SUPPRESSIVE EFFECT OF CALCIUM ON PARATHYROID-HORMONE RELEASE IN ADYNAMIC RENAL OSTEODYSTROPHY AND SECONDARY HYPERPARATHYROIDISM

Serum parathyroid hormone (PTH) levels are markedly lower in patients with the adynamic lesion (AD) of renal osteodystrophy than in those wi th secondary hyperparathyroidism (2 degrees HPT), but serum PTH values are often moderately elevated in AD when compared to subjects with no rmal renal and parathyroid gland function (NL). To study the inhibitor y effect of calcium on PTH release in AD and in 2 degrees HPT, the res ponse to two-hour intravenous calcium infusions was examined in 6 pati ents with AD, in 31 patients with 2 degrees HPT and in 20 NL. Basal se rum PTH levels were 88 +/- 51, 536 +/- 395, and 26 +/- 6 pg/ml, respec tively, in AD, 2 degrees HPT and NL, whereas basal ionized calcium lev els did nor differ. When expressed as a percentage of pre-infusion val ues, PTH levels at the end of two-hour calcium infusions were higher b oth in AD (23.2 +/- 5.6%) and in 2 degrees HPT (27.8 +/- 12.3%) than i n 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 degrees HPT than in NL, P < 0.05 for each parameter: corresponding va lues for each group, with 95% confidence intervals, were 77% (73 to 52 ) and 0.039 min(-1) (0.030 to 0.018) in AD, 72% (68 to 76) and 0.031 m in(-1) (0.025 to 0.036) in 2 degrees HPT and 87% (84 to 89) and 0.070 min(-1) (0.058 to 0.089) in NL. Neither variable differed between AD a nd 2 degrees HPT. Basal and nadir serum PTH levels were highly correla ted: r = 0.95 and P < 0.05 in AD; r = 0.90 and P < 0.01 in 2 degrees H PT; r = 0.75 and P < 0.01 in NL. The slope of this relationship was le ss, however, both in AD and in 2 degrees HPT than in NL, P < 0.05 by a nalysis of co-variance. Thus, serum PTH levels fell below 20% of pre-i nfusion values in fewer subjects with AD (1 of 6) or 2 degrees HPT (9 of 31) than in NL (17 of 20) (chi(2) = 17.51, P < 0.005). The results indicate thai the inhibitory effect of calcium on PTH release in vivo does not differ in AD and 2 degrees HPT despite marked differences in basal serum PTH levels. Variations in functional parathyroid gland mas s rather than disturbances in calcium-sensing by the parathyroids prob ably account not only for the lower basal serum PTH levels in patients with AD compared to those with 2 degrees HPT, but also for the modera tely elevated serum PTH values commonly seen in patients with AD.