The kidney as an endocrine organ involved in calcium homeostasis

Clinicians have for several decades recognized the existence of sever bone disease associated with chronic renal failure. This problem has become more acute in recent years with the continued improvement of patient management, especially with the use of chronic dialysis.The bone disease which develops as a result of chronic renal failure has many components, including osteomalacia and/or osteitis fibrosa cystica due to secondary hyperparathyroidism. The basic reason for the development of bone disease is still a matter of debate. Bricker et al [1] proposed the hypothesis that transient phosphate retention with each decrement in renal function is a major factor leading to secondary hyperparathyroidism. Although this theory still remains as an attractive possibility, recent developments have brought into focus a new possibility involving the functional metabolism of vitamin D to a hormonal form responsible for the mobilization of calcium from both intestine and bone. With this in mind the remainder of this review will develop this idea as it currently exists and will bring into focus new information which may bring both the Bricker hypothesis and the vitamin D metabolism hypothesis of renal osteodystrophy [2] closer together