A new study suggests that intravenous (IV) administration of Iron may reduce mitral infarction (MI) in patients with chronic kidney disease (CKD) undergoing dialysis.

Researchers at the University of Glasgow (United Kingdom), King’s College Hospital (London, United Kingdom), and other institutions participating in the Proactive IV Iron Therapy in Haemodialysis Patients (PIVOTAL) trial, conducted a study involving 2,141 patients at 50 sites in the United Kingdom in order to investigate the effects of both high and low dose IV iron on MI in patients on hemodialysis. The researchers examined rates of MI, fatal or non-fatal MI, types of heart attacks, prognostic importance, and the effects on maintenance hemodialysis.

The results revealed that over 2.1 years of follow-up, 8.4% of participants experienced a MI. Rates of type one MI (classic plaque rupture with thrombus formation) were 2.5 times higher than type two MI (non-occlusive), and non-ST-elevation MIs were six times higher than ST-elevation MIs. High-dose IV iron reduced the composite endpoint of non-fatal and fatal MI by 31%, when compared with reactive low-dose IV iron. There was less effect of high-dose IV iron on recurrent MI events than on the time-to-first event analysis. The study was published on December 7, 2021, in Cardiovascular Research.

“Very few therapies investigated in people on dialysis have been shown to improve outcomes. We are delighted that high dose iron given into people veins reduces heart attacks,” said lead author Mark Petrie, of the BHF Cardiovascular Research Centre at the University of Glasgow. “Our hope is that this treatment is used around the world in people with kidney failure on dialysis.”

Iron deficiency anemia is a common complication of CKD, due to increased blood loss during dialysis resulting from frequent phlebotomies, blood remaining in the dialysis tubing, and gastrointestinal bleeding from a combination of gastritis and platelet dysfunction. In addition, Iron is recycled when red blood cells are phagocytosed by reticuloendothelial macrophages. This process is mediated by hepcidin, which is filtered and degraded by the kidney. Hepcidin levels are increased in CKD, severely depleting Iron availability for erythroid precursors. 

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