Evaluation of the calcium-PTH axis and renal handling of phosphate by calcium and citrate clamp techniques in normal subjects and in patients with heavy proteinuria.

We studied the effect of induced hyper- and hypocalcemia on parathyroid function and renal handling of phosphate in healthy subjects (n = 10) and in patients with heavy proteinuria, mean 5.6 +/- 1.9 g/24 hours (n = 5). We used calcium and citrate clamp techniques. Hypercalcemia was rapidly induced by calcium infusion and maintained for 120 min, and correspondingly, hypocalcemia by citrate infusion. The suppression of intact PTH secretion during calcium clamp was similar (to the level of < or = 0.8 pmol/l) in both groups. The response of the parathyroid glands to hypocalcemia was similar in normal subjects and proteinuric patients. Both groups showed a peak of PTH secretion at 10 min, 18.9 +/- 6.7 pmol/l in healthy subjects and 20.4 +/- 7.4 pmol/l in patients. The peak levels were 4.8-7.2 times and 4.0-6.7 times the baseline level, respectively. Thereafter the plasma PTH concentration declined to a fairly constant steady-state level (twice the baseline level) in spite of maintained hypocalcemia. The area under the curve of the plasma concentrations of intact PTH at various times (AUC0-120) was 890 +/- 324 pmol/l/min in normal subjects and 989 +/- 331 pmol/l/min in proteinuric patients, the difference between the groups being again not significant. The renal threshold phosphate concentration (TmPO4/GFR) increased during calcium infusion and decreased during citrate infusion in both groups. During recovery from hypocalcemia PTH levels were lower than during hypocalcemic induction at corresponding serum calcium levels. Using calcium and citrate clamp techniques, we found that the response of the parathyroid glands in acute and maintained hypercalcemia and hypocalcemia, and renal phosphate handling in patients with heavy proteinuria was not different from that of healthy subjects.