Diabetic microvascular complications: possible targets for improved macrovascular outcomes

被引:16
作者
D'Elia, John A. [1 ]
Bayliss, George [1 ,2 ]
Roshan, Bijan [1 ]
Maski, Manish [1 ]
Gleason, Ray E. [1 ]
Weinrauch, Larry A. [1 ]
机构
[1] Beth Israel Deaconess Med Ctr, Joslin Diabet Ctr, Harvard Med Sch, Dept Med,Renal Unit, Boston, MA 02215 USA
[2] Brown Univ, Rhode Isl Hosp, Alpert Sch Med, Dept Med, Providence, RI 02912 USA
来源
INTERNATIONAL JOURNAL OF NEPHROLOGY AND RENOVASCULAR DISEASE | 2011年 / 4卷
关键词
angiotensin-converting enzyme inhibitor; pulsatile insulin; diabetic nephropathy; cardiac autonomic neuropathy; podocytes; beta cells;
D O I
10.2147/IJNRD.S14716
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
The results of recent outcome trials challenge hypotheses that tight control of both glycohemoglobin and blood pressure diminishes macrovascular events and survival among type 2 diabetic patients. Relevant questions exist regarding the adequacy of glycohemoglobin alone as a measure of diabetes control. Are we ignoring mechanisms of vasculotoxicity (profibrosis, altered angiogenesis, hypertrophy, hyperplasia, and endothelial injury) inherent in current antihyperglycemic medications? Is the polypharmacy for lowering cholesterol, triglyceride, glucose, and systolic blood pressure producing drug interactions that are too complex to be clinically identified? We review angiotensin-aldosterone mechanisms of tissue injury that magnify microvascular damage caused by hyperglycemia and hypertension. Many studies describe interruption of these mechanisms, without hemodynamic consequence, in the preservation of function in type 1 diabetes. Possible interactions between the renin-angiotensin-aldosterone system and physiologic glycemic control (through pulsatile insulin release) suggest opportunities for further clinical investigation.
引用
收藏
页码:1 / 15
页数:15
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