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Molecular Basis for the Management of Secondary Hyperparathyroidism in Chronic Renal Failure
Author(s) -
Fukagawa Masafumi,
Yi Hung,
Fukuda Naoko,
Kurokawa Kiyoshi
Publication year - 1995
Publication title -
artificial organs
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 76
eISSN - 1525-1594
pISSN - 0160-564X
DOI - 10.1111/j.1525-1594.1995.tb02287.x
Subject(s) - calcitriol , secondary hyperparathyroidism , hyperparathyroidism , calcitriol receptor , endocrinology , medicine , parathyroid gland , hyperplasia , chronic renal failure , vitamin d and neurology , parathyroid hormone , calcium
Recent clinical and experimental data suggest that the resistance of parathyroid cells to the physiological concentration of calcitriol plays an important role in the pathogenesis and the progression of secondary hyperparathyroidism in chronic renal failure. This resistance is due to the decreased density of the calcitriol receptor in parathyroid cells, which may result from impaired up‐regulation of calcitriol receptor. Since patients with larger parathyroid glands were more resistance to calcitriol pulse therapy than those with smaller glands and calcitriol receptor density inversely correlated with gland weight, the size of the parathyroid gland may serve as a marker for the degree of resistance to calcitriol. Furthermore, the possible role of phosphorus in the control of parathyroid function has been suggested recently. Thus, it is most important to prevent the progression of parathyroid hyperplasia in chronic renal failure by the early use of active vitamin D, calcitriol pulse therapy, and dietary phosphorus restriction.