II. RECOMMENDATIONS FOR THE MANAGEMENT OF RENAL OSTEODYSTROPHY Molecular mechanisms of secondary hyperparathyroidism

concentration, which is recognized by a sevenIntroduction transmembrane-domain receptor with a large extracellular amino-terminal region, the calcium-sensing The development of secondary hyperparathyroidism receptor [4]. A decrease in extracellular calcium is a major risk factor for the development of renal concentration leads not only to an increase in PTH osteodystrophy. In cases of chronic renal failure (CRF) secretion but also to increases in PTH mRNA levels where there is an inadequate increase in parathyroid and parathyroid cell proliferation. Hypocalcaemia hormone (PTH ) secretion, adynamic bone disease may increases PTH secretion in the short term, PTH mRNA develop. There is, therefore, a pressing clinical need to levels in hours and days and parathyroid cell number be able to fine-tune the synthesis and secretion of PTH after a more prolonged stimulus [5–7]. and the compensatory increase necessary in CRF. This requires an understanding of the physiological mechanisms involved in regulating PTH synthesis and secretion.