Non-suppressible secondary hyperparathyroidism in chronic progressive renal disease

Parathyroid hormone and calcitonin secretion in uraemic infants

“…The lack of hypercalcaemia after infusion of calcium in these two subjects may be due to the avidity for calcium of bone that has been more compromised by parathyroid hyperfunction [20]. The failure of calciuria to increase and of phosphaturia to decrease during the test seems to support the hypothesis of functional autonomy of the parathyroids [25], but other authors have shown that hyperparathyroidism is not autonomous in uraemia, and that the levels of PTH return to normal either during haemodialysis. or after kidney transplantation [9,20].…”

Hypercalcemia in Patients with Advanced Chronic Renal Failure Not Yet Requiring Dialysis

“…In patients with renal failure, this could be due to dimin ished binding of 1,25-dihvdroxyvitamin D to parathy roid tissue [28], as this hormone has been shown to reduce PTH secretion [29], Some authors [8,9] refute the existence of tertiary' hyperparathyroidism by suggest ing that true parathyroid autonomy is not present in patients whose parathyroid secretion responds to changes in calcium level induced by calcium infusion or EDTA [8,30]. Notwithstanding this contention, we choose to define tertiary hyperparathyroidism as para thyroid-mediated hypercalcemia occurring in the setting of long-standing secondary hyperparathyroidism.…”

“…Proponents of the trade-off hypothesis suggested that tertiary hyperparathyroidism simply re sulted when parathyroid hyperplasia was so massive that enough PTH secretion persisted to cause hypercalcemia despite normal suppression of the gland by calcium infu sion. The few non suppressible cases could be restored to suppressibility when subtotal parathyroidectomy was used to reduce the mass of parathyroid tissue [8,9], Although medical suppression of secondary and even tertiary hyperparathyroidism can be achieved [10], sur gical treatment is still employed frequently [11,12], if not without hazard [13][14][15][16][17], Studies of such excised parathyroid tissue have clearly shown an abnormality of calcium set point for parathyroid hormone in secondary and tertiary hyperparathyroidism independent of any increase in gland mass [18,19], Although tertiary hyperparathyroidism is probably the most common cause of hypercalcemia in patients with chronic renal failure not yet severe enough to warrant dialysis therapy, this subject has not been looked at care fully. In this report, we review the causes of predialysis hypercalcemia discovered at a large, multihospital univer sity medical center over a 5-year period and make sugges tions about its proper evaluation and management.…”

Relationship Between the Kidney and Parathyroid Hormone

“…Serial histo logical sections o f the parathyroid glands showed only chief cell hyperplasia, but their weights ranged between 2.0 and 4.4 g, respectively. Slatopolsky et al [151] also found that patients with nonsuppressible or poorly suppressible secondary hyperparathyroidism became readily suppressible following removal of 80% of their parathyroid tissue. These observations suggest that the same parathyroid tissue may be suppressible, as indicated by changes in TRP, when its size is reduced.…”