| [ Summary ] |
To understand the process and mechanism of parathyroid hyperplasia, induced by uremia, it is very important to prevent the progression of renal hyperparathyroidism and to select therapeutic options. Although it is well known that hypocalcemia, a deficiency of active vitamin D, and phosphate retention induce parathyroid cell proliferation, the mechanism and signals of the phenomena are not yet clear. It is speculated that these factors may independently contribute to the control of parathyroid cell numbers by acting as cell cycle regulators. In cases of prolonged uremia, the parathyroid glands progress from a state of polyclonal diffuse hyperplasia to one of nodular hyperplasia, with has some nodules having cells which proliferate monoclonally. It is suspected that in the cells constituting these nodules, the expression of calcium-sensing receptors and vitamin D receptors is different and the monoclonal origin of each nodule is independent. The mechanism of parathyroid tumorigenesis in primary hyperparathyroidism has gradually become clear. However, the mechanism of monoclonal proliferation of parathyroid cells in renal hyperparathyroidism is not well understood as yet. |