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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In vitro culture technique of bone marrow cells has been applied to study the cause of anemia in uraemic patients on maintenance haemodialysis. Incorporation of 59Fe into haem in bone marrow cells of the patients in the presence of erythropoietin, as well as the inhibitory effect of their plasma on the response of normal bone marrow cells to erythropoietin, was examined. Increase in haem synthesis rate by erythropoietin in the bone marrow cells of uraemic patients (n 14; 7.9 +/- 1.4) wasnot significantly different from that in normal bone marrow cells (n 9; 5.9 +/- 1.4,p greater than 0.05), thus indicating the presence of erythroid precursor cells with normal responsiveness to erythropoetin in uraemic patients. All the plasma from uraemic patients inhibited, in dose-dependent way, the response of normal bone marrow cells to erythropoietin. Levels of erythropoietin in the plasma samples of uraemic patients were much lower than those of the patients with iron deficiency anaemia with comparable Hb concentrations. On the basis of these results, the humoral inhibitory factor appears to play a significant role in the pathogenesis of renal anaemia, in addition to the low level of circulating erythropoietin.
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PMID:Response of uraemic bone marrow cells to erythropoietin in vitro. 100 62

1. The present studies have demonstrated that the titers of erythropoietin may be elevated to varying degrees in patients with anemia associated with end-stage renal disease. However, the increase in erythropoietin titers was apparently not sufficient to meet the increase in demand for new red blood cells created by their shortened life span and the inhibitors of heme synthesis and/or erythroid colony forming cells (CFU-E). 2. Inhibitors of heme synthesis were demonstrated in the plasma of some but not all patients with anemia associated with renal disease and in rabbits 72 hrs following bilateral nephrectomy. 3. CFU-E were both increased and decreased in the bone marrows of the chronic anemic uremic rabbits, when compared with that of sham operated controls, 14 and 21 days after 5/6th nephrectomy and depended on the rate of regeneration of the renal erythropoietic and excretory functions. CFU-E in marrows of 5/6th nephrectomy rabbits were decreased after 35 days. 4. An inhibitor of CFU-E was increased in the sera from chronic anemic uremic rabbits, when compared with that of the sham-operated controls, 35 days after 5/6th nephrectomy. 5. It is possible that in the anemia of uremia in addition to inadequate production of erythropoietin there is a defect in the differentiation of the CFU-E into the heme synthesizing erythroid series due to the presence of a specific inhibitor of CFU-E and/or heme synthesis.
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PMID:Studies on the mechanism of the anemia of renal insufficiency. 102 87

Erythropoietic activity produced by exogenous erythropoietin (Ep) is markedly reduced in Swiss mice rendered uremic by bilateral nephrectomy or bilateral ureteral ligation. Exogenous Ep causes a greater increase in erythropoiesis in germfree Swiss mice as compared with non-germfree mice, but the germfree mice show a more drastic reduction of erythropoiesis in uremia. Heme production in blood, spleen, and femoral marrow retains its typical pattern in uremia; there is no shift of erythropoiesis among the three sites. Production of endogenous Ep in uremic mice is less by a factor of 2-3 than that in intact mice whereas the reduction is by a factor of almost 100 in anephric mice. The data suggest that the anemia associated with uremia is the result of two phenomena: (1) a decreased production of Ep and (2) a diminished erythropoietic response to Ep.
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PMID:Erythropoietin activity in acutely uremic mice. 105 20

Erythroid colonies were grown in vitro in plasma clot cultures. Normal adult rat bone marrow responded to exogenous erythropoietin with the formation of an average of 2 colonies/10(3) cells plated. No erythroid colonies were observed in cultured normal spleen preparations. Shay chloro-leukemia cells administered iv induced an acute myelogenous leukemia. During the progressive stages of the disease, the numbers of erythrocyte colony forming units (CFU-E) in the marrow decreased; concomitantly, these progenitors appeared in leukemic spleen cultures. Paralleling changes in CFU-E, the numbers of nucleated red blood cells in the marrow declined but increased in the leukemic spleen. However, compensatory spleen erythropoiesis was transient, due to continued leukemia cell colonization. The loss of erythroid progenitor cells from the bone marrow played a significant role in the anemia associated with this leukemia.
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PMID:In vitro erythroid colony formation in acute myelogenous leukemia in the rat. 106 27

Erythropoietin level in the serum and urine of adult patients with acute leukaemia (AML, ALL, MML) was estimated by polycythaemic mouse bioassay in order to obtain more information about the associated anaemia. In AML and ALL patients the serum erythropoietin level as found to be increased and in a negative correlation with the blood haemoglobin concentration. In ALL patients erythropoietin in urine was increased regularly while in AML patients it was not. No correlation between the serum level and the urinary excretion of ESF, or between the blood Hb and the serum ESF, was found in MML patients. The results show that anaemia in leukaemia is not due to the low ESF level.
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PMID:Erythropoietin level in patients with acute leukaemia. 107 11

The widespread and ever expanding use of dialysis in the maintenance of patients with chronic renal disease has added an urgency to the study of the biogenesis of erythropoietin. It seems almost certain that erythropoietin could ameliorate, if not eliminate, the anemia of uremia, but unfortunately, erythropoietin is still not available in therapeutic quantities. Initially, erythropietin was though to be produced by the kidneys" but then the attention became directed at the liver. It was proposed that erythropoietin was produced there as an inactive precursor and that the kidney only acted as an oxygen sensor and as a producer of an erythropoietin-activating enzyme. Recent studies summarized here show that an isolated perfused kidney in the absence of any extrarenal substrate or precursor can synthesize erythropoietin. Consequently, it appears almost certain that the kidney is the endocrine organ of origin of erythropoietin. Further studies suggest that erythropoietin formation involves a phase of oxygen sensing and programming and a phase of synthesis. These phases probably occur in the same cell, and the renal cortex appears to be the most likely location for such cells. The current inability to extract erythropoietin from kidney homogenates is discussed but, unfortunately, not adequately explained.
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PMID:Renal biogenesis of erythropoietin. 109 Jan 49

Anemia is a frequent complication of renal failure. As in anemias of other origin, the resulting tissular hypoxia is partially compensated by an increased production of 2,3-diphosphoglycerate in red cells and a shift to the right of the oxygen hemoglobin dissociation curve. Two mechanisms are implicated in this anemia: increased hemolysis and depressed production of red cells. Decreased production of erythropoietin is probably the cause of reduced erythropoiesis, but the role of uremic intoxication has not been unequivocally excluded. In the course of chronic hemodialysis, iron deficiency anemia and occasionally hypersplenism develop. It is noteworthy that blood requirements in anephric patients are two to three times greater than those of nonanephric hemodialyzed patients. Accordingly, bilateral nephrectomy should be restricted to carefully selected cases. At the present time, androgens seem to be the best treatment of renal anemia. Qualitative anomalies of platelets are the main factor responsible for uremic bleeding and are corrected by hemodialysis.
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PMID:Hematologic disorders in renal failure. 109 56

Urinary erythropoietin was determined sequentially in four premature infants throughout their period of physiologic anemia. After the first day of life, no erythropoietin was found, even though there was a marked fall in hematocrit. Among seven premature infants with severe respiratory disease, three excreted elevated amounts of erythropoietin. Premature infants appear able to respond to hypoxia by increasing erythropoietin production. In the absence of hypoxia, however, diminution of erythropoiesis in the early weeks of life is not accompanied by elevated excretion of erythropoietin.
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PMID:Erythropoietin excretion in the premature infant. 111 82

Two experimental models for pure red cell aplasia (PRCA) were established. In the first one, administration of PRCA serum IgG in normal mice induced a sustained inhibitory effect on erythropoiesis, a progressive decline of the hematocrit values and an inverse rise of erythropoietin (Ep) levels in serum. Thus, the physiopathological pattern of PRCA type I (or A) was established, In the second model a rabbit producing anti-Ep crossreacting with endogenous Ep was subjected to a booster injection of Ep. The rise of the immune response was associated with decrease of Gct values and disappearance of erythroid precursors from marrow smears, and its subsequent decline with reticulocytosis and regression of the anemia, thus reproducing the physiopathological pattern of PRCA type II (or B).
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PMID:[Demonstration of 2 experimental models of pure chronic erythroblastopenia]. 111 20

Adult SI/SI-d mutant mice have severe macrocytic, normochromic anemia. Moreover these animals are unresponsive to the stimulation of erythropoietin in vivo. By means of a bone marrow cell suspension culture system, the present investigation shows that in adult SI/SI-d marrow, there are cells capable of responding in vitro to erythropoietin in a normal fashion. Moreover, the erythropoietin present in SI/SI-d serum is biologically active in vitro without any prior biochemical modification. These observations support the suggestion that there is a defect in differentiation in the erythroid cell lines of SI/SI-d mice in vivo due to an abnormal hemopoietic microenvironment.
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PMID:Erythropoiesis in steel mutant mice: effects of erythropoietin in vitro. 111 37


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