Intravenous Iron Repletion Does Not Significantly Decrease Platelet Counts in CKD Patients with Iron Deficiency Anemia

Purpose. We sought to investigate the effect of IV iron repletion on platelet (PLT) counts in CKD patients with iron deficiency anemia (IDA). Methods. We conducted a retrospective chart review, including all patients with CKD and IDA who were treated with iron dextran total dose infusion (TDI) between 2002 and 2007. Patient demographics were noted, and laboratory values for creatinine, hemoglobin (Hgb), iron stores and PLT were recorded pre- and post-dose. Results. 153 patients received a total of 251 doses of TDI (mean？±？SD？=？971？±？175？mg); age years and Creatinine ？mg/dL. All CKD stages were represented (stage 4 commonest). Hgb and Fe stores improved post-TDI ( ). There was a very mild decrease in PLT (pre-TDI 255 versus post-TDI 244, ). The mild reduction in PLT after TDI remained non-significant ( ) when data was stratified by molecular weight (MW) of iron dextran used (low versus high), as well as by dose administered (<1000 versus ≥1000？mg). Linear regression analysis between pre-dose PLT and Tsat and Fe showed R2 of 0.01 and 0.04, respectively. Conclusion. Correction of iron deficiency did not significantly lower PLT in CKD patients, regardless of MW or dose used. Correlation of PLT to severity of iron deficiency was very weak. 1. Introduction Intravenous (IV) iron has become a cornerstone of therapy for anemia in patients with chronic kidney disease (CKD)—both before hemodialysis and for those on hemodialysis. One of the earliest intravenous (IV) compounds used to treat iron deficiency anemia was iron dextran; however, its popularity as a first-line agent had waned considerably secondary to concerns regarding its safety and the introduction of newer compounds on the market. Iron deficiency often leads to reactive thrombocytosis [1–5], with platelet counts sometimes as high as 500,000 to 700,000 cells/mm3. The etiology of the thrombocytosis in iron deficiency remains uncertain. Platelet (PLT) counts have been reported to vary directly with the severity of iron deficiency in chronic hemodialysis patients. This has led some to hypothesize that iron deficiency may produce a relative thrombocytosis which may contribute to the thrombotic events noted in clinical trials of erythropoiesis stimulating agents (ESA’s) in CKD patients. Even more interestingly, PLTs were reduced after IV iron administration in hemodialysis patients in the recent DRIVE study [6–8]. However, the PLT count remained unchanged in patients in the treatment arm not given IV Iron. In a recent NKF abstract, Besarab et al. reported that correction of iron deficiency lowers PLT in