Futrakul Narisa, Butthep Punnee, Futrakul Prasit
Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
Clin Hemorheol Microcirc. 2008;38(3):201-7.
Current treatments of chronic kidney disease (CKD) patients frequently result in progressive decline in renal perfusion, leading to the end-stage renal disease. Such renal failures may be a reflection of the progressive nature of renal microvascular disease. The aim of the present study is to elucidate the mechanism of microvascular homeostasis in CKD patients with moderately impaired renal function. We determined biomarkers relevant to vascular homeostasis, such as circulating endothelial cell (CEC), and biomarkers of vascular repair, such as vascular endothelial growth factor (VEGF), angiopoietin-1, tie-2, angiopoietin-2 and VEGF-R2. The present result revealed an enhanced vascular injury which was reflected by increased number of circulating endothelial cells. In addition, a defective vascular repair was also reflected by deficiencies in angiogenic factors such as VEGF, and angiopoietin-1, whereas the anti-angiogenic factors such as angiopoietin-2 and VEGF-R2 were elevated. In conclusion, the activity against vascular injuries increased under the presence of defective ability of vascular repair in CKD with moderately impaired renal function. This finding may explain the present therapeutic failure in treating these CKD patients, and imply that treatment at an earlier stage of CKD should be implemented.
目前对慢性肾脏病(CKD)患者的治疗常常导致肾脏灌注逐渐下降,进而发展为终末期肾病。这种肾衰竭可能反映了肾微血管疾病的进展特性。本研究的目的是阐明肾功能中度受损的CKD患者微血管稳态的机制。我们测定了与血管稳态相关的生物标志物,如循环内皮细胞(CEC),以及血管修复的生物标志物,如血管内皮生长因子(VEGF)、血管生成素-1、酪氨酸激酶2(Tie-2)、血管生成素-2和血管内皮生长因子受体2(VEGF-R2)。目前的结果显示血管损伤加剧,这表现为循环内皮细胞数量增加。此外,血管生成因子如VEGF和血管生成素-1的缺乏也反映了血管修复存在缺陷,而血管生成素-2和VEGF-R2等抗血管生成因子则升高。总之,在肾功能中度受损的CKD患者中,血管修复能力存在缺陷的情况下,针对血管损伤的活性增加。这一发现可能解释了目前治疗这些CKD患者的失败原因,并提示应在CKD的早期阶段进行治疗。