Nosadini R, Abaterusso C, Dalla Vestra M, Bortoloso E, Saller A, Bruseghin M, Sfriso A, Trevisan M
Department of Clinical Medicine, University of Sassari, Italy.
Nephrol Dial Transplant. 1998;13 Suppl 8:44-8. doi: 10.1093/ndt/13.suppl_8.44.
The mechanism underlying the pathogenesis of microangiopathy and macroangiopathy in diabetes mellitus is hypothesized to be chronic hyperglycaemia. However, the values of blood glucose at which chronic diabetic complications develop at the renal and cardiac level are quite different. It is not clear whether this is due to different responses of kidney and heart tissues to the metabolic challenge of diabetes, or to the simultaneous role of other mechanisms contributing differently to the pathogenesis of chronic diabetic complications in renal and cardiac tissues. One of these mechanisms could be the simultaneous occurrence of arterial hypertension along with hyperglycaemia in diabetic patients. We reviewed the available evidence in the recent medical literature and provide information on the relationships between hyperglycaemia and cardiovascular and renal complications in insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). The majority of reports indicate that the values of blood glucose appearing to be at threshold level for the development of cardiovascular complications are significantly lower than those determining renal complications (5.4 vs 10.0 mmol/l blood glucose concentrations 2 h after an oral glucose tolerance test). This was the case both in cross-sectional and prospective studies and also in intervention studies aimed at decreasing blood glucose concentrations by using strict metabolic control methods (The Diabetes Control and Complications Trial Research Group), which succeeded in delaying the rate of occurrence of microangiopathic complications at the kidney and retinal level but not so effectively at the cardiac level. Therefore, alternative therapeutic or supplementary strategies to blood glucose control should be adopted in diabetes to prevent diabetic complications. To date, the most effective approach, from our point of view, is antihypertensive therapy in order to prevent end-stage renal disease. We extensively reviewed the available literature which reported comparisons between angiotensin-converting enzyme inhibitors (ACE inhibitors) and calcium channel blockers (CCBs) in the treatment of arterial hypertension in diabetes. Intensified antihypertensive therapy achieving a blood pressure level below 130/85 mmHg has been shown to be useful in decreasing the rate of occurrence of chronic diabetic complications in diabetes mellitus. Both ACE inhibitors and CCBs have been shown to significantly improve the course of renal function in diabetic patients with incipient and overt nephropathy.
糖尿病微血管病变和大血管病变发病机制的潜在原因被认为是慢性高血糖。然而，在肾脏和心脏水平出现慢性糖尿病并发症时的血糖值却大不相同。目前尚不清楚这是由于肾脏和心脏组织对糖尿病代谢挑战的反应不同，还是由于其他机制同时发挥作用，对肾脏和心脏组织中慢性糖尿病并发症的发病机制产生不同影响。其中一个机制可能是糖尿病患者同时存在动脉高血压和高血糖。我们回顾了近期医学文献中的现有证据，并提供了关于胰岛素依赖型糖尿病（IDDM）和非胰岛素依赖型糖尿病（NIDDM）中高血糖与心血管及肾脏并发症之间关系的信息。大多数报告表明，似乎处于心血管并发症发生阈值水平的血糖值显著低于决定肾脏并发症的血糖值（口服葡萄糖耐量试验2小时后血糖浓度分别为5.4和10.0 mmol/L）。在横断面研究、前瞻性研究以及旨在通过严格代谢控制方法降低血糖浓度的干预研究（糖尿病控制与并发症试验研究组）中都是如此，这些研究成功地延缓了肾脏和视网膜水平微血管并发症的发生速率，但对心脏水平的效果不太明显。因此，糖尿病患者应采用血糖控制之外的替代治疗或补充策略来预防糖尿病并发症。从我们的角度来看，迄今为止最有效的方法是抗高血压治疗以预防终末期肾病。我们广泛回顾了现有文献，这些文献报道了血管紧张素转换酶抑制剂（ACE抑制剂）和钙通道阻滞剂（CCB）在糖尿病动脉高血压治疗中的比较。强化抗高血压治疗使血压水平低于130/85 mmHg已被证明有助于降低糖尿病患者慢性糖尿病并发症的发生率。ACE抑制剂和CCB都已被证明能显著改善早期和显性肾病糖尿病患者的肾功能进程。
