Ketteler Markus, Westenfeld Ralf, Schlieper Georg, Brandenburg Vincent, Floege Jürgen
Department of Nephrology and Clinical Immunology, University Hospital Aachen, Pauwelsstrasse 30, 52057 Aachen, Germany.
Pediatr Nephrol. 2005 Mar;20(3):383-8. doi: 10.1007/s00467-004-1614-x. Epub 2004 Nov 10.
In the recent past, it has become increasingly clear that extracellular calcium and phosphate homeostasis is a tightly regulated process. Since the physiological serum concentrations of calcium and phosphate are several orders of magnitude above their solubility product, mechanisms inhibiting precipitation must be operative to prevent extraosseous calcification. A number of local and systemic calcification inhibitors, including fetuin-A, matrix Gla protein, and osteoprotegerin, have been identified in recent years. Deficiency and dysregulation of such factors may contribute to morbidity and even mortality. Extraosseous calcifications occur with high prevalence in patients with end-stage renal disease. In particular, vascular manifestations are clearly associated with cardiovascular events and decreased survival. In addition to the well-established roles of hyperphosphatemia and an increased calcium x phosphate product, the biological and potential clinical roles of disturbances in calcification inhibition in uremia are discussed in this overview.
近年来，越来越清楚的是，细胞外钙和磷的稳态是一个受到严格调控的过程。由于钙和磷的生理血清浓度比它们的溶度积高出几个数量级，因此抑制沉淀的机制必须发挥作用以防止骨外钙化。近年来已鉴定出多种局部和全身钙化抑制剂，包括胎球蛋白-A、基质Gla蛋白和骨保护素。这些因素的缺乏和失调可能导致发病甚至死亡。骨外钙化在终末期肾病患者中普遍存在。特别是，血管表现与心血管事件和生存率降低明显相关。除了高磷血症和钙磷乘积增加的既定作用外，本综述还讨论了尿毒症中钙化抑制紊乱的生物学和潜在临床作用。
