The lecture reveals the importance of iron deficiency correction in improving heart conditions in CKD patients, suggesting clinical significance.
It is theoretically reasonable to hypothesize that correcting of anemia could lead to better condition of the heart and prognosis in patients with chronic kidney disease (CKD) with/without cardiac disease. Unexpectedly, complete correction of anemia by erythropoietin stimulating agents (ESA) has not improved cardiovascular outcomes in patients with CKD. Iron is known to play a crucial role in oxygen transport as a component of hemoglobin and in cardiac and skeletal muscle metabolism as a component of oxidative enzymes. These physiological roles of iron led us to hypothesize that iron deficiency in itself may directly contribute to cardiac morphological and functional abnormalities independent of anemia. Recently, it is reported that a high prevalence of iron deficiency was seen at the initiation of dialysis and a marker of circulatory iron was inversely correlated with cardiothoracic ratio, as one of the surrogate markers of cardiac enlargement. These findings suggest that not only Hb but also circulatory iron may play an important role in promoting cardiac remodeling. The role of iron deficiency in patients with CKD, with or without anemia, therefore merits clinical awareness, and more insight into the pathophysiology and interplay between iron deficiency, anemia, and CKD is warranted, especially in patients with heart failure. Iron supplementation in the predialysis phase and dialysis phase of CKD may help prevent cardiac remodeling and would be a better outcome.
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Joki et al. (2022) studied this question.
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