Acute Kidney Injury Induces Remote Cardiac Damage and Dysfunction Through the Galectin-3 Pathway

Visual Abstract
Highlights • In 2 different mouse models, AKI increased Gal-3 expression and induced cardiac dysfunction, cardiac and systemic inflammation, cardiac macrophage infiltration, and fibrosis. • Cardiac consequences of AKI were dependent on the Gal-3 pathway and were prevented using Gal-3 knockout mice or modified citrus pectin as a pharmaceutical inhibitor. • Cardiac Gal-3 expression resulted from bone marrow-derived immune cells recruitment after AKI. • In critically ill patients, development of AKI is associated with increased plasma Gal-3 levels and increased biomarkers of cardiac injury and damage.
Summary Acute kidney injury is associated with increased risk of heart failure and mortality. This study demonstrates that acute kidney injury induces remote cardiac dysfunction, damage, injury, and fibrosis via a galectin-3 (Gal-3) dependent pathway. Gal-3 originates from bone marrow-derived immune cells. Cardiac damage could be prevented by blocking this pathway.