Parving H H
Hvidöre Hospital, Copenhagen, Denmark.
Diabetes Care. 1991 Mar;14(3):260-9. doi: 10.2337/diacare.14.3.260.
Diabetic nephropathy is the main cause of the increased morbidity and mortality in insulin-dependent diabetes mellitus (IDDM) patients. Elevated blood pressure accelerates and effective blood pressure reduction with beta-blockers and/or angiotensin-converting enzyme (ACE) inhibitors delays the progression of nephropathy and reduces albuminuria. All previous reports dealing with the natural history of diabetic nephropathy demonstrated a cumulative death rate between 50 and 77% 10 yr after onset of nephropathy. Effective antihypertensive treatment reduced the cumulative death rate to 15-20% 10 yr after onset of nephropathy. Recent randomized control studies indicate that ACE inhibition may delay and even prevent the development of diabetic nephropathy in normotensive IDDM patients with persistent microalbuminuria. Several cross-sectional and prospective studies suggest an association between elevated blood pressure and the development and progression of diabetic retinopathy. Furthermore, carotid insufficiency or other causes of unilaterally or bilaterally reduced retinal blood flow (pressure) diminish the development of diabetic retinopathy. Diabetic retinopathy is characterized by abnormal leakage of fluorescein through the blood-retinal barrier, an abnormality that can be reversed during antihypertensive treatment. It is well documented that elevated blood pressure, poor metabolic control, and diabetic microangiopathy independently enhance the endothelial leakage of plasma proteins in diabetes mellitus. A link between capillary hypertension, increased extravasation of plasma proteins, and the development and progression of diabetic microangiopathy has been suggested. Blood pressure reduction diminishes the extravasation of plasma proteins. The above results strongly support the case for early and effective treatment of arterial blood pressure elevation in diabetes.
糖尿病肾病是胰岛素依赖型糖尿病（IDDM）患者发病率和死亡率增加的主要原因。血压升高会加速肾病进展，而使用β受体阻滞剂和/或血管紧张素转换酶（ACE）抑制剂有效降低血压则可延缓肾病进展并减少蛋白尿。以往所有关于糖尿病肾病自然病史的报告均显示，肾病发病10年后的累积死亡率在50%至77%之间。有效的降压治疗可将肾病发病10年后的累积死亡率降至15%至20%。最近的随机对照研究表明，对于持续存在微量白蛋白尿的血压正常的IDDM患者，ACE抑制可能会延缓甚至预防糖尿病肾病的发生。多项横断面研究和前瞻性研究表明，血压升高与糖尿病视网膜病变的发生和进展之间存在关联。此外，颈动脉供血不足或其他导致单侧或双侧视网膜血流（压力）减少的原因会减缓糖尿病视网膜病变的发展。糖尿病视网膜病变的特征是荧光素通过血视网膜屏障异常渗漏，这种异常在降压治疗期间可逆转。有充分证据表明，血压升高、代谢控制不佳和糖尿病微血管病变会独立增加糖尿病患者血浆蛋白的内皮渗漏。有人提出毛细血管高血压、血浆蛋白外渗增加与糖尿病微血管病变的发生和进展之间存在联系。降低血压可减少血浆蛋白的外渗。上述结果有力地支持了早期有效治疗糖尿病患者动脉血压升高的观点。
