Altered Iron Metabolism in Dogs with Naturally Occurring Cardiac Disease

Cardiac disease represents a major cause of morbidity and mortality in dogs. In human cardiology, iron deficiency is a highly prevalent and clinically relevant comorbidity, contributing to exercise intolerance, symptom burden, and impaired quality of life independently of anemia, while correction with intravenous iron improves function and reduces hospitalization. Iron metabolism in dogs remains poorly characterized and typically considered only in the context of anemia. This study investigated iron metabolism and its regulatory pathways in dogs with cardiac disease, assessing whether alterations in iron handling and availability consistent with an iron-restricted phenotype are present. Hematologic indices, serum iron, total and unsaturated iron-binding capacity (TIBC, UIBC), ferritin, hepcidin, ceruloplasmin, C-reactive protein, and albumin were evaluated in 61 dogs comprising healthy controls, and dogs either with compensated cardiac disease (CCD group) or presenting acute decompensated congestive heart failure (ADCHF group). Dogs with cardiac disease exhibited evidence of systemic inflammation, reduced hematocrit, increased red blood cell distribution width, and decreased circulating iron. Both cardiac groups showed reduced TIBC and UIBC, suggesting decreased transferrin availability and reduced iron transport capacity, whereas ferritin concentrations did not differ between groups. Hepcidin concentrations were lower in CCD and not increased in ADCHF patients, suggesting complex and non-uniform regulation of iron homeostasis rather than a classic hepcidin-driven inflammatory pattern. In dogs with ADCHF, iron-binding capacity was independently associated with indices of cardiac remodeling, and additional correlation between inflammatory markers and iron-related parameters supported an interaction between inflammation, iron handling, and disease severity.