Abstract
Chronic renal failure is the primary cause of secondary hyperparathyroidism (SHPT). Patients with mineral metabolism disorders commonly present with low serum calcium levels, hyperphosphatemia, and calcitriol deficiency. In normal renal function subjects, parathyroid cells have a low turnover and rarely undergo mitoses. In uremic conditions, however, parathyroid glands become hyperplasic and leave quiescence. During the last ten years, new molecular mechanisms have been investigated to better understand the pathogenesis of SHPT: the emerging role of the Calcium Sensing Receptor (CaSR); the importance of the parathyroid expression of the Vitamin D receptor (VDR); the growing evidence on the central role of the Fibroblast Growth Factor 23 (FGF-23). In contrast, the discovery of a parathyroid phosphate sensor or receptor has yet to be made.
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