CALCIUM-REGULATED PARATHYROID-HORMONE SECRETION IN ADYNAMIC RENAL OSTEODYSTROPHY

Hypercalcemia and low serum parathyroid hormone (PTH) levels are featu res 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-regul ated PTH release in patients with either adynamic bone or secondary hy perparathyroidism (OF) as documented by bone biopsy and in normal volu nteers (NL). Patients had undergone CCPD for 20 +/- 4.2 months, and al l received calcium carbonate as the sole phosphate-binding agent Durin g two hours infusions of sodium citrate, the rate of decline in serum ionized calcium levels did not differ among groups; serum PTH levels r ose 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 baseli ne values in AD but only 146 +/- 9.7% of baseline in OF (P < 0.001), a nd the increase above baseline levels in AD did not differ from that i n NL (300 +/- 25%, NS). During calcium infusions, serum PTH levels fel l 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 percentag e 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 calc ium; 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 in dicate that abnormalities in the set point for calcium-regulated PTH r elease do not account for marked differences in serum PTH levels in pa tients with low-turnover and high-turnover skeletal lesions of renal o steodystrophy.