CALCIUM-REGULATED PARATHYROID-HORMONE RELEASE IN PATIENTS WITH MILD OR ADVANCED SECONDARY HYPERPARATHYROIDISM

Citation
Wg. Goodman et al., CALCIUM-REGULATED PARATHYROID-HORMONE RELEASE IN PATIENTS WITH MILD OR ADVANCED SECONDARY HYPERPARATHYROIDISM, Kidney international, 48(5), 1995, pp. 1553-1558
Citations number
36
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00852538
Volume
48
Issue
5
Year of publication
1995
Pages
1553 - 1558
Database
ISI
SICI code
0085-2538(1995)48:5<1553:CPRIPW>2.0.ZU;2-W
Abstract
Differences in the regulation of parathyroid hormone (PTH) release by calcium are thought to account for excess PTH secretion in patients wi th secondary hyperparathyroidism (2 degrees HPTH). To determine whethe r calcium-regulated PTH release varies with the severity of 2 degrees HPTH in patients with end-stage renal disease, dynamic tests of parath yroid gland function were done using the four-parameter model in 26 pa tients with 2 degrees HPTH documented by bone biopsy. Estimates of the set point did not differ among patients categorized as mild (basal se rum PTH < 400 pg/ml), moderate (basal PTH 400 to 600 pg/ml) or severe (basal PTH > 600 pg/ml) 2 degrees HPTH; values were 1.23 +/- 0.06 mmol /liter, 1.24 +/- 0.06 mmol/liter and 1.23 +/- 0.05 mmol/liter, respect ively, and none of these set point estimates differed from results obt ained in normal volunteers, 1.21 +/- 0.02 mmol/liter (NS). The slope o f the sigmoidal ionized calcium-PTH curve also did not differ among gr oups. Set point values did not correspond to basal serum PTH levels, t o the maximum serum PTH level observed during hypocalcemia or to the m inimum serum PTH level seen during hypercalcemia in patients with 2 de grees HPTH. In contrast, basal serum PTH values were positively correl ated with both the maximum serum PTH level observed during hypocalcemi a (r = 0.76, P < 0.01), and the minimum serum PTH level attained durin g calcium infusions (r = 0.78, P < 0.01). Calcium-regulated PTH releas e does not differ with the degree of 2 degrees HPTH, and set point abn ormalities do not account for excess PTH secretion in patients with ch ronic renal failure as judged by in vivo dynamic tests of parathyroid gland function. The results suggest that variations in parathyroid gla nd size are the major contributor to excessive PTH secretion in patien ts with chronic renal failure.