According to reservoir-wave analysis (RWA) arterial pressure is the sum of a reservoir pressure (RP) accounting for dynamic storage and release of blood from arteries, and of an excess pressure (XSP) analogous to flow. RP is the minimal left ventricular work required to generate aortic flow, while XSP corresponds to surplus cardiac workload. We have previously shown that kidney transplantation (KTx) improves aortic stiffness. We now aim to determine how the improvement of aortic stiffness after kidney transplantation will translate on the reservoir-wave analysis parameters. We hypothesize that kidney transplantation will result in a decrease of reservoir and excess pressure. This is a longitudinal observational study involving patients with kidney failure who were undergoing KTx. Before, 3, 6 and 24 months after KTx, carotid pressure waves were recorded using applanation tonometry calibrated using brachial diastolic and mean blood pressure. Using pressure only approach, reservoir-wave analysis was used to obtain RP, XSP and their integrals (RPI, XSPI). Generalized estimating equations were used to take into account repeated measures and adjust for changes in heart rate at each time point. Values are reported as estimated marginal means and standard errors. 75 patients (69% male, mean age 51 ± 13 years) were assessed. From baseline to 3 months Post-KTx, RP (121.4 ± 2.4 vs. 98.1 ± 1.5 mmHg; P<0.001) and RPI (11274 ± 9265; P<0.001) decrease significantly, and continuously declined further at 6 and 24 months (P<0.001 as compared to pre-KTx). There were no significant changes in XSP at 3 months (18.8 ± 1.1 vs. 18.6 ± 1.5 mmHg; P=0.898), and the values remained consistently stable at 6 and 24 months. However, XSPI, declined gradually at 3 months (393 ± 29 to 372 ± 26, P=0.5), and then at 6 months (315 ± 20 P=0.023), without it being significantly changed at 24 months (P=0.10). Kidney transplantation results in a continuous decrease in reservoir pressure and its integral (RP and RPI). As opposed to our hypothesis, excess pressure (XSP) does not change, while there was later reduction of its integral after KTx. Since XSP is analogous to flow and there is a possible alteration of flow after adding renal vessels to existing vascular network, potentially explaining why we do not see a decrease in excess pressure post KTx despite reduced arterial stiffness.