Jacobsen Peter Karl
Steno Diabetes Center, Gentofte, Denmark.
J Renin Angiotensin Aldosterone Syst. 2005 Mar;6(1):1-14. doi: 10.3317/jraas.2005.001.
Diabetic nephropathy is a major cause of diabetes- related morbidity and mortality; however the clinical course of the disease and the renal prognosis is highly variable among individuals. The current review will discuss the genetic influence on the development of end stage renal disease (ESRD) in diabetic patients and potential improvements to the current treatment strategy to slow the loss of kidney function in these patients. In this first part, the growing evidence that glucose-induced activation of the intra-renal and systemic renin-angiotensin systems plays an essential role in processes leading to destruction of renal function is summarised. Genetic variations, especially the angiotensin-converting enzyme (ACE)/ID polymorphisms in the gene coding for ACE, are involved in activation of the renin-angiotensin system and seem to influence the clinical course of diabetic nephropathy during treatment with ACE inhibitors. In addition, this polymorphism may interact with other polymorphisms within the renin-angiotensin system, leading to high risk of ESRD. As new genetic approaches and methods develop, further understanding of diabetic nephropathy will evolve and genotyping will help prevent ESRD in diabetic patients.
糖尿病肾病是糖尿病相关发病和死亡的主要原因；然而，该疾病的临床病程和肾脏预后在个体之间存在很大差异。本综述将探讨基因对糖尿病患者终末期肾病（ESRD）发生发展的影响，以及当前治疗策略的潜在改进措施，以减缓这些患者肾功能的丧失。在第一部分中，总结了越来越多的证据表明，葡萄糖诱导的肾内和全身肾素 - 血管紧张素系统激活在导致肾功能破坏的过程中起重要作用。基因变异，特别是编码血管紧张素转换酶（ACE）的基因中的ACE / ID多态性，参与肾素 - 血管紧张素系统的激活，并且似乎会影响使用ACE抑制剂治疗期间糖尿病肾病的临床病程。此外，这种多态性可能与肾素 - 血管紧张素系统内的其他多态性相互作用，导致ESRD的高风险。随着新的基因方法和技术的发展，对糖尿病肾病的进一步了解将会不断深入，基因分型将有助于预防糖尿病患者发生ESRD。
