Futrakul Narisa, Futrakul Prasit
Narisa Futrakul, Faculty of Medicine, King Chulalongkorn Memorial Hospital, Chulalongkorn University, Bangkok 10330, Thailand.
World J Nephrol. 2013 Nov 6;2(4):125-8. doi: 10.5527/wjn.v2.i4.125.
Under common practice, the conventional diagnostic marker such as microalbuminuria determination does not recognized early stage of diabetic kidney disease (normoalbuminuria, chronic kidney disease stage 1, 2); due to the insensitiveness of the available marker. Treatment at later stage (microalbuminuria) simply slows the renal disease progression, but is rather difficult to restore the renal perfusion. Intrarenal hemodynamic study in these patients revealed an impaired renal perfusion and abnormally elevated renal arteriolar resistances. Treatment with vasodilators such as angiotensin converting enzyme inhibitor and angiotensin receptor blocker fails to correct the renal ischemia. Recent study on vascular homeostasis revealed a defective mechanism associated with an impaired nitric oxide production which would explain the therapeutic resistance to vasodilator treatment in microalbuminuric diabetic kidney disease. This study implies that the appropriate therapeutic strategy should be implemented at earlier stage before the appearance of microalbuminuria.
在通常的临床实践中，传统的诊断标志物如微量白蛋白尿测定无法识别糖尿病肾病的早期阶段（正常白蛋白尿，慢性肾脏病1、2期）；这是因为现有标志物不敏感。在后期阶段（微量白蛋白尿）进行治疗只能减缓肾脏疾病的进展，但很难恢复肾脏灌注。对这些患者的肾内血流动力学研究显示肾脏灌注受损且肾小动脉阻力异常升高。使用血管扩张剂如血管紧张素转换酶抑制剂和血管紧张素受体阻滞剂进行治疗无法纠正肾脏缺血。最近关于血管稳态的研究揭示了一种与一氧化氮生成受损相关的缺陷机制，这可以解释微量白蛋白尿型糖尿病肾病对血管扩张剂治疗的抵抗性。这项研究表明，应在微量白蛋白尿出现之前的更早阶段实施适当的治疗策略。
