Sodium-glucose co-transporter 2 inhibitors (SGLT2i) increase hemoglobin and hematocrit, effects that have emerged as key statistical mediators of the cardiorenal benefits observed with SGLT2i therapies [1,2]. The underlying mechanisms of SGLT2i-induced erythrocytosis include enhanced iron mobilization and utilization, driven by upregulation of the erythropoietin-erythroferrone-transferrin receptor protein 1 (TfR1) axis [3]. Interestingly, data from observational studies and randomized clinical trials (RCTs) indicate that these hematologic effects occur independently of baseline anemia status [4–6].
