Martola Leena, Elinder Carl-Gustaf, Stenvinkel Peter
Njurmedicinska kliniken, Huddinge Universitetssjukhus.
Lakartidningen. 2003 Dec 11;100(50):4180-3.
Despite rapid improvement in dialysis technology during the last 20 years the mortality rate is still very high in patients with end-stage renal disease (ESRD), and is in fact comparable to that of many cancer patients with metastases. The main cause of mortality in ESRD is cardiovascular disease (CVD), and cardiac mortality for dialysis patients aged 45 years or younger is more than 100-fold greater than in the general population. Recent evidence suggests that the high cardiovascular mortality rate in this patient population is associated with extensive vascular and valvular calcification. Although hyperphosphatemia may be the major cause of vascular calcification in this patient group it has been suggested that chronic inflammation also contributes to this process. Indeed, recent evidence suggests that inflammatory mediators, such as pro-inflammatory cytokines and adipocytokines, may promote vascular calcification in vitro. Moreover, a2-Heremans Schmid glycoprotein (fetuin), an intrinsic inhibitor of the calcification process, is down-regulated during chronic inflammation. Lower levels of fetuin have recently been found to predict mortality in ESRD. Thus, further studies are needed to elucidate the roles of calcium-free phosphate binders as well as focused anti-inflammatory treatment strategies in the prevention of vascular and valvular calcification in ESRD.
尽管在过去20年里透析技术有了快速进步,但终末期肾病(ESRD)患者的死亡率仍然很高,实际上与许多有转移灶的癌症患者相当。ESRD患者死亡的主要原因是心血管疾病(CVD),45岁及以下透析患者的心脏死亡率比普通人群高出100多倍。最近的证据表明,该患者群体中心血管高死亡率与广泛的血管和瓣膜钙化有关。虽然高磷血症可能是该患者群体血管钙化的主要原因,但有人提出慢性炎症也促成了这一过程。事实上,最近的证据表明,炎症介质,如促炎细胞因子和脂肪细胞因子,可能在体外促进血管钙化。此外,钙化过程的内在抑制剂α2-赫曼斯·施密德糖蛋白(胎球蛋白)在慢性炎症期间会下调。最近发现较低水平的胎球蛋白可预测ESRD患者的死亡率。因此,需要进一步研究以阐明无钙磷结合剂以及针对性抗炎治疗策略在预防ESRD患者血管和瓣膜钙化中的作用。