Demer Linda, Tintut Yin
Department of Medicine, University of California, Los Angeles, California 90095-1679, USA.
Curr Opin Nephrol Hypertens. 2010 Jul;19(4):349-53. doi: 10.1097/MNH.0b013e32833a3d67.
This review highlights the most recent publications addressing the relationship between bone and vascular calcification in patients with chronic and end-stage kidney disease.
The relatively new term 'chronic kidney disease-mineral bone disorder' reflects the growing reach of chronic kidney disease research into the realm of systems physiology, involving a triad of renal, skeletal, and vascular tissues. Recent studies address underlying mechanisms of the bone and vascular complications of chronic kidney disease and point to a variety of biochemical factors, including phosphatonins (fibroblast growth factor-23, matrix extracellular phosphoglycoprotein), bone morphogenetic protein 7, osteoprotegerin, matrix GLA protein, ectonucleotide pyrophosphatase/phosphodiesterase 1, alkaline phosphatase, and lipid oxidation products. Studies also demonstrate that agents used for treatment of one component of the triad often act on the other components of the triad - beneficially or adversely. These findings emphasize the importance of avoiding the subspecialty, single organ viewpoint when treating individual components of chronic kidney disease-mineral bone disorder.
The consistent synchrony among chronic kidney disease, aortic calcification, and bone loss offers clues to underlying mechanisms for the systemic abnormalities.
本综述重点介绍了关于慢性肾脏病和终末期肾病患者骨与血管钙化关系的最新出版物。
相对较新的术语“慢性肾脏病 - 矿物质和骨异常”反映了慢性肾脏病研究在系统生理学领域的影响范围不断扩大，涉及肾脏、骨骼和血管组织的三联征。近期研究探讨了慢性肾脏病骨与血管并发症的潜在机制，并指出了多种生化因素，包括磷调节素（成纤维细胞生长因子 - 23、基质细胞外磷酸糖蛋白）、骨形态发生蛋白7、骨保护素、基质γ-羧基谷氨酸蛋白、胞外核苷酸焦磷酸酶/磷酸二酯酶1、碱性磷酸酶和脂质氧化产物。研究还表明，用于治疗三联征中一个组成部分的药物常常对三联征的其他组成部分产生有益或有害的作用。这些发现强调了在治疗慢性肾脏病 - 矿物质和骨异常的各个组成部分时，避免专科、单一器官观点的重要性。
慢性肾脏病、主动脉钙化和骨质流失之间持续的同步性为全身异常的潜在机制提供了线索。
