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Renal hyperfi ltration related to diabetes mellitus and obesity in human disease

与在人的疾病的糖尿病 mellitus 和肥胖有关的肾的 hyperfiltration

作     者:Alexa N Sasson David ZI Cherney 

作者机构:Division of Nephrology University Health Network University of Toronto Ontario M5G 2N2 Canada 

出 版 物:《World Journal of Diabetes》 (世界糖尿病杂志(英文版)(电子版))

年 卷 期:2012年第3卷第1期

页      面:1-6页

学科分类:1002[医学-临床医学] 100201[医学-内科学(含:心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基  金:Supported by A Canadian Diabetes Association-KRESCENT Program Joint New Investigator Award the CIHR and the Heart and Stroke Foundation of Canada to Cherney ZID 

主  题:Diabetes mellitus Metabolic syndrome Hy- perf iltration Glomerular f iltration rate 

摘      要:High intraglomerular pressure is associated with renal hyperf iltration, leading to the initiation and progression of kidney disease in experimental models of diabetes mellitus (DM). In humans, hyperf iltration is observed in patients with type 1 and type 2 DM, and is also seen in patients with pre-diabetic conditions, such as the metabolic syndrome. From a mechanistic perspective, both vascular and tubular factors likely contribute to the pathogenesis of hyperf iltration. Until now, human studies have primarily focused on the use of medications that inhibit the renin angiotensin system to reduce efferent vasoconstriction and thereby improve hyperfiltration. More recent advances in the development of investigational adenosine antagonists and inhibitors of sodium glucose cotransport may help to elucidate tubular factors that contribute to afferent vasodilatation. In this review, we summarize available data from experimental and human studies of type 1 and type 2 DM and obesity to provide an overview of factors that contribute to the hyperf iltration state. We have focused on the renin angiotensin system, cyclooxygenase-2 system, nitric oxide, protein kinase C and endothelin as vascular determinants of hyperfiltration. We also dis-cuss relevant tubular factors, since experimental models have suggested that inhibition of sodium-glucose cotransport may be renoprotective.

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