Renal and cardiac functions have close and complementary interconnections, and the communication between kidney and heart through a variety of bidirectional pathways causes significant pathological changes. The patients with heart failure with preserved ejection fraction (HFpEF) have multiple comorbidities, including chronic kidney disease (CKD) that is one of the prognostic risks for these patients. The link between functional kidney disease and HFpEF remains incompletely understood. We focused on diabetic cardiomyopathy, which is characterized by early onset of left ventricular (LV) diastolic dysfunction. Clinical data and our preclinical studies in mouse model of diabetes suggested that the dysregulation of Ca²⁺ signaling and the impairment of NO-cGC-PKG pathway are crucial for the development of LV diastolic dysfunction. Furthermore, several renal factors including erythropoietin, inflammatory cytokines, amphiregulin and circulating miRNAs underlie the association between CKD and LV diastolic dysfunction. Recent studies suggest SGLT2 inhibitors ameliorate not only CKD but also HFpEF. In this symposium, we would like to review the late-breaking findings on the mechanism underlying the homeostasis of cardiac function through cardio-renal interactions and its failure in diabetic cardiomyopathy.