Kalziumregulation aus nephrologischer Sicht – manches anders als gedacht?

Precise regulation of the extracellular calcium concentration within a very narrow range is mandatory for functioning of the organism. Via dose-dependent effects on kidney, bone, and the intestine, parathyroid hormone and active vitamin D regulate and synchronize these Ca-regulating organs to maintain the individual mid- to long-term extracellular Ca concentration. However, elegant animal studies have demonstrated that acute Ca regulation (i.e., on a minute-to-minute basis) is primarily independent of calciotropic hormones, cell-mediated bone remodeling, gastrointestinal uptake, and renal Ca handling. A rapidly exchangeable calcium pool (rECP) located at the bone surface has been postulated to act as a temporary buffer, storing or liberating Ca in the event of acute Ca loading or deprivation in order to counteract acute serum Ca deviations. This rECP function is thought to depend on physicochemical mechanisms involving amorphous calcium phosphate salts (e.g., brushite) and the presence of non-collagenous bone proteins (NCBPs) directly bound to hydroxyapatite at bone surfaces. Clinical studies assessing intradialytic Ca kinetics provided first evidence for the existence of an rECP in vivo and for the involvement of bone in acute Ca regulation by demonstrating an independent association of the NCBP osteocalcin with acute Ca-buffering capacity. The independent association of intradialytic calcium kinetics with the presence of coronary heart disease is first evidence for the clinical relevance of acute calcium regulation.