Montañez-Barragán Alejandra, Gómez-Barrera Isaias, Sanchez-Niño Maria D, Ucero Alvaro C, González-Espinoza Liliana, Ortiz Alberto
Escuela Superior de Medicina del Instituto Politécnico Nacional, Ciudad de México, Mexico.
Servicio de Nefrología, IdiPAZ, 28046, Madrid, Spain.
J Nephrol. 2014 Dec;27(6):607-17. doi: 10.1007/s40620-014-0092-x. Epub 2014 Apr 23.
Vascular calcification in chronic kidney disease (CKD) patients is associated to increased mortality. Osteoprotegerin (OPG) is a soluble tumor necrosis factor (TNF) superfamily receptor that inhibits the actions of the cytokines receptor activator of nuclear factor kappa-B ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL) by preventing their binding to signaling receptors in the cell membrane. OPG-deficient mice display vascular calcification while OPG prevented calcification of cultured vascular smooth muscle cells and protected kidney cells from TRAIL-induced death. OPG may be a biomarker in patients with kidney disease. Circulating OPG is increased in predialysis, dialysis and transplant CKD patients and may predict vascular calcification progression and patient survival. By contrast, circulating OPG is decreased in nephrotic syndrome. In addition, free and exosome-bound urinary OPG is increased in human kidney disease. Increased urinary OPG has been associated with lupus nephritis activity. Despite the association of high OPG levels with disease, experimental functional information available suggests that OPG might be protective in kidney disease and in vascular injury in the context of uremia. Thus, tissue injury results in increased OPG, while OPG may protect from tissue injury. Recombinant OPG was safe in phase I randomized controlled trials. Further research is needed to fully define the therapeutic and biomarker potential of OPG in patients with kidney disease.
慢性肾脏病(CKD)患者的血管钙化与死亡率增加相关。骨保护素(OPG)是一种可溶性肿瘤坏死因子(TNF)超家族受体,它通过阻止细胞因子核因子κB受体活化因子配体(RANKL)和TNF相关凋亡诱导配体(TRAIL)与细胞膜上的信号受体结合,从而抑制它们的作用。OPG基因缺陷小鼠表现出血管钙化,而OPG可防止培养的血管平滑肌细胞钙化,并保护肾细胞免受TRAIL诱导的死亡。OPG可能是肾病患者的一种生物标志物。在透析前、透析及肾移植的CKD患者中,循环中的OPG水平升高,且可能预测血管钙化进展及患者生存情况。相比之下,肾病综合征患者循环中的OPG水平降低。此外,人类肾病患者尿液中游离的和外泌体结合的OPG均增加。尿液中OPG增加与狼疮性肾炎活动相关。尽管OPG水平升高与疾病有关,但现有实验功能信息表明,在尿毒症背景下,OPG可能对肾病及血管损伤具有保护作用。因此,组织损伤导致OPG增加,而OPG可能保护组织免受损伤。重组OPG在I期随机对照试验中是安全的。需要进一步研究以全面确定OPG在肾病患者中的治疗和生物标志物潜力。