Kidney Medicine | 2019
Dialysate Calcium: A Lot More Than ‘Set It and Forget It’
Abstract
albumin and globulin), chelated, or circulating as ionized calcium. This ionized calcium has important roles in myocyte and cardiac contractility, nerve conduction, and vascular tone regulation. Simplistically, net calcium balance in a patient receiving maintenance hemodialysis is dependent on total dietary intake and the proportion absorbed through the gut; losses in sweat, stool, and urine (the latter of which is minimal in most dialysis patients); and the flux of calcium during dialysis sessions. Dialytic calcium balance is driven by the plasma-dialysate calcium gradient and through convective removal with ultrafiltration. However, this concept of “calcium balance” does not take into account the dysregulated intercompartmental (bone, extracellular fluid, and vasculature) calcium kinetics of dialysis patients resulting in maldistribution. Calcium homeostasis is normally tightly regulated by 1,25-dihydroxyvitamin D (calcitriol), parathyroid hormone (PTH), fibroblast growth factor 23 (FGF-23), and calcitonin. However, given abnormalities in all these hormones, impaired phosphate excretion, exogenous vitamin D receptor agonist administration, and the use of calcium-based phosphate binders, understanding the interior milieu of calcium in dialysis patients is challenging. The icing on this complicated cake is dialysate calcium, which can result in significant calcium flux and have important immediate and long-term consequences. As the search for the optimal dialysate calcium concentration continues, dialysate calcium concentrations commonly used in the United States have changed over time (Fig 1). Initially, a dialysate calcium concentration of 2.5 mEq/L was used because this closely matched the physiologic ionized calcium concentration. However, losses due to ultrafiltration and poor absorption of calcium from the gut due to deficiency of active vitamin D led to widespread hypocalcemia and secondary hyperparathyroidism with resulting hemodynamic and cardiac instability. To avoid these complications, higher calcium loads began being delivered, often with dialysis using a 3.5mEq/L dialysate calcium concentration (Fig 1). With the recognition that cardiovascular disease was the leading cause of death among dialysis patients and concerns that vascular calcification was complicit in cardiovascular