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

Considerable evidence suggests that insufficient EP production and the presence of a toxic factor inhibiting erythropoiesis are two major factors responsible for the production of anemia in patients with CRF. The toxic factor can be detected in a number of tissue culture systems. In order to evaluate its mechanism of action in a proliferation-dependent system, we studied the formation of erythroid colonies in plasma clots containing normal serum and CRF serum, using normal mouse marrow cells as the target organ. Fewer colonies were found in cultures containing uremic serum. This effect was greater as the concentration of serum was increased. No differences were found in the size or morphology of colonies formed. Addition of urea and creatinine to normal sera did not affect their ability to support colony growth. Uremic sera had no effect on white cell colony growth in the plasma clot system. We conclude that materials inhibitory to erythroid proliferation are present in CRF serum.
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PMID:The effect of serum from patients with chronic renal failure on erythroid colony growth in vitro. 68 22

Recent studies showed that the blood BFU-E, when subtracted from the uremic milieu, normally responds to the stimulating factor produced by T lymphocytes. The serum of uremic patients inhibits the in vitro growth of normal BFU-E, however, the inhibition is almost completely reversed by hemodialysis. These data allow to understand why the therapy with erythropoietin relieves the anemia of CRF. Uremic T lymphocytes fail to stimulate the BFU-E growth. Normal T lymphocytes are inhibited by uremic serum and the hemodialysis does not correct the defect. Lymphopenia, decreased number of both T4 and T8 lymphocytes and low T4/T8 ratio were found in 50% of patients. Cimetidine was still able to increase the burst-stimulating activity of uremic T lymphocytes through inhibition of the suppressor T subset. In conclusion, one can say that in CRF T8 lymphocytes are normal and that uremic toxins decrease both number and function of T4 lymphocytes. The deficiency of BPA appears to significantly contribute to the pathogenesis of the anemia of CRF. The experience from our and other Institutions shows the effectiveness of the recombinant human erythropoietin in relieving the anemia of CRF, notwithstanding the hematological milieu is highly modified by uremia.
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PMID:[Recent findings on the pathogenesis and therapy of anemia in chronic kidney failure]. 146 41

Anemia of CRF has been corrected by use of H-R-EPO both in hemodialysis and CAPD patients. Long term response to subcutaneous EPO and its relationship with serum EPO levels remain to be established. Twenty-five CAPD patients treated with CAPD during 30 +/- 28 (mean +/- SD) months were included in this study. The follow-up period was 6-24 months. All patients have been on CAPD at least 6 months and their Hemoglobin (Hb) level was lower than 8.5 g/dl. Twelve patients received EPO by subcutaneous route, at doses of 20 u./Kg daily and 13 other patients at doses of 2000 units twice a week. Thereafter, these doses were adjusted to obtain a Hemoglobin level ranging 10.5-13 g/dl. In conclusion, our results suggest that the subcutaneous route for H-R-Erythropoietin can be considered as the best choice for CAPD patients. Low doses twice a week seem to improve anemia in 2 months. Later, dose adjustment should be done according to the patient's response. The improvement in nutritional status we observed suggests a new positive aspect for EPO therapy. Our data did not show changes in peritoneal function.
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PMID:Medium term response to H-R erythropoietin in CAPD patients: the influence of erythropoietin plasmatic levels and the effects on peritoneal transport capacity. 168 Apr 50

Recombinant human erythropoietin represents a potential therapeutic alternative to red blood cell transfusions in a number of pediatric anemias. It is effective in correcting anemia associated with chronic renal failure and may significantly reduce the morbidity associated with childhood CRF. Most exposures to allogeneic blood products in pediatrics for treatment of anemia with blood transfusions occur in neonatal intensive care units. If proven effective in treating anemia in premature babies, r-HuEPO will be responsible for a major reduction in the use of blood transfusions in clinical neonatology. Carefully designed, placebo-controlled clinical trials will be required to establish the role of r-HuEPO in anemia of prematurity. Recombinant human erythropoietin also may be useful to increase the amount of blood that can be collected before elective surgical procedures. Another potential indication is to raise the hematocrits of infants with large intracardiac shunts who develop congestive heart failure coincident with the developmental fall in hemoglobin concentration after birth. Finally, r-HuEPO may one day play a role in modifying the expression of globin genes and, thereby, ameliorate the course of sickle cell disease and beta thalassemia. Many questions surrounding the use of r-HuEPO in infancy and childhood are being addressed in ongoing clinical trials.
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PMID:Recombinant erythropoietin in pediatrics: a clinical perspective. 218 91

Many factors complicate the effort for a recommendation on individual vitamin requirements in CRF. On the basis of our present incomplete knowledge about the handling of vitamins in uremia, suggestions for appropriate supplementation only of water-soluble vitamins are given. Patients with advanced CRF without dialysis treatment should receive daily supplements of vitamin B6 (5 mg), ascorbic acid (70-100 mg), and the normal recommended daily allowance of the other water-soluble vitamins in addition to the vitamin intake from the diet. We give folic acid only in patients taking antifolate drugs or in combination with iron in iron deficiency state and anemia (1 tablet of Folicombin contains 0.5 mg folic acid and 0.4 g elemental iron). There is still a pressing need for more data on the vitamin status, on vitamin requirements, and on long-term effects of vitamin administration in CRF.
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PMID:Vitamin status in patients with chronic renal failure. 304 75

In summary, the anemia of CRF results from several interactive processes, chief among these inadequate Ep production relative to the degree of anemia. The anemia of renal failure can be regarded as an endocrine deficiency state, which is corrected by the specific replacement therapy. The advances of molecular biology have provided a biosynthetic Ep, a potent tool for correction and prevention of the anemia of renal failure. However, new problems often arise as new treatments become available. The rapid improvement in hematocrit and the resultant lowering in plasma volume may affect dialysis clearances in hemodialysis patients. Since the well-being and appetite of the patients improves as the hematocrit rises, newer methods to increase the weekly dialysis clearances will be needed to prevent the complication of underdialysis in these patients.
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PMID:Pathogenesis of the anemia of chronic renal failure: the role of erythropoietin. 305 63

The paper is concerned with the efficacy of plasmapheresis with regard to red blood values in CRF patients on hemodialysis therapy. The probable mechanisms of this positive effect are discussed. Correlation between a degree of expression of the DIC-syndrome and anemia severity is demonstrated. An original method for reducing loss of blood in the dialyzer has been proposed.
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PMID:[Problems in the treatment of the anemic syndrome in patients with chronic kidney failure]. 376 67

The cardiac abnormalities that complicate chronic renal failure and renal replacement therapy are not well characterized in young people. These abnormalities are becoming more important because successful renal transplantation has resulted in children with end-stage renal failure living longer. Echocardiographic abnormalities of cardiac function and structure were studied in children and young adults (< 27 years old) with chronic renal failure (CRF, N = 32), end-stage renal failure treated with chronic peritoneal dialysis (CPD, N = 10) or renal transplantation (N = 30) or controls (N = 60). Left ventricular mass indexed for height (LVM/Ht and LVM/Ht2.7) and body surface area (LVM/SA), fractional shortening, measurement of left ventricular diastolic function (peak E and A wave velocities and the EA ratio) and structural (such as valvular) abnormalities were determined by echocardiography. The median (and range) of LVM/Ht in the groups were control 51.8 (23.1 to 119.8), CRF 60.2 (22.2 to 135.8), CPD 80.2 (14.5 to 100.9) and transplant group 97.8 (51.2 to 182.1) g/m. The increases in LVM/Ht, LVM/Ht2.7 and LVM/SA in the transplant group were significant (P < 0.01). The CRF group had significantly increased LVM/Ht2.7 and LVM/SA (P < 0.01). Systolic function was not significantly different between the groups. A significant correlation between creatinine and LVM indexed for height was found in the CRF group. Systolic or diastolic blood pressure could not be correlated with LVM indices in the transplant group. Changes in diastolic function were found (increased peak A wave velocity and decreased E/A ratios in the CRF and CPD groups, and increased peak E wave velocity in the transplant group). The study demonstrated that left ventricular hypertrophy is a frequent and often severe finding in children with chronic renal failure and those treated with renal replacement therapy. Factors other than hypertension and anaemia are important, and evidence was found for a link between serum creatinine and increased left ventricular mass prior to end-stage renal failure.
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PMID:Left ventricular abnormalities in children, adolescents and young adults with renal disease. 887 76

As with spontaneous growth, the height gain achieved by stimulation with recombinant human growth hormone (rhGH) in children with chronic renal failure appears to be inversely related to the degree of renal dysfunction. The secondary complications of CRF that may independently interfere with growth, such as metabolic acidosis, anaemia, and secondary hyperparathyroidism, do not explain the poorer response to rhGH in children with end-stage renal failure. Certain abnormalities of the somatotropic hormone axis, the severity of which is related to the degree of renal dysfunction, are more likely to explain the dependence of the rhGH treatment response on glomerular filtration rate. These derangements include partial GH receptor deficiency, increased plasma binding of IGF-I, and accumulation of non-competitive inhibitors of IGF-I action. Strategies to optimise growth-promoting treatment in end-stage renal failure will depend on the relative contribution of these different somatotropic hormone axis alterations to uraemia.
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PMID:Pathogenic mechanisms underlying the variable response to recombinant human growth hormone in children with chronic renal failure. 899 24

VLDL receptor (VLDL-R) is a novel member of the LDL receptor gene family with distinct tissue distribution and function. It binds and internalizes VLDL particles and is primarily expressed in skeletal muscle, heart, brain and adipose tissue, which use fatty acids for energy production or storage. CRF is associated with elevated serum triglyceride and VLDL concentrations and depressed VLDL and chylomicron clearance. We have recently shown marked down-regulation of lipoprotein lipase expression in CRF. This study was conducted to test the hypothesis that VLDL-R expression may be similarly depressed in CRF. To this end, VLDL-R mRNA (Northern blot) and protein mass (Western blot) of skeletal muscle (soleus) and heart were measured in male Sprague-Dawley rats six weeks after 5/6 nephrectomy (CRF group) or sham operation (NL group). A group of erythropoietin (EPO)-treated (150 U/kg twice weekly) CRF animals was included to determine the possible effect of EPO-deficiency anemia (EPO-CRF group). Subgroups of animals were studied at weeks 1, 3 and 6. The CRF group showed a fivefold increase in plasma triglyceride concentration. This was associated with an impressive fourfold reduction in heart and skeletal muscle VLDL-R mRNA and protein mass. VLDL-R mRNA levels in the heart and skeletal muscle were directly related to creatinine clearance and inversely related to serum triglyceride and VLDL concentrations. EPO therapy led to a mild improvement in CRF hypertriglyceridemia but failed to improve VLDL-R expression. Thus, the rise in plasma triglyceride and VLDL concentrations in CRF animals was associated with marked down-regulation of VLDL-R expression. Down-regulation of VLDL-R expression, shown here for the first time, reveals another facet of disturbed lipid metabolism in CRF.
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PMID:Down-regulation of VLDL receptor expression in chronic experimental renal failure. 906 30


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