Abstract
Patients on hemodialysis are exposed to calcium via the dialysate at least three times a week. Changes in serum calcium vary according to calcium mass transfer during dialysis, which is dependent on the gradient between serum and dialysate calcium concentration (d[Ca]) and the skeleton turnover status that alters the ability of bone to incorporate calcium. Although underappreciated, the d[Ca] can potentially cause positive calcium balance that leads to systemic organ damage, including associations with mortality, myocardial dysfunction, hemodynamic tolerability, vascular calcification, and arrhythmias. The pathophysiology of these adverse effects includes serum calcium changes, parathyroid hormone suppression, and vascular calcification through indirect and direct effects. Some organs are more susceptible to alterations in calcium homeostasis. In this review, we discuss the existing data and potential mechanisms linking the d[Ca] to calcium balance with consequent dysfunction of the skeleton, myocardium, and arteries.
Highlights
Patients with end-stage kidney disease (ESKD) have increased morbidity and mortality[1]; chronic kidney disease mineral bone disorder (CKD-MBD) is a consistent independent risk factor
Calcium disturbances and treatments that alter serum calcium have been addressed in several reviews, the impact of a positive calcium balance during hemodialysis due to calcium dialysate content - d[Ca] - on this outcome is rarely considered
The purpose of this review is to examine the evidence supporting a pathologic role of a positive calcium balance on end organ damage in patients undergoing hemodialysis
Summary
Patients with end-stage kidney disease (ESKD) have increased morbidity and mortality[1]; chronic kidney disease mineral bone disorder (CKD-MBD) is a consistent independent risk factor. The ratio of extracellular to intracellular calcium and the amount of calcium stored within the cells are tightly controlled[2] This homeostasis is disrupted in patients with chronic kidney disease (CKD) due to disruption of normal homeostatic loops with kidney function decline, with compensatory changes in several hormones (parathyroid hormone - PTH, vitamin D, fibroblast growth factor 23 - FGF23). Basile et al.[13] showed in 2001 that neither pre- nor post-dialysis systolic and diastolic blood pressures, predialysis serum bicarbonate and pH, and pre-dialysis serum sodium, potassium, calcium, or phosphorus were significantly different when comparing hemodialysis and hemodiafiltration Another potential confounding factor for the intradialytic calcium balance is the use of citrate instead of acetate in the dialysate. Summary of several studies showing calcium mass transfer (CMT) according to dialysate calcium concentration - d[Ca]
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