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Query: UMLS:C0035078 (renal failure)
 31,970 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

A review is given of clinical studies performed by use of a highly sensitive in-vitro erythropoietin assay (fetal mouse livercell culture) in large patients' populations to clarify the controversial role of erythropoietin deficiency in the pathogenesis of renal anemia. Studies involved a.) patients with chronic renal disease and varying degree of renal insufficiency in the predialysis phase b.) non-nephrectomized and anephric patients on regular hemodialysis treatment. The data available demonstrate that the initial phase of renal anemia is accompanied by a compensatory increase of serumerythropoietin concentration and therefore erythropoietin deficiency has to be excluded as a primary cause of the anemia of renal failure; merely a relative lack of erythropoietin seems to exist. In the terminal phase of renal failure, erythropoietin deficiency becomes absolute, such in 50% of the investigated non-nephrectomized hemodialysis patients and in all anephric patients. However in individual patients even in terminal renal failure a sustained regulatory feedback mechanism between serumerythropoietin concentration and hematocrit, probably working at lower hematocrit level, could be demonstrated.
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PMID:[Role of erythropoietin deficiency in the pathogenesis of renal anemia]. 39 76

The anemia of chronic renal disease has been attributed primarily to a decrease in erythropoietin (EP) production. Results of this study show that measurable levels of plasma EP can be demonstrated in a majority of patients with end-stage renal failure who are undergoing long-term hemodialysis. These levels were not related to the type of renal disease, nor were they greatly affected by androgenic therapy or by nephrectomy. Although EP elevations in such patients were somewhat less than in nonuremic patients with comparable anemia, the presence of measurable EP levels suggests that impaired end-organ response may play a role in the anemia of chronic renal failure.
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PMID:Plasma erythropoietin levels in patients undergoing long-term hemodialysis. 57 68

In a longitudinal study the individual values of serum erythropoietin (SEp) in end-stage renal failure were investigated in 15 patients. SEp was determined by use of the foetal mouse liver cell assay on three occasions: (A) 2--6 months before the onset of RDT, (B) on day of first dialysis, and (C) 2--6 months following the onset of RDT. In every patient SEp increased from (A) to (B), and decreased again from (B) to (C). Changes of haematocrit were exactly opposite to changes of SEp. The results demonstrate that even in the terminal stage of chronic renal failure erythropoietin production is stimulated or suppressed in response to variations in the degree of anaemia.
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PMID:Sustained negative feedback between haematocrit and serum erythropoietin concentration in end-stage renal failure. 74 Jun 77

Pure red cell aplasia is a selective aplasia of the marrow erythroid cells. Unlike aplastic anemia, the marrow has a normal cellularity and the patients generally have normal leukocyte and platelet blood counts. The congenital form of the disease occurs in the firlst 1 1/2 years of life and is often responsive to corticosteroids. The acquired form may be secondary to infections, drugs, chemicals, or hemolytic anemia (aplastic crisis). In these cases it is often acute and self-limited with cessation of the infection or drug ingestion. It may also be secondary to systemic lupus erythematosus, rheumatoid arthritis, acute severe renal failure, severe nutritional deficiency, or diverse neoplasms, and may remit with treatment of the primary condition. When a thymoma is present, it should be resected since a remission is produced in 29 per cent of these patients. The remaining patients have an acquired primary form of the disease that tends to be chronic and in some cases may have an immune pathogenesis. A cytotoxic immunoglobulin inhibitor of the marrow erythroid cells or erythropoietin has been described and these patients may respond to prednisone and/or to cytotoxic immunosuppressive drugs such as cyclophosphamide and 6-mercaptopurine. Pure red cell aplasia appears to be more common than the literature has revealed and has stimulated much investigation into an immune pathogenesis for marrow failure.
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PMID:Diagnosis and treatment of pure red cell aplasia. 78 16

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

Erythropoietin activity in serum was measured using 59Fe incorporation into erythrocytes in protein-starved, hypoxic mice. The activity in serum from 20 patients with untreated myelomatosis was not significantly different from that in 31 saline controls. Only three patients had detectable erythropoietin levels in serum: 0.24 IU/ml, 0.27 IU/ml and 0.50 IU/ml (standard B), respectively. The venous haematocrit was correlated positively with the glomerular filtration rate as measured by 51Cr EDTA-clearance. No correlation could be established between venous haematocrit and serum albumin or serum transferrin. The results are in agreement with the assumption of a defective erythropoietin activity due to renal failure in myelomatosis.
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PMID:Serum erythropoietin in myelomatosis. 88 35

The diminished erythropoiesis in the anemia of chronic renal disease has been attributed to three possible factors: (1) decreased erythropoietin production, (2) inhibition of erythropoietin activity, and (3) decreased bone marrow response to erythropoietin. In this report we isolated and evaluated these parameters in 19 patients with chronic renal disease, nine patients with iron-deficiency anemia, and seven control subjects. The results in patients with chronic renal failure were as follows: (1) erythropoietin enhanced heme synthesis in bone marrow cell cultures by 88 +/- 12 per cent in renal failure, as compared to 65 +/- 7 per cent in the control group; (2) plasma erythropoietin activity did not increase appropriately for the degree of anemia; and (3) erythropoietin inhibitor activity in renal failure was not greater than in a control group. In conclusion, the relative failure of erythropoiesis in chronic renal disease appears to be due primarily to decreased production of erythropoietin and not to diminished marrow response to erythropoietin.
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PMID:Erythropoiesis in chronic renal disease. 96 7

The effect of renal failure and bilateral nephrectomy on erythropoiesis and plasma erythropoietic activity was observed in a patient with polycythemia vera. For eight years the patient's hematocrit was maintained between 45 and 50 per cent by phlebotomy and in spite of the development of renal failure the hematocrit did not decline. Following rejection of a renal transplant, the hematocrit fell to 18 per cent but rose to 40 per cent with oral iron therapy. Following bilateral nephrectomy, the hematocrit fell to 29 per cent but subsequently increased to 37 per cent. After an episode of gastrointestinal bleeding the hematocrit was 21 per cent but subsequently rose to 32 per cent. Erythropoietin could not be detected in the plasma either before or after nephrectomy. In addition, erythropoietin failed to stimulate 59Fe incorporation into heme in vitro in the patient's marrow cells. The data incidate that, in polycythemia vera, erythropoiesis does not require erythropoietin.
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PMID:Polycythemia vera in an anephric man. 101 15

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


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