3 minute lightning oral presentation (and poster) ESA-SRB-APEG-NZSE 2022
A retrospective analysis of the prevalence of hypocalcaemia and hypophosphataemia post intravenous ferric carboxymaltose and iron polymaltose in the inpatient setting (#129)
Hypophosphataemia following intravenous iron infusion is increasingly recognised, mediated by inhibition of fibroblast growth factor 23 (FGF23) degradation, renal phosphate wasting and reduced calcitriol (1,2). Hypophosphataemia prevalence after intravenous iron infusion is 45-75% (3,4,5). Significant hypocalcaemia after iron infusion has rarely been reported (3,6,7,8) and the frequency of hypocalcaemia following intravenous iron in the inpatient setting has not been characterised.
In this single-centre retrospective study, we sought to characterise changes in plasma calcium and phosphate following intravenous iron in inpatients. We hypothesized that hypocalcaemia occurred more frequently following iron infusion, and was more likely to occur with concurrent vitamin D deficiency.
All inpatients who received intravenous iron polymaltose or ferric carboxymaltose at the Royal Brisbane and Women’s Hospital from January 2020 to September 2021, who had a general chemistry blood test within ten days prior to and following infusion, were included. We extracted all available results for corrected calcium (CCa) and phosphate (PO4) for 21 days before and after iron infusion. Seven-hundred-and-eighty-seven patients with 9168 blood samples were included.
The results showed a mean pre-infusion PO4 of 1.17mmol/L (range 0.47-1.91mmol/L) and post-infusion PO4 of 1.00mmol/L (range 0.33-1.85mmol/L), confirming a reduction in phosphate after iron infusion (p<0.0001). A significant increase in hypophosphataemia frequency after infusion was also demonstrated (7% vs 33%; p<0.0001). The temporal course of hypophosphataemia is shown in Figure 1. There was no significant difference between mean pre-infusion and post-infusion CCa, or in hypocalcaemia frequency. However, the temporal change in CCa showed an early post-infusion increase before a late decrease (Figure 2), suggesting an inverse relationship to PO4. Vitamin D levels were only available for 307 patients, however, deficiency was not associated with hypocalcaemia or hypophosphataemia occurring after iron infusion. In conclusion, our results confirmed significant hypophosphataemia following intravenous iron but did not demonstrate significant hypocalcaemia.
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