Reversibility of experimental secondary hyperparathyroidism

Parathyroid hormone regulation in normal and uremic rats. Reversibility of secondary hyperparathyroidism after experimental kidney transplantation.

Intensification of Anemia by Secondary Hyperparathyroidism in Hemodialysis Patients

The excessive amounts of parathyroid hormone in secondary hyperparathyroidism (SHPTH) is suggested to interfere with normal erythropoiesis.  In SHPTH, during chronic renal failure, due to the impairment of erythropoietin synthesis, this effect is more pronounced.  In the present study the role of secondary hyperparathyroidism in the severity of anemia was evaluated in hemodialysis patients (n=3...

Pathogenesis of secondary hyperparathyroidism.

Chronic renal failure is the primary cause of secondary hyperparathyroidism (SHPT). Patients with mineral metabolism disorders commonly present with low serum calcium levels, hyperphosphatemia, and calcitriol deficiency. In normal renal function subjects, parathyroid cells have a low turnover and rarely undergo mitoses. In uremic conditions, however, parathyroid glands become hyperplasic and le...

Pathogenesis of secondary hyperparathyroidism.

Hyperplasia of the parathyroid glands and increased concentrations of immunoreactive parathyroid hormone are among the earlier alterations of mineral metabolism in patients with chronic renal failure. In the past five years several investigators have demonstrated that phosphorus retention plays a key role in the development of secondary hyperparathyroidism and chief cell hyperplasia of the para...

Mechanisms of secondary hyperparathyroidism.

Small decreases in serum Ca(2+) and more prolonged increases in serum phosphate (P(i)) stimulate the parathyroid (PT) to secrete parathyroid hormone (PTH), and 1,25(OH)(2)D(3) decreases PTH synthesis and secretion. A prolonged decrease in serum Ca(2+) and 1,25(OH)(2)D(3), or increase in serum P(i), such as in patients with chronic renal failure, leads to the appropriate secondary increase in se...