Bone Abstracts

The pathophysiology of secondary hyperparathyroidism (II HPT) in the absence of renal disease is mainly due to lack of vitamin D, calcium deficiency being extremely rare. In case of chronic kidney disease (CKD), phosphate retention and increase in secretion of FGF23 by bone are among the earliest factors associated with II HPT occurrence. Then, the deficit in calcitriol synthesis induces lack of calcium intestinal absorption which worsens II HPT. As renal function declines, the loss of receptors for FGF (FGFR), vitamin D (VDR) and calcium (CaSR) in parathyroid glands is responsible for the progressive autonomisation of these glands leading, together with increase in parathyroid cell proliferation, to tertiary HPT. Tertiary HPT correspond to two histology types: hyperplasia or adenoma, both lesion being potentially associated. The primary management of II HPT is based upon natural vitamin D supplementation (ego/colecalciferol) in association with calcium. In non uremic patients, the use of other forms of vitamin D is not recommended, except when hypocalcemia is present, then treatment with 25OH vitamin D may be used. In CKD, both natural and 1 α vitamin D derivatives may be used in order to down regulate PTH secretion. Cinacalcet, a calcium sensing receptor agonist has, in few years, substantially changed the management of II HPT in CKD and considerably reduced the indication for parathyroid surgery.