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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Uremia interferes with erythropoiesis, granulocyte, platelet, and immune functions. As a result, uremic patients are almost invariably anemic, and have a high incidence of infections and hemorrhagic complications. The anemia of renal failure, which is caused primarily by damage to the site of erythropoietin production is often complex, and complicated by hemolysis from a variety of mechanisms, iron deficiency, and so forth. Although hemodialysis ameliorates some of the hematologic complications to a variable degree, they remain a serious hinderance to the well being of this group of patients. Progress in understanding the mechanism of these problems and their therapy has been reviewed here.
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PMID:Hematologic complications of chronic renal failure. 36 51

The percentage of fat-cell areas in bone marrow particles from 22 patients with untreated myelomatosis was estimated. In only 1 patient was the mean fat cell area below 25% of the bone marrow area measured. A negative correlation was found between the area of fat cells and plasma cells, indicating a displacement of the fat cell area by the plasma cells. 28% of the patients had empty bone marrow deposits of iron. However, based on a normal iron saturation of S-transferrin and a normal sideroblast count in the bone marrow, the supply of iron to the erythropoiesis was considered sufficient. All patients but one had normoblastic bone marrows. Using a deoxyuridine suppression test in 10 patients, no biochemical defect could be demonstrated. To judge from the correlation coefficient a minor degree (9-14%) of the variation in Hb values could be predicted from the cellularity in the bone marrow while a major degree (70%) could be predicted from the renal glomerular filtration rate. The results do not support a displacement of blood-forming elements, iron deficiency, vitamin B12 or folic acid deficiency to be of general significance in the pathogenesis of anaemia, but agrees with a causal relationship between anaemia and renal failure.
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PMID:Bone marrow studies in myelomatosis. 71 78

Hematocrit and plasma ESF titers were determined at 2 to 3 weeks intervals in 21 patients with chronic renal failure prior to and during a 15-weeks' period following initiation of chronic intermittent hemodialysis. While hematocrits increased from 22 to 27%, plasma ESF titers were found unchanged between 31 and 35 mU/ml. It can be excluded therefore that the improvement of erythropoiesis following initiation of dialysis was in part due to an increase in plasma ESF titers. The increased erythropoiesis observed is probably not dependent on increased ESF production. A 30-fold ESF deficit existed in patients with renal failure prior to the initiation of hemodialysis when compared with 5 patients with aplastic anemia (hematocrit 23%, plasma ESF titer 1115 mU/ml). At one exception ESF titers up to 500 mU/ml were found in dialysed patients only in combination with anemia due to acute bleeding or iron deficiency. ESF production is appropiate to the degree of anemia in patients with proper renal function after kidney transplantation.
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PMID:[Plasma erythropoietin and hematocrit under the influence of chronic hemodialysis treatment (author's transl)]. 83 18

Various factors are involved in the pathogenesis of anemia in dialysis patients. Reduced erythropoiesis is mainly attributed to erythropoietin deficiency. Stimulation of erythropoiesis may be promoted by androgens. Substitution of iron is recommended in case of iron deficiency. As a rule, supplementation of vitamin B12 is not necessary, but administration of folic acid is recommended. Treatment of anemia in renal failure is rendered more effective by increased technical efficiency in hemodialysis permitting a relatively protein-rich diet. Blood transfusions are not necessary during routine treatment of dialysis. Since bilateral nephrectomy will always provoke severe anemia, it should be reserved to special cases of severe hypertension. Until now, no conservative therapy has been developed which would allow optimal treatment of anemia in dialysis patients. Successful renal transplantation still is, and will be, the best therapeutic intervention.
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PMID:[Anemia in terminal kidney failure. Pathogenesis and therapy]. 83 56

Haemoglobin concentration was determined in all patients (530) over 70 years of age in a general practice in Oslo during an eight month period. 72 had anaemia and were investigated further. Iron deficiency was found in 13 patients and was most often caused by gastrointestinal blood loss. Chronic diseases, particularly chronic infections and rheumatoid arthritis, were responsible for anaemia in 34 patients. Renal failure caused anaemia in 14 patients. In 10 patients we found no explanation for the anaemia. Nine patients with a previously undiscovered disease were found, six of whom could be offered some kind of treatment. We conclude that anaemia in elderly patients in general practice is often caused by chronic diseases. The main cause of iron deficiency is blood loss, and routine prescription of iron is not justified in this age group. The therapeutic benefit from routine measurement of haemoglobin concentration is small and the test should be used selectively.
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PMID:Anaemia in elderly patients. Incidence and causes of low haemoglobin concentration in a city general practice. 175 48

Recombinant Human Erythropoietin (r-HuEPO) is efficient in the treatment of anaemia in terminal renal failure under dialysis. Five pediatric patients, who were under periodic hemodialysis, were treated and the interaction between the metabolism of iron and the response to r-HuEPO was studied in particular. In two patients it was noticed that a significant reduction of hematic ferritin levels occurred, while an efficient erythropoietic activity was maintained. On the contrary, three patients showed iron deficiency characterized by a reduced percentage of total transferrin saturation in the plasma, in the presence of high levels of ferritin in the blood. Also discovered was a missing increase or even a fall of the hemoglobin values that were obtained till now. In these cases, the increase of the hormone dose didn't lead to an improvement, that could only be obtained by the oral or parenteral administration of iron. The Authors in conclusion affirm that iron deficiency is the first cause to be searched for and to be corrected in the presence of missing hemoglobin increase even with adequate doses of r-HuEPO.
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PMID:[Influence of iron metabolism on the efficacy of r-HuEPO (recombinant human erythropoietin) treatment of anemia in children on hemodialysis]. 178 7

Several factors contribute to the pathogenesis of anemia due to renal failure. Hypoproliferation of red cell progenitors may be caused partially by an inhibitory effect of some 'uremic toxins' whose existence certainly is very controversial. Iron deficiency due to gastrointestinal and dialysis-related blood losses and occasionally aluminum intoxication may interfere with the maturation of the erythron. Moderate hemolysis with shortening of red cell survival to some 50% of normal may be an additional factor. The main cause of anemia is, however, inadequate production of erythropoietin by the diseased kidney. This latter factor has now become amenable to treatment.
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PMID:[Pathogenesis of anemia due to kidney disease]. 264 77

Fourteen nondialyzed patients with chronic renal insufficiency (serum creatinine 265 to 972 mumol/L [3.0 to 11.0 mg/dL]) and severe anemia (hematocrit less than 30%) were randomized to receive either recombinant human erythropoietin (r-HuEPO) or a placebo subcutaneously thrice weekly for 12 weeks or until reaching a hematocrit of 38% to 40%. Anemia was significantly ameliorated in the treated patients. No acceleration in the progression of renal failure (1/serum creatinine v time) or change in serum potassium was noted for either the placebo or treated group over the 12-week period. Six of seven treated patients had a significant decrease in serum ferritin and percent transferrin saturation (plasma iron/total iron-binding capacity). This resulted in functional iron deficiency and the requirement for iron supplementation. The average systolic and diastolic blood pressure did not differ significantly between the two groups of patients during the study. Quality of life was improved in all r-HuEPO-treated patients but not in those in the placebo group. This study demonstrates the safety and efficacy of r-HuEPO in the correction of anemia in predialysis patients without adverse effects on renal function over a 12-week period. Improved patient well-being as a result of the correction of anemia resulted in one patient refusing appropriate initiation of dialysis therapy.
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PMID:The use of recombinant human erythropoietin in the correction of anemia in predialysis patients and its effect on renal function: a double-blind, placebo-controlled trial. 268 5

rEPO therapy provides a unique opportunity to correct anemia in end-stage renal failure patients. Complete correction of the anemia, although possible, has some obvious disadvantages over a partial correction with a target hemoglobin of 10-13 g/dl or a hematocrit of 30-35%, respectively. Unresponsiveness to rEPO seems to be rare; in most cases the predicted hemoglobin increase could be seen as soon as an underlying iron deficiency was treated adequately. Blood loss and aluminum toxicity are the next most frequent reasons for an inadequate response to rEPO. Hypertension (and its complications) as well as fistula clotting are the most important side-effects which require close attention when patients at risk for these complications are treated with rEPO.
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PMID:Recombinant human erythropoietin in nephrology. 269 56

The authors studied 35 marrow biopsies from 32 patients with rheumatoid arthritis, systemic lupus erythematosus, mixed connective tissue disease, polymyositis, and psoriatic arthritis. Reasons for biopsy included cytopenia, fever of unknown origin, and malignancy. Cellularity was abnormal in 71%. Plasma cells were increased in 60% and associated with lymphoid aggregates. Immunoperoxidase stains showed polyclonal perivascular plasma cells and increased T-cells forming lymphoid aggregates. Two patients had granulomas without documented infection. Anemic patients had findings consistent with anemia of chronic disease, erythroid aplasia, hemolysis, and iron deficiency. Iron stores were variable. Platelet and granulocyte precursors were variably altered and did not predictably correlate with the presence, absence, or cause of thrombocytopenia and neutropenia. Myelodysplastic syndromes were present in two patients with rheumatoid arthritis. Osteomalacia and osteoporosis were seen, resulting from renal failure and steroids. Marrow findings are unpredictable and reflect the diverse causes of cytopenias in patients with connective tissue disorders.
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PMID:Bone marrow findings in connective tissue disease. 281 17


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