Anemia in Patients with Chronic Renal Failure and in Patients undergoing Chronic Hemodialysis. Anemia is defined as a reduction in the oxygen carrying capacity of blood, measured in the laboratory as a low hemoglobin concentratioin, or a low hematocrit (the percentage of the blood volume that is occupied by red blood cells or erythrocytes). In a normal person, the hemoglobin is approximately 1. It occurs when the balance between the normal rates of blood loss and blood production is disturbed. There are three basic mechanisms by which this occurs: (1) blood loss, (2) excessive destruction of red blood cells (hemolysis), and (3) abnormally low production of red blood cells by the bone marrow. In chronic renal failure, anemia is almost always present, and can be a result of any of the mechanisms listed above. However, the typical . This hormone is a necessary stimulus for normal bone marrow to produce red blood cells. In addition, other factors associated with renal failure, including the accumulation of so- called uremic toxins, may play a role in depressing bone marrow function. Excess stores of aluminum may accumulate in the bone marrow of long term dialysis patients and can contribute to anemia as well. Platelets, which are small constituents of blood which aid in blood clotting, do not work normally in uremia. The defective blood clotting seen in uremia makes bleeding more common. Rapid bleeding. Very slow loss of blood can also cause anemia by depleting the body. Normally, red blood cells survive for about four months before being destroyed. This life span is reduced in renal failure, probably because of chemical effects of uremia and decreased flexibility of the red blood cells. This hemolysis is usually mild and a person with a normal bone marrow could easily compensate for it by increasing red blood cell production. However, in renal failure, the bone marrow. The effectiveness of dialysis in reversing any complication of uremia depends on the nature of that complication. Those disturbances which are due to accumulation of a uremic toxin may be reversible if that toxin is dialyzable and if the removal rate by dialysis outstrips its generation rate. Some improvement in red blood production is seen with initiation of dialysis, probably by decreasing the toxic effect of uremia on the marrow. Dialysis, however, does not replace the hormone producing functions of the kidney and therefore does not by itself correct the main cause of anemia, namely deficient production of erythropoietin. Anemia is not a single disease but a condition, like fever, with many possible causes and many forms. Causes of anemia include nutritional deficiencies, inherited. More than a quarter of the world's population is anemic, with about one-half of the burden from iron deficiency. The prevention and treatment of iron deficiency is a.
Dialysis does correct the bleeding tendency seen in uremia, but not to normal. Iron deficiency can result from unavoidable dialyzer blood loss, clotted dialysis membranes, and frequent blood sampling. Hemolysis may occur if there are problems with the dialysate (temperature problems, contamination with aluminum, fluoride, copper, chlorine, or chloramine). Anemia results from lack of iron, folic acid, B vitamins and other nutrients. These home remedies for anemia are excellent ways to replenish nutrients in your body. Folate, a water soluble vitamin necessary for normal red blood cell production, is dialyzable. Generally, dialysis patients are given oral supplementation with folic acid in case their normal diet does not supply them with sufficient folate to keep up with its loss through dialysis. In an otherwise healthy patient with chronic renal failure, a hematocrit of approximately 2. The presence of other medical problems, particularly heart and lung disease, can decrease a patient. Anemia is a condition in which the blood does not have enough red blood cells or enough hemoglobin – the iron-containing, oxygen-carrying protein molecules found in.Patients who have undergone bilateral kidney removal (nephrectomies) often have hematocrits which are significantly lower, probably because they cannot make any erythropoietin at all. Patients whose kidney failure is a result of polycystic kidney disease generally do not have anemia. Until recently, the principal treatments were transfusion of red blood cells and administration of the hormone testosterone. Although transfusions will rapidly correct a low blood count, repeated transfusions are associated with some problems, including iron overload, the development of certain antibodies, and the possibility of viral infections. Testosterone may stimulate red blood cell production by the bone marrow, but the effect is generally small, and its use is often associated with virilizing side effects. In 1. 98. 3, the gene for erythropoietin was isolated, then cloned. Subsequently this led to the mass production of erythropoietin and finally to its use in renal failure patients in 1. Chapter 2. 0). It is administered either intravenously at dialysis or subcutaneously. In anemic patients with chronic renal failure, treatment with erythropoietin is now standard practice and has dramatically reduced the need for blood transfusions. The increase in hematocrit seen with patients treated with erythropoietin has generally resulted in improvement in exercise tolerance and overall sense of well- being. It is important to moniter the iron status of treated patients, as iron deficient patients will not respond appropriately to administration of erythropoietin. The use of erythropoietin is constrained by the extremely high cost of this hormone and the reimbursement policies of insurance companies and Medicare. It has multiple causes, the most important of which is decreased production of erythropoietin by the kidney. The availability of the recombinant form of this hormone is revolutionizing treatment of this form of anemia.
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