Abstract

time) and iron deficiency (measured by hypochromic red cells) in hemodialysis patients, and which speculated that the hemostasis impairment might affect (functional) iron deficiency, most likely by facilitating excessive blood loss (1). This explanation is plausible, but we would like to say that iron deficiency itself could also affect platelet-related hemostasis impairment. Although not as yet extensively studied, Caliskan et al. showed that collagenor adenosine diphosphate-induced platelet aggregation was decreased in patients with iron deficiency anemia (2), and Pati et al. also demonstrated that the rate and degree of platelet aggregation with all agonists (except the lowest concentration of adenosine diphosphate) were significantly lower in anemic patients than in control and post-iron therapy subjects (P < 0.05–0.001) (3). Although it has been reported that uremic patients have decreased shear-induced platelet aggregation mediated by the decreased availability of glycoprotein IIb-IIIa receptors (4), and defective platelet aggregation in uremia is transiently worsened by hemodialysis (5), iron deficiency itself might also cause additional platelet-related hemostasis impairment in hemodialysis patients. However, further studies will be necessary to evaluate whether iron therapy could reverse defective platelet aggregation due to iron deficiency or reduce excessive blood loss in hemodialysis patients in the future.

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