Chronic kidney disease (CKD) is characterized by clustered age-independent concentric LV geometry, geometry-independent systolic dysfunction, and age and heart rate-independent diastolic dysfunction. Concentric LV geometry is always associated with echocardiographic markers of abnormal LV relaxation and increased myocardial stiffness, two hallmarks of diastolic dysfunction. Non hemodynamic mechanisms such as metabolic and electrolyte abnormalities, activation of biological pathways, and chronic exposure to cytokine cascade and myocardial macrophage system also impact myocardial structure and impair the architecture of myocardial scaffold, producing and increasing reactive fibrosis, and altering myocardial distensibility. This review addresses pathophysiology of diastole in CKD, and relations with cardiac mechanics, hemodynamic loading, structural conditions, non-hemodynamic factors, and metabolic characteristics. The three mechanisms of diastole will be examined: elastic recoil, active relaxation, and passive distensibility and filling. Based on current evidence, we briefly give indications on methods for quantification of diastolic function and discuss on whether diastolic dysfunction represents a distinct characteristic in CKD or rather a proxy of the severity of cardiovascular condition, with the potential to be predicted by the general cardiovascular phenotype. Finally, the review discusses the opportunity of assessment of diastolic function in the context of CKD, with special emphasis on end-stage kidney disease, to indicate whether and when in-depth measurements might be helpful for clinical decision making in this context.