Anemia and Kidney Disease
Anemia is common in people with chronic kidney disease impacting over 35 million people in the U.S. Anemia may begin to develop in the early stages of kidney disease, when patients still have 20 to 50 percent of normal kidney function. Anemia tends to worsen as kidney disease progresses and is most often due to the diseased kidney’s inability to produce sufficient erythropoietin. Erythropoietin, is a hormone that stimulates the production of red blood cells in the bone marrow. Since the patient’s kidneys are no longer functioning, erythropoietin is not being produced.
Anemia is a significant medical condition for hemodialysis patients that requires ongoing treatment. Patients undergoing hemodialysis also develop anemia due to the blood loss that accompanies their treatment. This blood loss occurs because of needle sticks, blood that is trapped in the bloodlines or dialyzer and frequent blood draws. In fact, on average, hemodialysis patients lose 5-7 milligrams of iron each dialysis treatment. This loss of iron may also lead to anemia.
To effectively treat anemia, both bio-available iron and an erythropoiesis-stimulating agent (ESA) need to be present at the same time. An ESA, designed to replicate Erythropoietin, is administered to patients with failed kidneys to correct their anemia. Patients are also treated with IV iron repletion therapy to increase the effectiveness of ESA. However, because of the molecular structure of IV iron, the vast majority of iron received by the patient is stored in the liver as Ferritin and never released. In fact, only 2-6% of IV iron administered to the patient actually gets released to the bone marrow for red blood cell creation. IV iron stored in the liver is known to cause inflammation and iron overload. Because the liver is overloaded with iron there is also an increased risk of infections, cardiovascular disease and many other side effects. In addition, because IV iron is recognized by the body as a foreign matter when injected, there is a risk of severe anaphylaxis and allergic reactions associated with its use.
Because of the limitations to IV iron, there is an unmet need for replacing lost iron and maintaining hemoglobin in hemodialysis patients without producing iron overload.
Triferic is the answer to that unmet need. Triferic is the only FDA approved drug indicated for the replacement of iron to maintain hemoglobin in hemodialysis patients and was launched commercially in the United States on September 30, 2015.
Triferic is a true iron maintenance therapy. It delivers 5-7 milligrams of iron each dialysis treatment, simply replacing the lost iron each patient experiences during their treatment. In contrast to IV iron repletion therapy, Triferic is not stored in the liver. Once Triferic crosses the dialyzer membrane and enters the blood, it immediately binds to transferrin (the iron carrying protein) where it is carried to the bone marrow for healthy red blood cell production. Also, unlike IV iron repletion therapy, Triferic does not require any needles or syringes for administration. A nurse simply adds Triferic to the liquid bicarbonate concentrate for seamless administration via dialysate to each patient during their dialysis treatment.