How the kidney hyperfiltrates in diabetes:From molecules to hemodynamics

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.

Central blood pressure and chronic kidney disease

In this review, we focused on the relationship between central blood pressure and chronic kidney diseases(CKD). Wave reflection is a major mechanism that determines central blood pressure in patients with CKD. Recent medical technology advances have enabled non-invasive central blood pressure measurements. Clinical trials have demonstrated that compared with brachial blood pressure, central blood pressure is a stronger risk factor for cardiovascular(CV) and renal diseases. CKD is characterized by a diminished renal autoregulatory ability, an augmented direct transmission of systemic blood pressure to glomeruli, and an increase in proteinuria. Any elevation in central blood pressure accelerates CKD progression. In the kidney, interstitial inflammation induces oxidative stress to handle proteinuria. Oxidative stress facilitates atherogenesis, increases arterial stiffness and central blood pressure, and worsens the CV prognosis in patients with CKD. A vicious cycle exists between CKD and central blood pressure. To stop this cycle, vasodilator antihypertensive drugs and statins can reduce central blood pressure and oxidative stress. Even in early-stage CKD, mineral and bone disorders(MBD) may develop. MBD promotes oxidative stress, arteriosclerosis, and elevated central blood pressure in patients with CKD. Early intervention or prevention seems necessary to maintain vascular health in patients with CKD.