Chronic kidney disease is observed in most patients with CHF with preserved ejection fraction (HFpEF) and presents a major risk factor facilitating development and progression of LV diastolic dysfunction. The review focused on the effect of chronic kidney disease on intracellular signaling pathways affecting stiffness and diastolic relaxation of cardiomyocytes in response to inflammation and endothelial dysfunction of coronary capillaries, excessive sympathetic activation, and dysregulation of natriuretic peptides, which directly participate in the development of CHF. Elucidation of these mechanisms allows to identify new cell targets for new approaches to drug therapy for patients with HFpEF.
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