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Excessive soft tissue and vascular calcifications are typical complications of chronic kidney disease (CKD) and disorders of phosphate homeostasis are considered to be a major contributor to the pathogenesis. However, at least in some individuals, calcium administration also increases the risk, and furthermore, it is widely accepted that there is a link between bone disease and vascular pathology. In this review, we discuss the role of the bone exchangeable calcium pool (ECP) in the acute regulation of the serum calcium concentration (Ca(s)) in health and CKD. This pool is able to buffer an acute calcium load as well as to maintain a stable Ca(s) during acute calcium deprivation. Indeed, the minute-to-minute regulation of Ca(s) appears to depend exclusively on this mechanism without any obvious contribution of other factors like parathyroid hormone, which nonetheless define the Ca(s) steady state set point. It is tempting to speculate that a reduction of the bone ECP plasticity in some patients with CKD leads to short-lasting increases in Ca(s) above the individual mid- to long-term set point as observed during haemodialysis or after the ingestion of calcium-containing phosphate binders. This could contribute to and partially explain the propensity of these subjects to develop extraosseous calcifications. An improved understanding of the processes involved and the availability of new techniques to assess the capacity of this pool, at least in dialysis patients, will make this area an attractive target for new investigations.
Pirklbauer et al. (Thu,) studied this question.