Calcium balance and intact PTH variations during haemodiafiltration

Recent approaches to prevent and treat secondary hyperparathyroidism in dialysis patients include decreasing dialysate Ca content from 1.75 to 1.5 mM or lower. We have recently observed that by decreasing dialysate Ca to 1.25 mM a rise in intact parathormone serum levels occurs despite adequately controlled predialysis Ca and phosphate serum levels. In that study complementary treatment with high-dose 1 alpha(OH) vitamin D3 was required to suppress the parathormone. In the present study we aimed to assess the total Ca balance as well as the modifications in parathormone induced by the dialysis session in order to understand the reasons for which the rise in parathormone was induced.

Fourteen HD patients treated with haemodiafiltration three times/week gave their informed consent for the study. They were distributed in two groups with identical treatment but for the dialysate Ca content which was 1.5 and 1.25 mM respectively and for the amount of oral CaCO3 received. Total and ionized Ca, phosphate, pH, and albumin as well as parathormone were measured in serum before and after dialysis and in the spent dialysate during two dialysis sessions.

Serum ionized Ca (normalized to pH 7.4) did not change during 1.25 mM dialysate Ca and significantly increased with 1.5 mM (P < 0.001). The end-dialysis values being 1.25 +/- 0.02 and 1.38 +/- 0.02 mM respectively. Total Ca significantly decreased with 1.25 mM dialysate Ca (P < 0.04) and increased with 1.5 mM (P < 0.003), the end-dialysis values being 2.51 +/- 0.03 and 2.75 +/- 0.04 mM respectively. In the dialysate the difference in ionized Ca concentrations, fresh minus spent dialysate was -1.78 +/- 1.12 mmol/l (NS) and 4.26 +/- 1.47 mmol/l (P < 0.02) respectively for 1.25 and 1.5 mM dialysate Ca. The difference in total Ca concentrations, fresh minus spent dialysate was -0.1 +/- 0.01 mmol/l (P < 0.05) and -0.002 +/- 0.01 mmol/l (NS) respectively. Phosphate removal was higher in 1.25 mM dialysate-Ca-treated patients (40.4 +/- 1.75 mmol/session versus 34 +/- 1.3 mmol/session respectively, P < 0.015). The use of 1.25 mM dialysate Ca did not result in a change in serum parathormone, while the use of 1.5 mM resulted in a decrease of 43 +/- 15% (P < 0.02) in patients with marked hyperparathyroidism.

Our data remind us of the difficulty in assessing Ca balances and identifies the phosphate content as one of the factors influencing the amount of ionized Ca in the dialysate. Although the long-term parathormone increase we observed using 1.25 mM dialysate Ca may well not be explained only by the acute intradialytic modifications, the negative Ca balance identified here (which was missed with the analysis of ionized Ca alone), and the lack of parathormone inhibition may participate in the relapse of hyperparathyroidism.