Anemia: In the vast majority of cases, “lowered hemoglobin” is equivalent with the general medical diagnosis of anemia. Anemia is defined by Webster’s Seventh New Collegiate Dictionary, as “a condition in which the blood is deficient in red blood cells, hemoglobin or in total volume…” Hemoglobin is the chemical within the red blood cells which gives color to blood and carries oxygen to the tissues. So, low hemoglobin essentially means that the patient has anemia. To best understand how this might occur, some explanation regarding how the kidney can affect anemia, as well as a review of the various causes of anemia, may be in order. Type of Anemia Common Name or Example Hereditary diseases Sickle cell, Thalassemia, other Hemolytic anemia Toxin, other cause for cell breakage Impaired red cell synthesis Vitamin or nutritional deficiency Hypochromic anemia Blood loss, cancer, iron deficiency Bone marrow failure Leukemia, drug effects Miscellaneous causes Infection, alcoholism, chronic illnesses
The Kidney and Anemia When considering prevention and treatment of anemia, the kidney is one of the most important organs in the body. This is because the kidney produces a hormone called erythropoietin (EPO) that stimulates the bone marrow where blood cells are produced in order to make more red blood cells. Since a red blood cell made today lives only 120 days, replenishment must be a continuous process. When the bone marrow and kidneys are functioning normally, there is a normal balance of EPO and supply of blood cells such that the blood count is normal and anemia is absent. If the kidney is diseased and does not produce EPO, bone marrow is not sufficiently stimulated, fewer red blood cells are produced and anemia occurs. Thus, to minimize anemia, many patients with kidney failure must take EPO while on dialysis. Other medications, such as iron, may also be given to treat patients with chronic kidney disease (CKD) and anemia. Normally, the transplanted kidney produces adequate amounts of EPO so the balance of blood cell production and kidney hormonal output results in a correction of anemia, which affects most kidney failure patients. The question as to why a long-term transplant recipient would develop anemia must be answered both in terms of how the transplanted kidney might allow anemia to develop, as well as other causes of anemia not related to kidney function. Anemia Related to the Kidney Transplant Following kidney transplantation, in the vast majority of patients, there is correction of previous anemia from the new kidney making normal amounts of EPO, and the bone marrow responds appropriately. In certain cases, the transplanted kidney may produce insufficient quantities of EPO for several reasons. First, the kidney could be from an older donor of smaller stature and may not have produced normal amounts of EPO in the donor. Second, there could be kidney tissue damage during the time the kidney was prepared for transplantation and was stored in a cold state. Third, the kidney may initially produce normal amounts of EPO, but with time chronic damage from either rejection or other causes could alter the ability to produce adequate amounts of EPO. Important in the immunosuppressive treatment plan of all kidney transplant patients is the drug treatment plan designed to prevent rejection. At least two types of drugs can affect the kidney or bone marrow so the patient might become anemic after a long period of normal kidney transplant function. The first class of such drugs is called calcineurin inhibitors (cyclosporin and FK 506). These drugs, while preventing rejection of the kidney, actually have some degree of toxic effect upon the kidney. Taken over many years, they may alter function of the transplanted kidney and actually contribute to CKD, leading to diminished production of EPO and anemia. Another class of drugs that prevent rejection is the antimetabolite group (ImuranĀ®, CellCeptĀ® and RapamuneĀ®). These drugs have a well-known effect on the marrow and can cause anemia. In rare cases, these drugs can cause life-threatening anemia or other bone marrow abnormality. Non-Kidney-Related Causes of Anemia The long-term transplant patient could be subject to a number of reasons for having anemia, many of which may not be related to the transplant or its medications at all. These cases, which can affect anyone, are generally grouped into categories depicted in the table. The cause of lowered hemoglobin in the stable long-term kidney transplant patient may be due to many things. Some causes may be related to the kidney itself or medications given to prevent rejection. Additional causes may relate to the many and varied reasons that patients become anemic. Interestingly, a number of CKD patients may have a cause for kidney disease that also relates to anemia independently. An example may be sickle cell anemia, which can not only cause a very difficult problem with red blood cells, but also affect the kidney in an adverse fashion. What Should Be Done? All transplant patients should be aware of the reasons for anemia, and should be followed on a regular basis with a complete blood count (CBC) at appropriate intervals. The CBC will allow the treating physician to determine whether further tests or treatment should be considered for the anemia. Most transplant patients respond nicely to treatment of anemia when its cause has been determined. Most often, anemia treatment is quite compatible with ongoing therapy to prevent rejection and maintain normal kidney transplant function. Answer provided by Thomas Peters, MD, a transplant surgeon at the Jacksonville Transplant Center at Shands Jacksonville Medical Center, Jacksonville, Fla. Dr. Peters also serves on the AAKP Board of Directors and AAKP Medical Advisory Board. The Dear Doctor column provides readers with an opportunity to submit renal related health questions to healthcare professionals who specialize in the area of concern. The answers are not to be construed as a diagnosis and therefore, altercations in current healthcare should not occur until the patient's physician is consulted. This article originally appeared in the January 2005 issue of aakpRENALIFE, Vol. 20, No. 4.
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