CALCIUM-REGULATED PARATHYROID-HORMONE SECRETION IN ADYNAMIC RENAL OSTEODYSTROPHY

Hypercalcemia and low serum parathyroid hormone (PTH) levels are features of the adynamic lesion (AD) of renal osteodystrophy, but there is little information about parathyroid gland function in this disorder. Therefore, the four parameter model was used to evaluate calcium-regulated PTH release in patients with either adynamic bone or secondary hyperparathyroidism (OF) as documented by bone biopsy and in normal volunteers (NL). Patients had undergone CCPD for 20 +/- 4.2 months, and all received calcium carbonate as the sole phosphate-binding agent During two hours infusions of sodium citrate, the rate of decline in serum ionized calcium levels did not differ among groups; serum PTH levels rose from 136 +/- 38 to 342 +/- 140 pg/ml in AD and from 691 +/- 99 to 869 +/- 121 pg/ml in OF. Maximum PTH levels were 322 +/- 42% of baseline values in AD but only 146 +/- 9.7% of baseline in OF (P < 0.001), and the increase above baseline levels in AD did not differ from that in NL (300 +/- 25%, NS). During calcium infusions, serum PTH levels fell from 164 +/- 75 to 39 +/- 11 pg/ml in AD and from 622 +/- 76 to 171 +/- 29 pg/ml in OF; minimum serum PTH levels, expressed as a percentage of pre-infusion values, were 25 +/- 2% in AD and 26 +/- 5% in OF (NS). The slope of the sigmoidal calcium-PTH curve was less in AD than in OF (54 +/- 27 versus 127 +/- 149 pg/ml/mmol, P < 0.05), suggesting a decrease in sensitivity of the parathyroids to changes in ionized calcium; however, set point values were 1.20 +/- 0.01, 1.22 +/- 0.01 and 1.21 +/- 0.01 mmol/liter in AD, OF and NL, respectively. The results indicate that abnormalities in the set point for calcium-regulated PTH release do not account for marked differences in serum PTH levels in patients with low-turnover and high-turnover skeletal lesions of renal osteodystrophy.