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Anemia

Introduction
The intention of this paper is to explore causal factors and consequences of anemia as it relates to renal failure; to examine agents used to combat anemia for those who suffer from renal failure and undergo hemodialysis and how administration of the essential trace element iron is utilized in current treatments.  The structure of this paper will consist of five segments beginning with a brief review of anemia, followed by a short discussion of iron deficiency anemia.  Then the relationship between renal failure, anemia and iron deficiency will be explored. Finally, current measures used in combating anemia in hemodialysis patients such as recombinant human erythropoietin will be examined. 

Anemia 
Anemia is a pathological deficiency in the number of red blood cells (erythrocytes), usually measured in unit volume concentration of hemoglobin.  Hemoglobin is an iron-containing protein that enables the transport of oxygen from the lungs to all of the body's muscles and organs.  Oxygen provides the body with the energy needed to perform normal activities.  The structure of hemoglobin consists of a globin portion which is made up of polypeptide chains (two á-chains and two â-chains) and four heme groups.  Each heme molecule contains one iron ion ligand in its center which allows for the binding of oxygen (Gropper, p. 427, 2005).   Anemia occurs when the number of red blood cells or the hemoglobin within the cells fall below normal ranges (normal hemoglobin for men is 14 -18 g/dl and normal hemoglobin for women is 12-16g/dl [Understanding Anemia, 2005]).  When hemoglobin levels fall below ll-12 g/dl, the transport of oxygen becomes compromised, hence leaving the body without the energy needed to function properly.  If left untreated, the consequences of anemia lead to substantial morbidity and mortality.
There are several types of anemia which include the following:
Anemia - B12 deficiency
Anemia - folate deficiency
Anemia - iron deficiency
Anemia due to chronic disease
Hemolytic anemia
Hemolytic anemia - G-6-PD deficiency
Idiopathic aplastic anemia
Idiopathic autoimmune hemolytic anemia
Immune hemolytic anemia
Immune hemolytic anemia - drug-induced
Megaloblastic anemia
Pernicious anemia
Secondary aplastic anemia
Sickle cell anemia
As the above list indicates, there is a wide range of potential causes of anemia such as blood loss, nutritional deficits, various diseases, reactions to medications and problems with bone marrow (Brose, M., 2004).  For the purpose of this paper we shall examine the occurrence of anemia as a result of renal failure and the consequences of iron deficiency.

Iron deficiency, Anemia and Renal Failure
Iron deficiency is a worldwide common nutritional problem causing iron-deficiency anemia in more than 500 million people.  Iron deficiency is associated with low birth weight,..."defects in cognitive and psychomotor development in children and impaired work capacity for adults" (Gupta, et al, 1999).  Since iron is a central component of hemoglobin, deficiencies in iron inhibit hemoglobin synthesis.  The amount of iron present in the body varies with sex, age, and body size. Normal adults have between 2 - 5 g of iron present in the body; 4 g for average adult males; 2 g for average adult females.  A majority of iron is found in hemoglobin (65%) with roughly 25% in storage as ferritin and hemosiderin primarily stored in bone marrow.  The main iron transport protein is transferrin.  Each molecule of transferrin can bind two iron (Ferric) atoms. 
Anemia is a significant obstacle for hemodialysis patients with chronic renal failure and understanding the underlying cause of anemia and iron deficiency is imperative for appropriate treatment.

The kidneys play a pivotal role in the production of red blood cells. Erythropoiesis (red cell production) takes place in bone marrow.  For this process to begin the kidney cells must release the hormone erythropoietin (EPO), a glycoprotein that is a growth factor for red blood cell stem cells. The release occurs when oxygen content in blood is low.  The hormone travels to bone marrow and stimulates red blood cell precursors to divide and terminally differentiate into reticulocytes (immature red blood cells) which then develop into mature cells over a period of 24 - to - 48 hours (Rolfes, Pinna & Whitney, 2005).   As renal failure progresses, adequate EPO is not produced by kidney cells and red blood cell production is compromised.

The most commonly used therapy to combat anemia for hemodialysis patients is the use of a recombinant human erythropoietin (rHuEPO) (Berns, Elzein, Lynn, Fishbane, Meisels & DeOreo, 2003), epoetin alfa and while this therapy improves physiologic quality of life, raises hemotocrit and hemoglobin concentrations, 25 - 37% of patients still fail to achieve normal hemoglobin levels (Folkert, Javier, & O'Mara 2002; Frankenfield, Neu, Warady, Fivush, Johnson & Brem, 2003).  This is primarily due to secondary conditions, such as iron deficiency, which is the most common causal factor that diminishes response to treatment with epoetin alfa (Hudson & Comstock, 2001). 
It is recommended for hemodialysis patients to have iron saturation of transferrin above 20% and to have ferritin levels greater than 200 ng/ml (Asuncion, 2002). Iron deficiency develops in more than 50% of hemodialysis patients (Folkert, Javier, & O'Mara 2002) for a number of reasons; there is chronic blood loss during the hemodialysis procedure (blood remaining in dialyzers and the dialysis lines) (Eschback,  Cook, Scribner & Finch, 1977) and during diagnostic sampling as well as the occurrence of gastrointestinal bleeding which can be a result of erosions and ulcers from gastrointestinal complications that often develop during end stage renal disease (Bickford, 2002; Folkert, Javier, & O'Mara 2002; Foret, 2002).  These losses increase the demand for sufficient iron absorption and studies show that this cannot be accomplished via the gastrointestinal tract alone (Bickford, 2002).  For rHuEPO therapy to successfully combat anemia it is necessary to accurately determine the patient's iron status. 

In dialysis facilities, hemoglobin and hemotocrit are measured frequently, which dictates adjustments to the rHuEPO dosage (Berns, et al., 2003). Unfortunately, current laboratory parameters used to measure iron status such as serum iron, total iron binding capacity (TIBC), serum ferritin and transferrin saturation have proven to be problematic and imprecise for hemodialysis patients due to extraneous factors.  For example, serum iron indicates the amount of transferrin-bound iron in circulation but levels fluctuate during the day and the results can not be used to accurately determine iron status.  TIBC measures the presence of receptor protein transferrin.  The amount of transferrin circulating often correlates with iron concentration but transferrin is altered by factors other than iron, such as malnutrition.  In healthy people, serum ferritin roughly reflects iron stores and a low value is often indicative of iron depletion.  However, serum ferritin is an acute-phase reactant and conditions such as chronic renal disease, infection that develops from inserting catheters, and inflammation, which is a common characteristic of chronic renal failure, can elevate serum ferritin levels regardless of iron status and normal values do not necessarily equate adequate iron stores.  More importantly, serum ferritin is not a measure of available iron needed for erythropoiesis and does not allow for accurate estimation of iron requirements for rHuEPO.   Finally, the measurement of transferrin saturation refers to the degree to which the iron-bound transport protein transferrin is filled with iron, which is reflective of circulating iron available for heme synthesis.  Accuracy of this measurement is compromised because it is also an acute-phase reactant and can decrease with infections, inflammation and surgical procedures (Bickford, 2002; Foret, 2002). 

In light of the issues surrounding the accuracy of determining iron status for hemodialysis patients who are treated with rHuEPO, it is important to differentiate between absolute iron deficiency and functional iron deficiency (Bickford, 2002).  In absolute iron deficiency there is no iron available for the production of hemoglobin.

When iron stores are completely depleted delivery of iron to erythroid marrow does not occur and this condition will be reflected by serum ferritin levels < 12 ng/ml and TSAT of

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