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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 dependson 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 reninangiotensin system will be also reviewed.
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 as 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 reninangiotensin system will be also reviewed.