Loss of blood associated with
hemodialysis procedures and laboratory testing, together with impaired
iron absorption due to elevation of
hepcidin, invariably cause
iron deficiency in
end-stage renal disease patients. For this reason, nearly all
ESRD patients require intravenous
iron to replete
iron stores. Unfortunately, intravenously administered
iron is often used routinely with inadequate attention to the body
iron stores or severity of systemic
inflammation. This has led to an epidemic of
iron overload in the
ESRD population. Only a minute amount (3-4 mg) of the total body
iron (3-4 g in an adult man) resides in the plasma bound to
transferrin, which serves as a safe vehicle for
iron transport in the circulation. IV
iron products are generally administered as bolus
injections of 100 to 1000 mg, which far exceeds the available pool of free
transferrin and represents a huge quantity compared to the intestinal
iron absorption of 1 to 2 mg/day in the course of 3 to 4 meals. Administration of these products results in an increased plasma level of catalytically active non-
transferrin bound
iron and the rise in the
biomarkers of oxidative stress and
inflammation. IV
iron bypasses the
biological safeguards for the transport and handling of
iron and helps to intensify
chronic kidney disease-associated oxidative stress and
inflammation. As briefly described in this review, indiscriminate use of IV
iron can accelerate
cardiovascular disease, promote microbial
infections, aggravate viral
hepatitis, and worsen diabetes and
diabetic complications in such patients. For these reasons IV
iron should be used judiciously in this vulnerable population.