Nephrol Dial Transplant (2001) 16: 1214-1221
© 2001 European Renal Association-European Dialysis and Transplant Association
Rate dependence of acute PTH release and association between basal plasma calcium and set point of calcium–PTH curve in dialysis patients
1 Departments of Nephrology and Dialysis, Hospital of Sondrio, Sondrio, 2 Medical Statistics, University of Pavia, Pavia, Italy
Background. In vivo, the control of calcium-mediated acute PTH release during induced hypo- or hypercalcaemia is linked not only to plasma calcium concentration per se but also to the rate and direction of calcium change. In fact, during induced hypocalcaemia, the predominant mechanism that causes PTH to be released is the reduction of plasma Ca2+ irrespective of the absolute starting concentration of ionized calcium. This mechanism, which is rate-dependent and even activated in conditions of hypercalcaemia, may be involved in the association, reported in several papers, between the basal Ca2+ and the set point of the calcium–PTH curve.
Methods. The calcium–PTH relationship was studied in 12 dialysis patients under conditions of induced low and high predialysis plasma Ca2+. At each level of basal Ca2+, dynamic tests were conducted using two methodological approaches. In method A patients underwent low (0.5 mmol/l) calcium dialysis in the stimulation test and high (2 mmol/l) calcium dialysis in the inhibition test, while the dialysate calcium (CaD) was kept constant during each test. In this way a higher but variable rate of change in plasma Ca2+ was achieved. In method B, CaD was progressively decreased (stimulation test) and increased (inhibition test) during the tests in order to obtain a lower but more constant rate of change in plasma Ca2+. Consequently, for each patient, four calcium–PTH curves were produced: low basal Ca2+ with methods A and B, and high basal Ca2+ with methods A and B.
Results. Basal plasma Ca2+ was similar in A and B at low (1.16±0.02 vs 1.15±0.02 mmol/l) and high (1.25±0.02 vs 1.26±0.02 mmol/l) basal plasma Ca2+. The set point was higher in A than in B both at low (1.12±0.02 vs 1.10±0.02 mmol/l, P=0.01) and high (1.20±0.02 vs 1.16±0.02 mmol/l, P=0.03) basal Ca2+ as was the slope (542±41 vs 426±44%/mmol, P=0.02; 615±73 vs 389±25%/mmol, P=0.01). No significant difference was found between A and B as regards minimal PTH and plasma Ca2+ at minimal PTH (Camin) in both calcaemic states. Maximal PTH was slightly higher in B at low (510±97 vs 548±107 pg/ml, P=NS) and high basal plasma Ca2+ (410±97 vs 464±108 pg/ml, P=0.02). Plasma calcium at maximal PTH (Camax) was significantly higher in A (1.1±0.03 vs 0.99±0.02 mmol/l, P=0.001) at high basal plasma Ca2+. The set point was strictly related to basal plasma Ca2+ in both methods, but the slope of the linear regression was significantly steeper with method A. The set point was predicted to increase by 0.881 (CI 0.772–0.990) mmol/l for each mmol/l of increase in basal plasma Ca2+ with method A and by 0.641 (CI 0.546–0.737) mmol/l for each mmol/l of increase in basal plasma Ca2+ with method B.
Conclusions. (i) Higher and variable rates of change in plasma Ca2+ produce a higher set point value and a steeper slope of the calcium–PTH curve when compared to lower and more constant rates of calcium change. (ii) The different slope of the linear correlations between basal plasma Ca2+ and set point in the two methods suggests that the rate-dependent mechanism of acute PTH release plays a significant role in the association between set point and basal plasma Ca2+. (iii) The significance of the set point is questionable when the calcium–PTH curve is carried out in vivo.
Keywords: acute PTH secretion; basal plasma calcium; four-parameter model; hysteresis; rate of change in plasma calcium; set point
Correspondence and offprint requests to: Vincenzo De Cristofaro, Department of Nephrology and Dialysis, Hospital of Sondrio, Via Stelvio 25, I-23100 Sondrio, Italy.
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