Divalent ion metabolism and osteodystrophy in chronic renal failure.

The widespread use of clhronic dialysis and renal homotransplantation, while prolonging the lives of patients with chronic renal failure, have concomitantly resulted in the appearance of severe disorders of calcium and phosphorus metabolism and disabling renal osteodystrophy (retardation of growth and dwarfism, osteitis fibrosa, rickets or osteomalacia and, at times, osteosclerosis). Furthermore, it is apparent that the usual conservative measures, i.e., giving high doses of calcium, correcting acidosis with alkali, restricting phosphates, and giving phosphate-binding antacids orally, frequently fail to correct hypocalcemia and osteodystrophy or to reduce symptoms. Some of these measures, including chronic dialysis, may actually worsen abnormalities in osseous structure and metabolism as well as contribute to deposition of calcium salts in the soft tissue. Thus, abnormalities in calcium and phosphorus metabolism present a major obstacle to the rehabilitation of the patient with chronic renal failure. Stanbury and Lumb1 have stressed the need for interpreting the biochemical abnormalities in the plasma in relation to the osseous changes.