Secondary hyperparathyroidism is a frequent complication of chronic renal f
ailure (CRF) and a major factor in the pathogenesis of renal osteodystrophy
. A high serum phosphate, decreased levels of serum 1,25(OH)(2)D-3 and the
subsequently low serum calcium are the major metabolic abnormalities in CRF
, which lead to the secondary hyperparathyroidism. At the level of parathyr
oid hormone (PTH) secretion there is insensitivity to the ambient serum cal
cium. PTH mRNA levels are increased by a post-transcriptional mechanism tha
t involves the binding of PT cytosolic proteins to the PTH mRNA 3'-untransl
ated region (UTR). In a dietary model of secondary hyperparathyroidism due
to hypocalcemia there is increased binding of parathyroid proteins to the 3
'-UTR and decreased degradation as determined by an in vitro degradation as
say. Changes in serum phosphate also dramatically regulate PTH mRNA stabili
ty. There is also regulation at the level of PT cell proliferation. PT cell
proliferation is increased by experimental hypocalcemia or hyperphosphatem
ia and decreased by hypophosphatemia and administered 1,25(OH)(2)D-3. The u
nderstanding of the molecular mechanisms involved in the genesis of seconda
ry hyperparathyroidism will allow the design of new effective strategies in
the management of this troubling condition.