Background: Low dialysate calcium (LdCa) concentration is used to prevent or treat hemodialysis (HD)-induced hypercalcemia, but its use has been complicated by intradialytic hypotension in some patients. Our goal was to explore the possibility that dialysis calcium profiling (dCaP) can ameliorate intradialytic hypotension in HD patients who need to have dialysis performed with LdCa.
Methods: In a randomized crossover design, eighteen HD patients underwent one four-hour HD session with LdCa of 1.25 mmol/L (LdCa group) and one four-hour HD session with LdCa of 1.25 mmol/L during the first two hours and high dCa of 1.75 mmol/L during the remaining two hours (dCaP group). After that, they underwent another four-hour HD session with medium dCa of 1.5 mmol/L (MdCa group). Before HD and at four 60-minute intervals during the HD sessions, blood pressure (BP), heart rate (HR) and noninvasive measurements of cardiac index (CI), using bioelectrical impedance, were obtained. Ionized serum calcium (iCa) also was measured before HD and at 120 and 240 minutes into the HD session. In a separate study, eight HD patients were treated for three weeks with 1.25 mmol/L dCa and three weeks with the dCaP technique described above, in random order. A three-week treatment with MdCa followed. BP and symptoms were recorded during each HD session.
Results: During the LdCa treatment the iCa values remained unchanged, whereas mean arterial pressure (MAP) and CI decreased by 16.5 +/- 8.3% and 14.2 +/- 14.6%, respectively, at the end of HD. During the first half of the dCaP treatment, iCa, MAP and CI decreased by 2.2 +/- 4.1%, 12.6 +/- 12.3%, and 9.6 +/- 13.4%, respectively, whereas during the second half of the same treatment, iCa, MAP and CI values increased by 10.2 +/- 3.3%, 7.8 +/- 7.2% and 10.8 +/- 9.1%, respectively, from the middle HD values. ANOVA showed that the time x treatment effect was significant for iCa, MAP and CI. Total peripheral resistance and HR changes were insignificant and similar among treatments. Hemodynamic effects were comparable between LdCa and MdCa treatments. Intradialytic events were reduced (P < 0.05) only with the dCaP treatment.
Conclusions: The drop in BP observed during the last two hours of HD in both the LdCa and MdCa groups was abolished in the dCaP group. The latter was accomplished via an increase in cardiac output, due to an iCa-induced increase in myocardial contractility. Therefore, dCaP, by individualizing the dCa concentrations used and timing the switching between them, may improve intradialytic BP instability and simultaneously minimize the risk for HD patients to develop hypercalcemia.