An iron infusion is a medical procedure where iron is delivered directly into the bloodstream through an intravenous (IV) line to quickly replenish iron stores. This method treats severe iron deficiency anemia when oral supplements are ineffective, poorly tolerated, or when a rapid increase in iron levels is necessary. Since the kidneys play a large role in blood health, patients often question the potential impact of this treatment on their renal function.
Iron Metabolism and Kidney Function
The kidneys maintain a close relationship with the body’s iron stores, primarily through the production of a hormone called erythropoietin (EPO). EPO is synthesized by the kidneys and acts on the bone marrow to stimulate the production of new red blood cells, a process that requires a sufficient supply of iron. When kidney function declines, as occurs in chronic kidney disease (CKD), the production of EPO is often significantly reduced, leading to anemia.
Patients with CKD frequently develop iron deficiency anemia because of this EPO deficiency, chronic inflammation, and sometimes blood loss from dialysis. Inflammation interferes with the body’s ability to utilize stored iron effectively, a condition known as functional iron deficiency. Therefore, administering intravenous iron is a standard and often more effective approach than oral supplementation to restore iron levels and support red blood cell formation in this patient population.
How Intravenous Iron Can Affect Kidney Function
Historically, older formulations of intravenous iron, particularly high molecular weight iron dextran, carried a greater risk of adverse events. These risks included rare instances of acute kidney injury (AKI), thought to be related to the release of free, or “labile,” iron. This labile iron could cause oxidative stress and direct tissue damage within the kidneys.
Modern, non-dextran iron compounds, such as iron sucrose and ferric carboxymaltose, have largely replaced older agents and are associated with a much lower risk of severe allergic reactions or acute toxicity. However, a specific kidney-related side effect has been increasingly recognized, particularly with certain newer formulations like ferric carboxymaltose: renal phosphate wasting, which leads to hypophosphatemia (abnormally low levels of phosphate in the blood).
This phosphate wasting occurs because certain intravenous iron compounds can increase the level of a hormone called Fibroblast Growth Factor 23 (FGF23). High levels of FGF23 act directly on the kidney tubules, causing them to excrete too much phosphate into the urine. While often temporary and without symptoms, severe or prolonged hypophosphatemia can cause symptoms such as muscle weakness and fatigue. This reflects a direct, albeit usually reversible, impact on the kidney’s ability to manage mineral balance. This specific effect is less common with other modern formulations like iron sucrose or ferric derisomaltose.
Pre-Existing Risk Factors and Safety Measures
Patients with pre-existing conditions affecting mineral balance may be at a higher risk for developing symptomatic hypophosphatemia after an infusion. Those with chronic kidney disease or who require large, repeated doses of iron may also warrant closer observation. Physicians take several proactive safety measures to mitigate risks, including administering the infusion slowly and observing the patient for a period following the treatment to monitor for acute reactions.
Before administering an iron infusion, physicians assess iron status and check baseline kidney function using tests like serum creatinine and estimated Glomerular Filtration Rate (eGFR). Monitoring phosphate levels, particularly when using formulations associated with phosphate wasting, is becoming common practice to detect hypophosphatemia early. Patients should report any new or worsening symptoms following an infusion, such as changes in urination patterns, severe muscle pain, or profound weakness, as these could signal a mineral imbalance or other adverse reaction.