Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recombinant human erythropoietin 50 units/kg intravenous twice a week was given to 9 anemic patients and end stage renal disease (ESRD) who were undergoing dialysis at the Kidney Centre. Of the total, 8 required no transfusion since the initiation of therapy and their haematocrit increased to approximately 29% or more with the improvement in general condition, sense of well being and exercise tolerance. One patient showed an increase in serum creatinine and two iron deficiency during therapy. In all cases blood pressure remained adequately controlled. No organ dysfunction or any other complication was observed.
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PMID:Experience of erythropoietin in anemia of end stage renal disease. 177 May 62

10 anemic (HB less than 9.0 g/dl) predialysis patients with chronic renal failure were treated for three months with s.c. administration of r-Epo. Blood morphological parameters were estimated using hematological autoanalyser Technicon H1. An increase of the mean hemoglobin (Hb) level from 8.39 to 10.57 g/dl was observed. In 8 patients Hb concentration after 3 months therapy ranged from 9.4 to 12.7 g/dl, but in the remaining two of them Hb was lower than 9.0 g/dl. Appearance of a high percentage of hypochromic erythrocytes is probably the most characteristic response to r-Epo treatment. This phenomenon was caused by iron deficiency. A significant increase of serum creatinine and BUN levels were observed in treated patients, without the concomitant decrease of endogenous creatinine clearance. No clinical symptoms suggesting deterioration of the renal function were observed. Subcutaneous therapy with r-Epo appeared an effective and convenient method of treatment of anemia in predialysis patients.
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PMID:[Subcutaneous administration of recombinant human erythropoietin (R-EPO) in the treatment of anemia in predialysis patients with chronic renal failure]. 189 96

To assess the effects of iron therapy on platelet monoamine oxidase (MAO) activity and urinary excretion of total metanephrines (MN) in infants and young children with iron deficiency anemia, 24 subjects were tested before and after one month of oral iron treatment. Thirteen healthy children comprised the control group. In the control group, platelet MAO level was 0.21 +/- 0.02 U/mg protein (mean +/- SE), urinary total metanephrine was 2.51 +/- 0.47 micrograms/mg creatinine. In cases with iron deficiency, mean platelet MAO level was 47.6% lower (p less than 0.005) whereas mean urinary metanephrine plus normetanephrine (MN-NMN) was only 20.7% lower (p greater than 0.05) than the control values. After one month, the anemic patients receiving oral iron therapy showed a significant increase in hemoglobin concentration, per cent transferrin saturation and platelet MAO activity (p less than 0.05). However, urinary metanephrine excretion was found to be lower in this group when compared to the metanephrine levels in iron deficiency before the medication (p less than 0.05). Although hemoglobin and transferrin saturation did not return to normal levels, these findings suggested that platelet MAO activity increased and urinary excretion of metanephrines decreased after iron medication.
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PMID:Iron deficiency anemia and catecholamine metabolism. 205 11

A group of 50 patients (26 men and 24 women, mean age 50 +/- 19 years and range 21 to 67) on chronic hemodialysis (HD) and with basal levels of hemoglobin (Hb) less than or equal to 8 g/dl was treated with recombinant human erythropoietin (r-HuEpo) during 3 months. r-HuEpo was started at 50 U/kg I.V. 3 times a week, immediately after each session of HD, for 4 weeks, and this dose was increased in steps of 25 U/kg until a Hb level of 12 g/dl or a maximum dose of 100 U/kg were reached. Complete blood counts and biochemical profile were performed before the first dose of r-HuEpo and once weekly and monthly respectively during the period of treatment. In 8 patients the red-cell life span was studied with cromium 51 labelled erythrocytes just before and after treatment. One patient had a grand mal seizure and the r-HuEpo was discontinued. In 44 patients the mean hematocrit increased from 21.8% to 32.1% and in the other 5 there were no response because of iron deficiency. There were no changes in leucocytes and platelets counts and consistent decreases in iron and ferritin serum concentrations were observed despite oral supplementation of iron. In the 8 patients studied the shortened erythrocyte survival did not suffer any significant variation with r-HuEpo. Predialysis creatinine, urea and phosphorus blood levels increased significantly at 3th month of treatment but there was no increase in potassium. In 32.6% of previously normotensive and hypertensive patients an increase in blood pressure was founded. Thrombosis of arteriovenous fistulas and other severe clinical side effects were not observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of anemia in patients with chronic kidney insufficiency in hemodialysis with erythropoietin]. 222 Apr 24

Therapy with recombinant human erythropoietin (rHuEPO) can reverse anemia and improve the quality of life in anemic hemodialysis patients. However, therapy is costly and must be used efficiently. An initial rHuEPO dose less than 50 U/kg intravenously three times weekly may be adequate to achieve a hematocrit of 30-33% in many patients. Acquired iron deficiency is a common problem during rHuEPO therapy and must be prevented with oral and parenteral iron replacement to maintain the efficacy of rHuEPO. Patients should be monitored carefully for additional problems including: an increase in blood pressure; onset of seizures or headaches; increased blood potassium, phosphate, and creatinine concentrations; enhanced coagulability resulting in dialyzer and vascular access clotting; and myalgias with a 'flu-like' syndrome.
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PMID:Practical approach to initiation of recombinant human erythropoietin therapy and prevention and management of adverse effects. 226 Jun 19

Terminal renal dysfunction (TRD) was induced in 2 groups of dogs by partial surgical ablation of the kidney. Dogs of a control group and of 1 of the TRD groups were maintained on a diet containing normal phosphorus concentration, whereas dogs of the other TRD group were maintained on a low-phosphorus diet. Mild anemia developed in dogs of both TRD groups and could not be attributed to iron deficiency, increased erythrocyte concentration of 2,3-diphosphoglycerate, or absolute deficiency of erythropoietin (EP). Subsequently, all dogs were acutely depleted of approximately 25% of their blood volume. Erythropoietin concentration in dogs of the TRD groups was lower than that of controls, however, erythroid regenerative capacity was comparable with that of control dogs when plasma parathyroid hormone (PTH) concentration was lowered by reduced dietary intake of phosphorus. The PCV in dogs of the chronic TRD groups had a slight positive correlation with serum EP concentration, and a significant (P less than 0.05) negative correlation with plasma PTH and serum phosphorus and creatinine concentrations, using a correlation matrix. There was no longer a significant correlation between plasma PTH concentration and PCV after controlling for serum creatinine concentration by use of a multiple linear regression analysis. A significant (P less than 0.05) negative correlation also was observed between plasma PTH and serum EP concentrations, but not between serum EP and phosphorus or creatinine concentrations. Significance of the EP and PTH association was reduced when analyzed, using a multiple linear regression analysis that included serum creatinine values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of parathyroid hormone in the anemia of chronic terminal renal dysfunction in dogs. 261 21

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

Urinary and proximal tubular iron are increased after subtotal nephrectomy, and iron depletion has been shown to be beneficial in proteinuric models of chronic renal disease in rats. In this study, iron depletion by low iron pair-fed diet and periodic phlebotomy was induced for 6 months in rats with partial (5/6) nephrectomy, resulting in a reduction in hematocrit and serum iron in all iron-deficiency subgroups. Tubular iron, assessed by energy dispersive analysis and electron microscopy, was reduced in quantity but not number of iron-containing lysosomes only within 1 subgroup of severe iron deficiency (p < 0.05). There was no improvement in serial isotopic glomerular filtration rate measurements, urinary protein and transferrin excretion, tubular damage scores, serum creatinine, or measures of reactive oxygen species (ROS) generation. In a subgroup of rats with no supplementation of sulfhydryl amino acids (cysteine and methionine) which can act as ROS scavengers, iron deficiency increased urinary protein excretion (213.3 +/- 23.0 mg/24 h, mean +/- SEM, vs. 87.4 +/- 16.1, p < 0.001), urinary transferrin excretion (p < 0.05), kidney weight (p < 0.05) and tissue malondialdehyde, a lipid peroxidation product (0.78 +/- 0.16 nmol/mg protein vs. 0.57 +/- 0.19, p < 0.05), consistent with increased ROS generation. Hence, no beneficial effect of iron-deficiency was demonstrated by any measure of structure of function in the remnant kidney, and it may enhance damage if sulfhydryl repletion is not provided.
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PMID:Iron depletion in the remnant kidney. 747 24

The purpose of this study was to evaluate the sensitivity and specificity of laboratory methods in the diagnosis of posterythropoietin-era, iron-deficient, chronic renal failure patients. The patient population comprised 25 anemic (hemoglobin < 11 g/dL) patients with creatinine greater than 3 mg/dL; 20 were dialysis patients, two were transplant patients, and three patients had renal failure from other causes. Criteria for study inclusion were as follows: bone marrow iron was the reference standard and was graded 0 to +4, ranging from absent to diffuse homogeneous iron staining; serum ferritin concentration and serum transferrin saturation were tested in terms of sensitivity and specificity. The reference standard indicated that iron deficiency existed in 40% of patients. Neither serum ferritin nor transferrin saturation were completely adequate diagnostic tools. Serum ferritin levels less than 200 ng/dL were 100% specific for the diagnosis but only 41% sensitive. Transferrin saturation of less than 20% was 88% sensitive, but only 63% specific. By excluding patients with hypoproteinemia (transferrin values of < 150 mg/dL), the sensitivity of the test increased to 100% and the specificity to 80%. We conclude that transferrin saturation is an adequate screening tool in anemic chronic renal failure patients, provided that hypoproteinemia is not present. By determining both the serum ferritin concentration and the transferrin saturation, a high sensitivity and specificity can be achieved, even in patients with hypoproteinemia. Furthermore, we believe that on this basis, iron therapy in patients with renal insufficiency can be improved.
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PMID:Diagnosis of iron deficiency anemia in renal failure patients during the post-erythropoietin era. 862 43

To evaluate the role of erythropoietin (Epo) in the erythroid abnormalities often found in athletes, Epo was evaluated by radioimmunoassay in endurance runners (ER). In a first study, 46 experienced ER, 11 with iron deficiency (ID group), were studied during a training period. In ID and non-ID runners, serum Epo (SEpo) levels were similar to sedentary controls (ID = 19.1 +/- 4.9 U/L, non-ID = 19.7 +/- 5.5 U/L and controls 19.7 +/- 9.2 U/L). In a second study, serum and urine erythropoietin (UEpo) levels were evaluated in 17 ER during a 6-hour race. Samples were taken before the race (pre-race), immediately following (6-hour) and 4 days after (post-race). No differences were observed in SEpo levels (pre-race = 19.8 +/- 4.1 U/L, 6-hour = 21.2 +/- 4.9 U/L and post-race = 21 +/- 4 U/L), but UEpo increased following the race (pre-race = 15.4 +/- 9.6 U/L, 6-hour = 26.1 +/- 6.2 U/L and post-race = 14.1 +/- 6.5 U/L) (p < 0.0001) and this UEpo increase was related to urine creatinine changes (rs = 0.79, p < 0.00001). In conclusion, SEpo in ER does not differ from sedentary values and does not vary with competition; however, UEpo increases during a long-distance race. These data may be important for a correct evaluation of Epo abusers and sports anemia.
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PMID:Evaluation of erythropoietin in endurance runners. 780 89


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