Deferrari G, Repetto M, Calvi C, Ciabattoni M, Rossi C, Robaudo C
Department of Internal Medicine, University of Genova, Italy.
Nephrol Dial Transplant. 1998;13 Suppl 8:11-5. doi: 10.1093/ndt/13.suppl_8.11.
This brief review will focus on the major factors leading to incipient diabetic nephropathy (i.e. microalbuminuria) progressing to overt nephropathy (i.e. macroalbuminuria) and particularly on the role of glycaemic control and hypertension. Both experimental and cohort studies support the role of hyperglycaemia in the development of diabetic nephropathy. Some recent long-term interventional studies in microalbuminuric patients show conflicting results regarding the role played by good metabolic control in reducing the incidence of overt nephropathy. However, strict metabolic control, which is fundamental in normoalbuminuric patients, is of little use even in microalbuminuric patients. In general, levels of glycosylated haemoglobin less than two standard deviations above the upper normal range, commonly <7.5-8%, seem to protect patients from developing nephropathy. The results of many cross-sectional studies have shown that the progression of renal damage regularly is accompanied by arterial hypertension both in insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). Many long-term interventional studies have been performed in order to understand the effect of antihypertensive treatment on the incidence of proteinuria in both normotensive and hypertensive patients with IDDM or NIDDM. These data show a marked effect of antihypertensive therapy in preventing the onset of overt nephropathy, and suggest the superiority of angiotensin-converting enzyme (ACE) inhibitors. We believe that optimal blood pressure values are approximately 120/70-75 mmHg in younger patients and 125-130/80-85 mmHg in older patients. In conclusion, antihypertensive treatment, ACE inhibitors per se and possibly strict metabolic control reduce the development of nephropathy, thus playing a striking role in the secondary prevention of renal failure.
本简要综述将聚焦于导致早期糖尿病肾病（即微量白蛋白尿）进展为显性肾病（即大量白蛋白尿）的主要因素，尤其关注血糖控制和高血压的作用。实验研究和队列研究均支持高血糖在糖尿病肾病发展中的作用。近期一些针对微量白蛋白尿患者的长期干预研究，在良好代谢控制对降低显性肾病发生率所起作用方面得出了相互矛盾的结果。然而，严格的代谢控制对正常白蛋白尿患者至关重要，但即便对微量白蛋白尿患者也用处不大。一般来说，糖化血红蛋白水平低于正常范围上限两个标准差，通常<7.5 - 8%，似乎能保护患者不发生肾病。许多横断面研究结果表明，在胰岛素依赖型糖尿病（IDDM）和非胰岛素依赖型糖尿病（NIDDM）中，肾脏损害的进展通常伴有动脉高血压。为了解降压治疗对IDDM或NIDDM的血压正常和高血压患者蛋白尿发生率的影响，已开展了许多长期干预研究。这些数据显示降压治疗在预防显性肾病发生方面有显著效果，并提示血管紧张素转换酶（ACE）抑制剂更具优势。我们认为，年轻患者的最佳血压值约为120/70 - 75 mmHg，老年患者为125 - 130/80 - 85 mmHg。总之，降压治疗、ACE抑制剂本身以及可能的严格代谢控制可减少肾病的发生，从而在肾衰竭的二级预防中发挥显著作用。
