title: How the kidney hyperfiltrates in diabetes: From molecules to hemodynamics.
abstract: In this review, we focused on two molecules, connexin and sodium-glucose cotransporter, which can link to diabetic hyperfiltration. In diabetic kidney, the activation of renin-angiotensin system occurs simultaneously with glomerular hyperfiltration. The latter largely depends on pathophysiological afferent arteriolar dilation in the presence of high angiotensin II. As a mechanistic basis for the above, tubular hypothesis has been proposed for type 1 diabetic patients as well as experimental models. Although tubular hypothesis has not been well evaluated in type 2 diabetes, clinical observations support that tubular hypothesis is true also in type 2 diabetes. Recent results on tubular hypothesis along with connexin abnormality in type 2 diabetes were revisited. In addition, the importance of sodium-glucose cotransporter in diabetic hyperfiltration is discussed. The link between salt paradox and the activation of renin-angiotensin system will be also reviewed.
authors.affiliation: Tsuneo Takenaka, Department of Medicine, International University of Health and Welfare, Tokyo 107-0052, Japan.
authors.forename: Tsuneo
authors.initials: T
authors.lastname: Takenaka
authors.affiliation: Tsuneo Takenaka, Department of Medicine, International University of Health and Welfare, Tokyo 107-0052, Japan.
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Inoue
authors.affiliation: Tsuneo Takenaka, Department of Medicine, International University of Health and Welfare, Tokyo 107-0052, Japan.
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Watanabe
keywords: Connexin; Glomerular hyperfiltration; Salt paradox; Sodium-glucose co-transporter; Tubuloglomerular feedback