Renal Division, Emory University School of Medicine, Atlanta, Georgia, USA.
Kidney Int. 2010 Dec;78(12):1232-9. doi: 10.1038/ki.2010.334. Epub 2010 Sep 22.
Vascular calcification is common in patients with advanced chronic kidney disease and is associated with poorer outcomes. Although the pathophysiology is not completely understood, it is clear that it is a multifactorial process involving altered mineral metabolism, as well as changes in systemic and local factors that can promote or inhibit vascular calcification, and all of these are potential therapeutic targets. Current therapy is closely linked to strategies for preventing disordered bone and mineral metabolism in advanced kidney disease and involves lowering the circulating levels of both phosphate and calcium. The efficacy of compounds that specifically target calcification, such as bisphosphonates and thiosulfate, has been shown in animals but only in small numbers of humans, and safety remains an issue. Additional therapies, such as pyrophosphate, vitamin K, and lowering of pH, are supported by animal studies, but are yet to be investigated clinically. As the mineral composition of vascular calcifications is the same as in bone, potential effects on bone must be addressed with any therapy for vascular calcification.
血管钙化在晚期慢性肾脏病患者中很常见,与预后较差有关。尽管其病理生理学尚未完全阐明,但很明显,它是一个涉及矿物质代谢改变的多因素过程,以及可促进或抑制血管钙化的全身和局部因素的变化,所有这些都是潜在的治疗靶点。目前的治疗方法与预防晚期肾脏病中骨和矿物质代谢紊乱的策略密切相关,包括降低循环中磷和钙的水平。在动物中已经证明了专门针对钙化的化合物(如双膦酸盐和硫代硫酸盐)的疗效,但在人类中只有少数病例,安全性仍然是一个问题。动物研究支持其他治疗方法,如焦磷酸盐、维生素 K 和降低 pH 值,但尚未在临床上进行研究。由于血管钙化的矿物质成分与骨相同,因此任何血管钙化治疗方法都必须考虑对骨骼的潜在影响。