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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma levels of erythropoietin (EPO) were estimated in 14 patients with noninflammatory acute renal failure during the oliguric anuric and polyuric phase respectively. During the anuric oliguric phase plasma EPO levels were 4 times higher than in healthy subjects, while during the polyuric phase normal plasma levels were found in spite of the presence of anaemia. Results presented in this paper suggest presence of an abnormal feedback between EPO secretion and degree of anaemia in patients with acute noninflammatory renal failure both during the anuric/oliguric and polyuric phase respectively. Abnormal EPO secretion does not seem to be the only or even dominant factor involved in the pathogenesis of anaemia in patients with noninflammatory acute renal failure.
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PMID:[Plasma erythropoietin levels in patients with noninflammatory acute renal failure]. 189 1

In order to investigate the clinical usage of SNB-5001 (recombinant human erythropoietin), two types of anemic models induced by drugs were prepared. One group of rats was intravenously injected with 8 mg/kg of cisplatin. These rats temporarily showed leucopenia and thrombocytopenia. Since 2 weeks after the cisplatin injection, rats chronically showed renal failure and moderate anemia. Another group was subcutaneously injected with 15 mg/kg of puromycin, 4 times a week, for 3 weeks. These rats showed hypercholesteremia and hypoalbuminemia, and they showed chronic renal failure and severe progressive anemia. Anemic rats received SNB-5001 (50 or 500 U/kg) once a day for 7 days. In the anemic rats induced by cisplatin, more than 50 U/kg of SNB-5001 dose-dependently increased reticulocytes, red blood cells (RBC), hemoglobin (HGB) and hematocrits (HCT). SNB-5001 apparently improved the anemia induced by cisplatin. On the other hand, in anemic rats induced by puromycin, 50 U/kg of SNB-5001 increased reticulocytes, but did not increase RBC, HGB and HCT. SNB-5001 at the dose of 500 U/kg stopped the progress of anemia in puromycin treated rats. It was suggested that SNB-5001 is useful for the improvement of renal anemia induced by drugs, but the effects are affected by the uremic condition and the stage of renal anemia.
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PMID:[Effects of recombinant human erythropoietin (SNB-5001) on renal anemic rats induced by drugs]. 191 43

To investigate the possible effect of preeclampsia on erythropoietin metabolism, we measured plasma and urine erythropoietin concentrations and complete blood count in 19 women with preeclampsia and nine healthy gravidas. Hemoglobin concentration and hematocrit values in the preeclamptic patients did not differ significantly from those of the normal pregnant controls. However, the plasma erythropoietin concentration tended to be higher in the preeclamptic group than in the normal pregnant controls (26.9 +/- 31.2 versus 11.2 +/- 9.9 mU/mL), though the difference was not statistically significant. Plasma erythropoietin concentration correlated negatively with both hemoglobin concentration and hematocrit (r = -0.85, P less than .01). The pattern and magnitude of the erythropoietin response to anemia paralleled that previously reported in individuals with iron deficiency anemia. No significant correlation was found between urinary erythropoietin excretion and blood pressure, qualitative albumin excretion, hematocrit, hemoglobin concentration, or plasma erythropoietin concentration. Based on our results, the erythropoietin response to anemia appears to be intact in preeclampsia, at least in the absence of renal failure.
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PMID:Erythropoietin in preeclampsia. 192 99

Changes in exercise tolerance occurring after correction of anemia with recombinant human erythropoietin in a group of patients with end-stage renal failure were evaluated. Ten patients, aged 29 +/- 11 years, on chronic hemodialysis treatment, with no associated diseases, were evaluated by cardiopulmonary bicycle exercise testing and M-mode, 2-dimensional and pulsed doppler echocardiography before and after anemia correction. After 1 and 3 months of therapy, hemoglobin plasma levels increased from 5.9 +/- 1.2 to 7.7 +/- 1.3 and 9.9 +/- 1.4 g/dl, with a concomitant increase in peak oxygen consumption (VO2) from 21.4 +/- 4.3 to 24.4 +/- 4.3 and 26.6 +/- 4.6 ml/kg/min and of VO2 at the ventilatory threshold from 15.0 +/- 3.7 to 17.3 +/- 3.7 and 16.8 +/- 3.4 ml/kg/min. After 3 months of therapy, systolic blood pressure significantly decreased both at peak exercise (159 +/- 35 to 134 +/- 22 mm Hg) and ventilatory threshold (140 +/- 27 to 123 +/- 19 mm Hg), whereas cardiac index at rest decreased from 3.3 +/- 0.7 to 2.8 +/- 0.5 liters/min/m2 and heart rate from 77 +/- 12 to 70 +/- 10 beats/min. However, no significant relation was found between hemoglobin plasma levels and peak VO2, whereas a significant relation was found between hemoglobin concentration and cardiac index at rest.
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PMID:Improvement in exercise capacity after correction of anemia in patients with end-stage renal failure. 192 20

Recombinant human erythropoietin (epoetin) is a remarkably safe and effective biological product. Many dialysis patients are benefiting from the use of this drug when administered intravenously (IV) or subcutaneously (SC) three times a week. However, many patients are not receiving optimal therapy. Optimal therapy requires an understanding of the principles of effective usage and a definition of an optimal hematocrit (Hct) level. These therapeutic principles include (1) the erythroid response to epoetin is dose-dependent, but variable within a given dose; (2) the SC route of injection is as effective, if not more so, than IV injections; (3) the frequency of administration is route-dependent; (4) adequate iron stores are necessary for optimal response; (5) blood pressure may increase as the Hct increases, but may improve with time due to hemodynamic adjustments; (6) the anemia is primarily a hormone-deficiency state and not due to uremia; and (7) infections and traumatic (ie, surgical) inflammation may blunt the response to epoetin. Many patients with the anemia of renal failure have yet to benefit from treatment. These include patients with progressive renal failure or chronic transplant rejection, and dialysis patients who have had incomplete correction of their anemia.
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PMID:Erythropoietin 1991--an overview. 192 76

Mechanisms for the development of anemia and the effects of recombinant human erythropoietin (r-HuEPO) on hematological parameters were studied in new congenital adult type polycystic kidney (DBA/2FG-pcy) mice. The majority of DBA/2FG-pcy mice showed progressive anemia and an elevation of blood urea nitrogen, while a minority showed progressive anemia following polycythemia. Kidneys with numerous cysts in the cortex and medulla occupied virtually the entire abdominal cavity, and the combined kidney weight taken as a percentage of body weight reached 13.5% in the DBA/2FG-pcy mouse. The osmotic fragility of DBA/2FG-pcy mice erythrocytes was significantly increased compared with that of normal control mice. In addition, two-fold increases in serum EPO levels, determined by radioimmunoassay, and a decreased number of colony forming unit-erythroid (CFU-E) were observed in the DBA/2FG-pcy mice. The administration of r-HuEPO during anemia significantly increased the red blood cell count, hemoglobin concentration, hematocrit and reticulocyte percentage in a dose-dependent manner. These findings indicate that anemia in the DBA/2FG-pcy mouse is due to increased fragility of erythrocytes, a deficiency in EPO for the degree of anemia and a decreased number or a decreased response of erythroid progenitor cells. We suggest that the DBA/2FG-pcy mouse is a useful spontaneous model of chronic progressive renal failure.
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PMID:Anemia in new congenital adult type polycystic kidney mice. 194 61

Anemia (hematocrit less than 25%) predictably accompanies chronic renal failure and is present in over 90% of patients on chronic dialysis. Relative erythropoietin deficiency is the proximate cause. Recombinant human erythropoietin recently became available for research and clinical use. Erythropoietin production is regulated by a single copy gene located on chromosome 7; its expression has been shown in the kidney, liver, and macrophages. It is glycosylated protein of 166 amino acids with a molecular weight of 34,000 D. When given to patients with the anemia of renal failure, erythropoietin causes a dose-dependent rise in hematocrit to the normal range within 8 to 14 weeks. Complications of this response are minimal except for a significant incidence of hypertension. When the anemia is corrected, the patient's quality of life, cognitive function, and brain electrophysiology improve dramatically. Recombinant human erythropoietin represents a major breakthrough in the treatment of patients with chronic renal failure. Current reimbursement constraints limit its full application.
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PMID:Recombinant human erythropoietin and renal anemia: molecular biology, clinical efficacy, and nervous system effects. 202 6

The erythropoietic factors present in an anephric patient with nearly normal hematocrit were isolated from plasma by reversed-phase and gel permeation HPLC. The most active fraction was purified and the analysis of its N-terminal sequence was identical to the published sequence of the human insulin-like growth factor I (IGF I). Recombinant human IGF I had identical elution positions as the isolated erythropoietic factor on reversed-phase HPLC and the same molecular weight on gel permeation HPLC. Furthermore, hrIGF I stimulated erythroid colony formation in human bone marrow cultures as was previously shown for the isolated human erythropoietic factor. These results suggest that IGF I may replace erythropoietin as a stimulator of erythropoiesis in some patients with anemia and renal failure.
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PMID:The N-terminal sequence of the major erythropoietic factor of an anephric patient is identical to insulin-like growth factor I. 199 27

The development and widespread availability of recombinant products will effect blood centers through reduced product use, replacement of current products, and novel applications of new products. The greatest amount of clinical experience to date has dealt with the use of recombinant human erythropoietin (r-HuEPO) in the treatment of anemia in end-stage renal failure. Data also support its use in anemia associated with acquired immune deficiency syndrome (AIDS), cancer, and chronic inflammatory diseases. This article will focus on the effect of erythropoietin on the demand for erythrocyte use.
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PMID:Cytokine biology. Implications for transfusion medicine. 201 73

Six patients with acute renal failure, in five cases due to acute crescentic glomerulonephritis and in one case due to total bilateral renal cortical necrosis, were studied. All had serum erythropoietin (EPO) concentrations in the normal range, despite a relatively severe anaemia. Half-life and plasma clearance of intravenously injected recombinant human erythropoietin (rhEPO) were determined. The results indicate that the lack of compensatory increase in serum EPO to the anaemic stimulus is not due to increased catabolism, but to decreased synthesis of the renal hormone. Two patients were treated with rhEPO (Eprex). In marked contrast to untreated controls, both patients responded with vigorous reticulocytosis and normalization of haemoglobin levels while they were still in severe renal failure. These results are similar to our previous findings in patients with acute renal failure due to tubular necrosis. Under all three conditions the defective EPO synthesis is probably the dominant pathogenetic factor for the largely aregeneratory anaemia of prolonged cases, and for the sluggish restoration of red cell mass during recovery of renal function. It is concluded that defective synthesis of EPO is not only a permanent and irreversible feature of severe chronic renal failure, but that it is also present, usually in a transient and reversible form, in different types of acute renal failure.
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PMID:Erythropoietin deficiency in acute crescentic glomerulonephritis and in total bilateral renal cortical necrosis. 202 90


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