Ravera M, Re M, Deferrari G
Dipartimento di Cardionefrologia, Azienda Ospedaliera Universitaria San Martino, Genova, Italy.
G Ital Nefrol. 2007 Sep-Oct;24 Suppl 38:13-9.
Diabetic nephropathy is one of the most frequent causes of end-stage renal disease (ESRD), and there has been a dramatic increase in the number of patients entering renal replacement therapy in the last few years. Moreover, diabetic nephropathy is associated with elevated cardiovascular morbidity and mortality. Prevention and treatment of diabetic nephropathy is based on optimal metabolic and blood pressure control, proteinuria reduction, and renin-angiotensin-aldosterone system (RAAS) inhibition. In the normoalbuminuric patient, optimal glycemic control (HbA1c below 7.0%) plays a fundamental role in the primary prevention of ESRD. Furthermore, blood pressure levels below 130/80 mmHg are strongly recommended. In the microalbuminuric stage, strict glycemic control (HbA1c below 7.0%) likely reduces the incidence of overt nephropathy, while blood pressure values less than 130/80 mmHg are recommended. Moreover, there is evidence that inhibition of RAAS, either by angiotensin-converting-enzyme inhibitors (ACE-I) or angiotensin-receptor blockers (ARB), reduces the development of overt nephropathy, regardless of the blood pressure levels. ACE-I are recommended as the drugs of choice in type 1 diabetes, while both ACE-I and ARB are considered first-choice drugs in type 2 diabetes. Once overt proteinuria has developed, it is uncertain whether glycemic control affects the progression of nephropathy, which is strongly influenced by blood pressure and proteinuria. Optimal blood pressure levels are < 130/80 mmHg in patients with proteinuria < 1 g/day and < 120/75 mmHg in patients with proteinuria > or =1 g/day. In type 1 diabetes there is consensus on the renoprotective role of ACE-I, while in type 2 diabetes, ARB have been shown to be more effective than conventional therapy or calcium-channel blockers in slowing the progression of nephropathy. Lastly, a multifactorial therapeutic approach based on optimal glycemic control, intensive antihypertensive therapy, inhibition of RAAS, statins and aspirin is pivotal in the prevention and treatment of diabetic nephropathy.
糖尿病肾病是终末期肾病(ESRD)最常见的病因之一,在过去几年中,接受肾脏替代治疗的患者数量急剧增加。此外,糖尿病肾病与心血管疾病发病率和死亡率升高相关。糖尿病肾病的预防和治疗基于最佳的代谢和血压控制、蛋白尿减少以及肾素 - 血管紧张素 - 醛固酮系统(RAAS)抑制。在正常白蛋白尿患者中,最佳血糖控制(糖化血红蛋白低于7.0%)在ESRD的一级预防中起关键作用。此外,强烈建议血压水平低于130/80 mmHg。在微量白蛋白尿阶段,严格的血糖控制(糖化血红蛋白低于7.0%)可能会降低显性肾病的发生率,同时建议血压值低于130/80 mmHg。此外,有证据表明,通过血管紧张素转换酶抑制剂(ACE-I)或血管紧张素受体阻滞剂(ARB)抑制RAAS,可减少显性肾病的发生,无论血压水平如何。ACE-I被推荐为1型糖尿病的首选药物,而ACE-I和ARB均被视为2型糖尿病的首选药物。一旦出现显性蛋白尿,血糖控制是否会影响肾病进展尚不确定,而肾病进展受血压和蛋白尿的影响很大。蛋白尿<1 g/天的患者最佳血压水平为<130/80 mmHg,蛋白尿≥1 g/天的患者最佳血压水平为<120/75 mmHg。在1型糖尿病中,ACE-I的肾脏保护作用已达成共识,而在2型糖尿病中,ARB已被证明在减缓肾病进展方面比传统治疗或钙通道阻滞剂更有效。最后,基于最佳血糖控制、强化降压治疗、RAAS抑制、他汀类药物和阿司匹林的多因素治疗方法在糖尿病肾病的预防和治疗中至关重要。