Contemporary intravenous iron formulations allow administration of high doses of 
elemental iron and enable correction of total iron deficit in one or two 
infusions. An important but underappreciated complication of certain 
formulations is hypophosphatemia caused by increased secretion of the 
phosphaturic hormone, fibroblast growth factor 23 (FGF23). The pathophysiology 
of FGF23-induced hypophosphatemia due to certain intravenous iron formulations 
has been recently investigated in prospective clinical trials. To reach the 
correct diagnosis, clinicians must recognize the typical clinical manifestations 
of intravenous iron-induced hypophosphatemia and identify a specific pattern of 
biochemical changes (hyperphosphaturic hypophosphatemia triggered by high FGF23 
that causes low 1,25 (OH)2 vitamin D, hypocalcemia and secondary 
hyperparathyroidism). Physicians and patients should be aware of 
hypophosphatemia as a common complication of intravenous iron therapy and 
monitor serum phosphate concentrations in patients receiving repeated doses of 
specific intravenous iron formulations. Symptoms of hypophosphatemia are 
associated with severity and duration. Persistent hypophosphatemia can occur 
with iron therapy and can cause debilitating diseases including myopathy, 
osteomalacia and fractures. This review summarizes the current understanding of 
the iron-phosphate axis as well as complications of intravenous iron-induced 
hypophosphatemia.