Cozzolino Mario
Department of Health Sciences, Renal Division, San Paolo Hospital, University of Milan, Milan, Italy.
Clin Kidney J. 2018 Feb;11(1):70-72. doi: 10.1093/ckj/sfx116. Epub 2017 Oct 12.
Patients with chronic kidney disease (CKD) are affected by mineral and bone disorder (MBD), resulting in abnormalities in serum calcium (Ca), phosphorous (P) and parathyroid hormone (PTH). Changes in mineral metabolism have also been associated with higher rates of both all-cause and cardiovascular-related mortality. The majority of haemodialysis patients are also deficient in the endogenous hormone 1,25-dihydroxyvitamin D (calcitriol), often contributing to increased secondary hyperparathyroidism (SHPT) and consequently to abnormal levels of Ca, P and PTH. Thus P overload and SHPT are well-known targets of medical treatments, such as P binders, vitamin D and calcimimetics, although with still limited evidence-based advantages in terms of survival. The tough hedge that is still keeping nephrologists far from a conclusive and winning approach against CKD-MBD is reasonably related to the still partial comprehension of the molecular pathways involved in a complex, multifactorial and extreme process.
慢性肾脏病（CKD）患者会受到矿物质和骨代谢紊乱（MBD）的影响，导致血清钙（Ca）、磷（P）和甲状旁腺激素（PTH）异常。矿物质代谢的变化还与全因死亡率和心血管相关死亡率的升高有关。大多数血液透析患者还缺乏内源性激素1,25 - 二羟基维生素D（骨化三醇），这通常会导致继发性甲状旁腺功能亢进（SHPT）增加，进而导致Ca、P和PTH水平异常。因此，磷过载和SHPT是医学治疗的众所周知的靶点，如磷结合剂、维生素D和拟钙剂，尽管在生存方面基于证据的优势仍然有限。仍然使肾病学家难以找到针对CKD - MBD的决定性和成功方法的棘手障碍，合理地与对这个复杂、多因素和极端过程中涉及的分子途径的仍然部分理解有关。
