been recognized as a late manifestation of protracted uremia, the rarity of its appearance in the natural course of the disease once made it a feature of interest more to the student preparing for an examination or the serious nephrologist than to the busy practitioner. All this was changed by the development of techniques for repeated hemodialysis and the chronic dialysis program for terminal uremic patients. Now the life expectancy of the uremic patient can be indefinitely prolonged so long as he has access to the facilities for regular treatment. Unfortunately, hemodialysis, so effective in removing metabolic end products and in controlling hyperphosphatemia, hypocalcemia, and electrolyte and acid-base balance, has failed to protect the patient from the skeletal complications of his disease. Indeed, renal rickets, or renal osteodystrophy as it is more properly called, is rapidly being revealed not only as an inevitable accompaniment of