Vascular Calcification: The Killer of Patients with Chronic Kidney Disease

被引:414
|
作者
Mizobuchi, Masahide
Towler, Dwight [2 ]
Slatopolsky, Eduardo [1 ]
机构
[1] Washington Univ, Sch Med, Div Renal, Dept Med, St Louis, MO 63110 USA
[2] Washington Univ, Dept Med, Div Bone & Mineral Dis, Cardiovasc Res Ctr, St Louis, MO 63110 USA
来源
基金
美国国家卫生研究院;
关键词
SMOOTH-MUSCLE-CELLS; MATRIX GLA PROTEIN; STAGE RENAL-DISEASE; VITAMIN-D ANALOGS; HUMAN ATHEROSCLEROTIC PLAQUES; GAMMA-CARBOXYGLUTAMIC ACID; BONE MORPHOGENETIC PROTEIN; TRANSCRIPTION FACTOR RUNX2; OSTEOPONTIN MESSENGER-RNA; BEAM COMPUTED-TOMOGRAPHY;
D O I
10.1681/ASN.2008070692
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Cardiovascular complications are the leading cause of death in patients with chronic kidney disease (CKD). Vascular calcification is a common complication in CKD, and investigators have demonstrated that the extent and histoanatomic type of vascular calcification are predictors of subsequent vascular mortality. Although research efforts in the past decade have greatly improved our knowledge of the multiple factors and mechanisms involved in vascular calcification in patients with kidney disease, many questions remain unanswered. No longer can we accept the concept that vascular calcification in CKD is a passive process resulting from an elevated calcium-phosphate product. Rather, as a result of the metabolic insults of diabetes, dyslipidemia, oxidative stress, uremia, and hyperphosphatemia, "osteoblast-like" cells form in the vessel wall. These mineralizing cells as well as the recruitment of undifferentiated progenitors to the osteochondrocyte lineage play a critical role in the calcification process. Important transcription factors such as Msx 2, osterix, and RUNX2 are crucial in the programming of osteogenesis. Thus, the simultaneous increase in arterial osteochondrocytic programs and reduction in active cellular defense mechanisms creates the "perfect storm" of vascular calcification seen in ESRD. Innovative clinical studies addressing the combined use of inhibitors that work on vascular calcification through distinct molecular mechanisms, such as fetuin-A, osteopontin, and bone morphogenic protein 7, among others, will be necessary to reduce significantly the accrual of vascular calcifications and cardiovascular mortality in kidney disease. In addition, the roles of oxidative stress and inflammation on the fate of smooth muscle vascular cells and their function deserve further translational investigation.
引用
收藏
页码:1453 / 1464
页数:12
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