Suppressive effect of calcium on parathyroid hormone release in adynamic renal osteodystrophy and secondary hyperparathyroidism

W. G. Goodman, Johannes D Veldhuis, T. R. Belin, H. Juppner, I. B. Salusky

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Serum parathyroid hormone (PTH) levels are markedly lower in patients with the adynamic lesion (AD) of renal osteodystrophy than in those with secondary hyperparathyroidism (2°HPT), but serum PTH values are often moderately elevated in AD when compared to subjects with normal renal and parathyroid gland function (NL). To study the inhibitory effect of calcium on PTH release in AD and in 2°HPT, the response to two-hour intravenous calcium infusions was examined in 6 patients with AD, in 31 patients with 2°HPT and in 20 NL. Basal serum PTH levels were 88 ± 51, 536 ± 395, and 26 ± 6 pg/ml, respectively, in AD, 2°HPT and NL, whereas basal ionized calcium levels did not differ. When expressed as a percentage of pre-infusion values. PTH levels at the end of two-hour calcium infusions were higher both in AD (23.2 ± 5.6%) and in 2°HPT (27.8 ± 12.3%) than in NL. (11.9 ± 5.8%, P < 0.001). Both the amplitude of suppression (%) and the rate of decline (min - 1) in serum PTH were less in AD and 2°HPT than in NL, P < 0.05 for each parameter; corresponding values for each group, with 95% confidence intervals, were 77% (73 to 82) and 0.039 min -1 (0.030 to 0.048) in AD, 72% (68 to 76) and 0.031 min -1 (0.025 to 0.036) in 2°HPT and 87% (84 to 89) and 0.070 min -1 (0.058 to 0.089) in NL. Neither variable differed between AD and 2°HPT. Basal and nadir serum PTH levels were highly correlated: r = 0.95 and P < 0.05 in AD; r = 0.90 and P < 0.01 in 2°HPT; r = 0.75 and P < 0.01 in NL. The slope of this relationship was less, however, both in AD and in 2°HPT than in NL, P < 0.05 by analysis of co-variance. Thus, serum PTH levels fell below 20% of pre-infusion values in fewer subjects with AD (1 of 6) or 2°HPT (9 of 31) than in NL (17 of 20) (χ 2 = 17.81, P < 0.005). The results indicate that the inhibitory effect of calcium on PTH release in vivo does not differ in AD and 2°HPT despite marked differences in basal serum PTH levels. Variations in functional parathyroid gland mass rather than disturbances in calcium-sensing by the parathyroids probably account not only for the lower basal serum PTH levels in patients with AD compared to those with 2°HPT, but also for the moderately elevated serum PTH values commonly seen in patients with AD.

Original languageEnglish (US)
Pages (from-to)1590-1595
Number of pages6
JournalKidney International
Volume51
Issue number5
StatePublished - 1997
Externally publishedYes

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Chronic Kidney Disease-Mineral and Bone Disorder
Secondary Hyperparathyroidism
Parathyroid Hormone
Calcium
Serum
Parathyroid Glands
Intravenous Infusions
Analysis of Variance

ASJC Scopus subject areas

  • Nephrology

Cite this

Goodman, W. G., Veldhuis, J. D., Belin, T. R., Juppner, H., & Salusky, I. B. (1997). Suppressive effect of calcium on parathyroid hormone release in adynamic renal osteodystrophy and secondary hyperparathyroidism. Kidney International, 51(5), 1590-1595.

Suppressive effect of calcium on parathyroid hormone release in adynamic renal osteodystrophy and secondary hyperparathyroidism. / Goodman, W. G.; Veldhuis, Johannes D; Belin, T. R.; Juppner, H.; Salusky, I. B.

In: Kidney International, Vol. 51, No. 5, 1997, p. 1590-1595.

Research output: Contribution to journalArticle

Goodman, WG, Veldhuis, JD, Belin, TR, Juppner, H & Salusky, IB 1997, 'Suppressive effect of calcium on parathyroid hormone release in adynamic renal osteodystrophy and secondary hyperparathyroidism', Kidney International, vol. 51, no. 5, pp. 1590-1595.
Goodman, W. G. ; Veldhuis, Johannes D ; Belin, T. R. ; Juppner, H. ; Salusky, I. B. / Suppressive effect of calcium on parathyroid hormone release in adynamic renal osteodystrophy and secondary hyperparathyroidism. In: Kidney International. 1997 ; Vol. 51, No. 5. pp. 1590-1595.
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abstract = "Serum parathyroid hormone (PTH) levels are markedly lower in patients with the adynamic lesion (AD) of renal osteodystrophy than in those with secondary hyperparathyroidism (2°HPT), but serum PTH values are often moderately elevated in AD when compared to subjects with normal renal and parathyroid gland function (NL). To study the inhibitory effect of calcium on PTH release in AD and in 2°HPT, the response to two-hour intravenous calcium infusions was examined in 6 patients with AD, in 31 patients with 2°HPT and in 20 NL. Basal serum PTH levels were 88 ± 51, 536 ± 395, and 26 ± 6 pg/ml, respectively, in AD, 2°HPT and NL, whereas basal ionized calcium levels did not differ. When expressed as a percentage of pre-infusion values. PTH levels at the end of two-hour calcium infusions were higher both in AD (23.2 ± 5.6{\%}) and in 2°HPT (27.8 ± 12.3{\%}) than in NL. (11.9 ± 5.8{\%}, P < 0.001). Both the amplitude of suppression ({\%}) and the rate of decline (min - 1) in serum PTH were less in AD and 2°HPT than in NL, P < 0.05 for each parameter; corresponding values for each group, with 95{\%} confidence intervals, were 77{\%} (73 to 82) and 0.039 min -1 (0.030 to 0.048) in AD, 72{\%} (68 to 76) and 0.031 min -1 (0.025 to 0.036) in 2°HPT and 87{\%} (84 to 89) and 0.070 min -1 (0.058 to 0.089) in NL. Neither variable differed between AD and 2°HPT. Basal and nadir serum PTH levels were highly correlated: r = 0.95 and P < 0.05 in AD; r = 0.90 and P < 0.01 in 2°HPT; r = 0.75 and P < 0.01 in NL. The slope of this relationship was less, however, both in AD and in 2°HPT than in NL, P < 0.05 by analysis of co-variance. Thus, serum PTH levels fell below 20{\%} of pre-infusion values in fewer subjects with AD (1 of 6) or 2°HPT (9 of 31) than in NL (17 of 20) (χ 2 = 17.81, P < 0.005). The results indicate that the inhibitory effect of calcium on PTH release in vivo does not differ in AD and 2°HPT despite marked differences in basal serum PTH levels. Variations in functional parathyroid gland mass rather than disturbances in calcium-sensing by the parathyroids probably account not only for the lower basal serum PTH levels in patients with AD compared to those with 2°HPT, but also for the moderately elevated serum PTH values commonly seen in patients with AD.",
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T1 - Suppressive effect of calcium on parathyroid hormone release in adynamic renal osteodystrophy and secondary hyperparathyroidism

AU - Goodman, W. G.

AU - Veldhuis, Johannes D

AU - Belin, T. R.

AU - Juppner, H.

AU - Salusky, I. B.

PY - 1997

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N2 - Serum parathyroid hormone (PTH) levels are markedly lower in patients with the adynamic lesion (AD) of renal osteodystrophy than in those with secondary hyperparathyroidism (2°HPT), but serum PTH values are often moderately elevated in AD when compared to subjects with normal renal and parathyroid gland function (NL). To study the inhibitory effect of calcium on PTH release in AD and in 2°HPT, the response to two-hour intravenous calcium infusions was examined in 6 patients with AD, in 31 patients with 2°HPT and in 20 NL. Basal serum PTH levels were 88 ± 51, 536 ± 395, and 26 ± 6 pg/ml, respectively, in AD, 2°HPT and NL, whereas basal ionized calcium levels did not differ. When expressed as a percentage of pre-infusion values. PTH levels at the end of two-hour calcium infusions were higher both in AD (23.2 ± 5.6%) and in 2°HPT (27.8 ± 12.3%) than in NL. (11.9 ± 5.8%, P < 0.001). Both the amplitude of suppression (%) and the rate of decline (min - 1) in serum PTH were less in AD and 2°HPT than in NL, P < 0.05 for each parameter; corresponding values for each group, with 95% confidence intervals, were 77% (73 to 82) and 0.039 min -1 (0.030 to 0.048) in AD, 72% (68 to 76) and 0.031 min -1 (0.025 to 0.036) in 2°HPT and 87% (84 to 89) and 0.070 min -1 (0.058 to 0.089) in NL. Neither variable differed between AD and 2°HPT. Basal and nadir serum PTH levels were highly correlated: r = 0.95 and P < 0.05 in AD; r = 0.90 and P < 0.01 in 2°HPT; r = 0.75 and P < 0.01 in NL. The slope of this relationship was less, however, both in AD and in 2°HPT than in NL, P < 0.05 by analysis of co-variance. Thus, serum PTH levels fell below 20% of pre-infusion values in fewer subjects with AD (1 of 6) or 2°HPT (9 of 31) than in NL (17 of 20) (χ 2 = 17.81, P < 0.005). The results indicate that the inhibitory effect of calcium on PTH release in vivo does not differ in AD and 2°HPT despite marked differences in basal serum PTH levels. Variations in functional parathyroid gland mass rather than disturbances in calcium-sensing by the parathyroids probably account not only for the lower basal serum PTH levels in patients with AD compared to those with 2°HPT, but also for the moderately elevated serum PTH values commonly seen in patients with AD.

AB - Serum parathyroid hormone (PTH) levels are markedly lower in patients with the adynamic lesion (AD) of renal osteodystrophy than in those with secondary hyperparathyroidism (2°HPT), but serum PTH values are often moderately elevated in AD when compared to subjects with normal renal and parathyroid gland function (NL). To study the inhibitory effect of calcium on PTH release in AD and in 2°HPT, the response to two-hour intravenous calcium infusions was examined in 6 patients with AD, in 31 patients with 2°HPT and in 20 NL. Basal serum PTH levels were 88 ± 51, 536 ± 395, and 26 ± 6 pg/ml, respectively, in AD, 2°HPT and NL, whereas basal ionized calcium levels did not differ. When expressed as a percentage of pre-infusion values. PTH levels at the end of two-hour calcium infusions were higher both in AD (23.2 ± 5.6%) and in 2°HPT (27.8 ± 12.3%) than in NL. (11.9 ± 5.8%, P < 0.001). Both the amplitude of suppression (%) and the rate of decline (min - 1) in serum PTH were less in AD and 2°HPT than in NL, P < 0.05 for each parameter; corresponding values for each group, with 95% confidence intervals, were 77% (73 to 82) and 0.039 min -1 (0.030 to 0.048) in AD, 72% (68 to 76) and 0.031 min -1 (0.025 to 0.036) in 2°HPT and 87% (84 to 89) and 0.070 min -1 (0.058 to 0.089) in NL. Neither variable differed between AD and 2°HPT. Basal and nadir serum PTH levels were highly correlated: r = 0.95 and P < 0.05 in AD; r = 0.90 and P < 0.01 in 2°HPT; r = 0.75 and P < 0.01 in NL. The slope of this relationship was less, however, both in AD and in 2°HPT than in NL, P < 0.05 by analysis of co-variance. Thus, serum PTH levels fell below 20% of pre-infusion values in fewer subjects with AD (1 of 6) or 2°HPT (9 of 31) than in NL (17 of 20) (χ 2 = 17.81, P < 0.005). The results indicate that the inhibitory effect of calcium on PTH release in vivo does not differ in AD and 2°HPT despite marked differences in basal serum PTH levels. Variations in functional parathyroid gland mass rather than disturbances in calcium-sensing by the parathyroids probably account not only for the lower basal serum PTH levels in patients with AD compared to those with 2°HPT, but also for the moderately elevated serum PTH values commonly seen in patients with AD.

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