See related article, pp 61–67 Normal arterial aging is characterized by arterial enlargement, wall thickening, and stiffening, which predominates at large arteries.1 Patients with chronic kidney disease (CKD) have an early vascular aging,2 characterized by an accelerated arterial enlargement and stiffening, which occurs in parallel with the decline in glomerular filtration rate (GFR).3 The relationships between central hemodynamics (either arterial stiffness or central blood pressure) and GFR decline are complex and depend mainly on both the stage of the disease—early CKD, advanced CKD or end-stage renal disease—and the level of blood pressure—optimal blood pressure, high normal, and grade 1 to 2 hypertension.3–5 O’Rourke and Safar6 suggested that the torrential flow and low resistance to flow in the kidney expose small arterial vessels of the glomerulus to the high-pressure fluctuations that exist in the renal arteries. Such fluctuations, measurable as central pulse pressure, increase 3- to 4-fold with age. For instance, the loss of renal blood flow autoregulation, because of altered myogenic tone in hypertension, can expose small glomerular vessels to higher pulsatile pressure and flow and favor higher dissipation in the microcirculation, leading to hyperfiltration and glomerulosclerosis.3 Indeed, central pulse pressure was reported to be significantly and independently associated with GFR or proteinuria in cross-sectional studies in patients with CKD.4,7 However, in the longitudinal Nephrotest study5 following prospectively CKD patients for a mean of 3.1 years, central pulse pressure was not significantly and independently associated with the decline in GFR. Thus, it is possible that an adequate autoregulatory capability of the GFR could be maintained for years. The influence of aortic stiffness on GFR is also not straightforward. Although several cross-sectional studies showed a significant and independent association between GFR and aortic stiffness measured through carotid-femoral pulse wave …