Anemia is defined as a reduction in one or more of the major red blood cell measurements: hemoglobin concentration, hematocrit, or red blood cell count. Hemoglobin is an iron-rich protein that gives the red color to blood. It carries oxygen from the lungs to the rest of the body. Anemia has three main causes: blood loss, lack of red blood cell production, and high rates of red blood cell destruction. While some types of anemia are short-term and mild, others can last for a lifetime. Left untreated, anemia may be life-threatening. The National Kidney Foundation defines anemia as a hemoglobin concentration of less < 13.5 g/dL in men and < 12.0 g/dL in women.
There are many anemia types, some people are born with certain types of anemia (inherited), or develop due to chronic disease, or due to nutritional deficiencies, especially iron-deficiency.
Anemia can cause physical and mental dysfunction due to a lack of oxygen supply to the body with symptoms of malaise, fatigue, weakness, dyspnea, impaired cognition, headache, dizziness, slow wound healing, skin rashes, cold hands and feet, and other symptoms such as impaired sexual function. It can also cause cold hands and feet, pale skin, irregular heartbeats, and chest pain.
New research has found a relationship between anemia and impaired thinking. In the elderly, mild anemia may be an independent risk factor for cognitive decline and executive function impairment such as problem solving, planning, and assessing dangers. Executive function impairment may happen early in the process with patients becoming unable to carry on with instrumental day-to-day living activities, such as shopping, cooking, taking medications, paying bills, walking, etc., then memory loss occurs.
Infections & Anemia
Mycobacterial infections frequently lead to the development of anemia. The mechanisms of anemia development during mycobacterial infections are not fully understood. Whether mycobacteria-induced anemia is due to iron restriction in response to infection or to a block in RBC formation is still a matter of debate. The development of anemia correlates with an increased risk of death in mycobacterium tuberculosis patients.
Viruses have also been linked to anemia. Epstein-Barr virus, cytomegalovirus, varicella-zoster virus, human herpes virus 6 (HHV-6), B19 parvovirus, human immunodeficiency virus, hepatitis A and C viruses and the putative viral agent associated with non-A-G post-hepatitis aplastic anemia have been reported in association with anemia. The ability of the bone marrow to generate copious amounts of blood cells required on a daily basis depends on a highly orchestrated process of proliferation and differentiation of hematopoietic stem and progenitor cells. This process can be rapidly adapted under stress conditions from viruses to meet the specific cellular needs of the immune response to the physiological changes. The virus itself and the ensuing immune response can have a tremendous impact on the hematopoietic process. Inflammatory cells produced by the immune system can cause hematopoietic cell death.
Iron Deficiency Anemia
Iron deficiency anemia is a type of anemia caused by an insufficient amount of iron. Without adequate iron, the body can't produce enough hemoglobin to support red blood cells to carry oxygen. As a result, the patient may experience tiredness and shortness of breath. The cause of iron deficiency anemia includes loss of blood, malnutrition without enough iron intake, low vitamin B12, as well as infections.
Iron is an essential element in maintaining oxygen carrying function by the red blood cells. Iron is also a critical nutrient for growth and survival for nearly all infectious microorganisms including bacteria, viruses, and fungus. Successful bacterial pathogens have therefore evolved to compete successfully for iron in a highly iron-stressed environment of the host's tissues and body fluids. On the other side, in reaction to an infection, the body has developed a protective mechanism to decrease iron levels and deprive microbes of iron to help the body get rid of the infection. The iron absorption in the digestive tract is under the control of a protein, hepcidin, produced by the liver. Hepcidin is a key regulator of the entry of iron into circulation in mammals. During infection or inflammation, the liver will release abnormally high amounts of hepcidin which suppresses gut iron absorption and triggers the macrophages and liver cells to trap the iron inside the cell, leading to a reduced serum iron level. When the infection and inflammation is over, the liver should decrease the secretion of hepcidin and iron absorption should return to normal. However, in some patients, their liver keeps secreting high levels of hepcidin resulting in long lasting decreased iron absorption which causes chronic iron deficiency anemia. For patients with chronic infections or inflammation, iron deficiency anemia is a common complication.
CKD & Anemia
The prevalence of CKD‐associated anemia is approximately 50%. The major causes of anemia in CKD patients are decreased erythropoietin (EPO) syntheses. EPO is a glycoprotein secreted by the kidneys interstitial fibroblasts and is essential for the growth and differentiation of red blood cells in the bone marrow. In CKD, tubular atrophy and tubulointerstitial fibrosis compromises renal erythropoietin synthetic capacity and results in anemia.
In CKD patients complicated with diabetes, anemia can contribute to retinopathy, neuropathy, or diabetic foot ulcer. Anemia can directly cause further progression of kidney disease. Renal ischemia due to reduced oxygen worsens renal medullary hypoxia, leading to renal interstitial injury and fibrosis. Anemia also causes increased renal sympathetic nerve activity, resulting in increased glomerular pressure and proteinuria which in turn accelerates the progression of kidney disease.
Under anemic conditions, the heart contracts harder to meet the body’s oxygen demand. Over time it causes left ventricular hypertrophy (LVH) and heart failure. Heart failure causes further renal function deterioration and leads to a vicious cycle termed the “cardiorenal anemia syndrome” which significantly increases morbidity and mortality of CKD patients.