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 ...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.展开更多
文摘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.
