The mechanisms of parathyroid hyperplasia and its regression

Parathyroid gland (PTG) is a unique endocrine organ in which the quiescent glandular cells begin to proliferate in the progressive course of renal failure, leading to secondary hypereparathyroidism (SHPT). SHPT is characterized by continuous over-secretion of parathyroid hormone (PTH) and parathyroid hyperplasia, and the major contributing factors are a deficiency of active vitamin D, hypocalcemia and phosphate retention. Many experimental and human studies have revealed that the down-regulations of vitamin D receptor (VDR), calcium (Ca) -sensing receptor (CaSR), and retinoid X receptor (RXR) in parathyroid hyperplasia of SHPT, especially nodular hyperplasia, which is a severe form of hyperplasia. These also contribute to progression of parathyroid hyperplasia. Recently, mechanisms by which active vitamin D and Ca regulate parathyroid hyperplasia via their receptors have been clarified. In this paper, we review mechanisms for progression of parathyroid hyperplasia and the possibility for regression of parathyroid hyperplasia.