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

We studied the significance of free erythrocyte protoporphyrin (FEP) in relation to iron status, aluminum levels and anemia in uremic patients on chronic dialysis. All but 1 patient showed high FEP values closely related to the degree of anemia. Increased FEP levels are due to a defective heme synthesis, not related to iron deficiency or aluminum overload. Treatment of anemia with recombinant human erythropoietin reduced FEP values. We therefore hypothesize that recombinant human erythropoietin ameliorates an enzymatic defect in heme synthesis.
Nephron 1992
PMID:Recombinant human erythropoietin reduces free erythrocyte protoporphyrin levels in patients on chronic dialysis. 152 41

To evaluate the influence of body iron stores on the serum aluminum (Al) level, we studied the correlation between iron status (the serum ferritin, serum iron and transferrin saturation) and serum Al levels in 68 severely anemic hemodialysis patients. Among them, 36 underwent the desferrioxamine (DFO) mobilization test. These 68 patients were divided into three groups according to their serum ferritin level. The basal Al level in the patient group was 41.4 +/- 37.4 micrograms/l (control, 4.1 +/- 2.4 micrograms/l). The serum Al level after DFO infusion of the patient group was 111.1 +/- 86.8 micrograms/l. A significantly higher basal Al and peak Al level after DFO infusion were found in group 1 patients (serum ferritin less than 300 micrograms/l) when compared to group 2 (serum ferritin 300-1,000 micrograms/l) and group 3 (serum ferritin greater than 1,000 micrograms/l) patients. A significant negative correlation between serum ferritin and basal serum Al (r = -0.544, p = 0.0001), as well as peak serum Al after DFO infusion (r = -0.556, p = 0.0001), was noted. Similarly, a negative relationship between serum Al (both basal and peak) and either serum iron or transferrin saturation was noted. However, there was no correlation between the serum Al level and the dosage of aluminum hydroxide. In conclusion, serum ferritin, serum iron and transferrin saturation were inversely correlated with serum Al in our hemodialysis patients. Iron deficiency may probably increase Al accumulation in these patients.
Nephron 1992
PMID:Effect of body iron stores on serum aluminum level in hemodialysis patients. 163 May 39

The study was carried out in order to evaluate in maintenance hemodialysis (MH) patients: (1) the reliability of serum ferritin (SF) measurement in iron deficiency diagnosis and therapy; (2) the possibility to improve iron stores assessment through laboratory indexes routinely used in clinical practice; (3) the most effective iron deficiency treatment. After a preliminary assessment of SF reference values in 250 healthy volunteers, we studied 72 MH patients divided into three groups according to their SF baseline values: high (group A), normal (group B), low (group C) (normal range 19-191 ng/ml). Each group was further divided into three subgroups receiving three different iron treatments for 6 months: (1) oral administration of 67.5 mg/day of Fe3+ as Fe-ferritin (subgroups A1, B1, C1); (2) oral administration of 60 mg/day of Fe3+ as Fe-chondroitin sulfate (subgroups A2, B2, C2); (3) i.v. administration at the end of each dialytic session of 31 mg of Fe3+ as Fe-gluconate-Na (subgroups A3, B3, C3). The response to the iron therapy was considered positive when the hemoglobin (Hb) and the hematocrit (Ht) increased to greater than or equal to 15% of the baseline values. The rate of positive responses in each subgroup was as follows: A1 0/5, A2 0/5, A3 0/7, B1 2/10, B2 1/6, B3 5/11, C1 1/7, C2 3/7, C3 10/16. We concluded that SF values above 191 ng/ml allow to exclude iron deficiency whereas SF values less than or equal to the normal range are inadequate. In an attempt to improve diagnostic sensitivity we divided patients of subgroup B3 and C3 into responders (R) and nonresponders (NR).(ABSTRACT TRUNCATED AT 250 WORDS)
Nephron 1991
PMID:Iron deficiency in maintenance hemodialysis patients: assessment of diagnosis criteria and of three different iron treatments. 190 85

Serum ferritin (SF) and erythrocyte ferritin (EF) were evaluated in 35 patients on chronic hemodialysis treatment (CHD), in 45 healthy subjects and in 22 nonnephropathic females with iron deficiency anemia. Twenty-five CHD patients with basal SF less than 500 micrograms/l were treated orally with 200 mg of Fe2+ for 2 months and the positive (hemoglobin increase greater than 1 g/dl) or negative response to the therapy was correlated to the basal levels of SF and EF. Three groups of CHD patients could be defined on the basis of their basal SF levels (hypo-, normo- or hyperferritinemic). Nine patients with increased SF levels had also EF levels significantly higher than the other CHD patients and controls since they were probably iron-overloaded. In the other 2 groups of CHD patients, EF levels were significantly higher than in controls for each level of SF probably because of the reduced utilization of iron by uremic bone marrow. Among the 25 treated CHD patients, only 5 responded to the therapy: 3 were hypoferritinemic while the other 2 responders had basal SF within the normal range. Four hypoferritinemic patients did not respond to the therapy. Four out of five responders had the lowest EF levels among CHD patients. EF measurement could be an important and useful test in detecting the presence of an iron deficiency erythropoiesis in CHD patients.
Nephron 1990
PMID:Erythrocyte ferritin in patients on chronic hemodialysis treatment. 231 39

Several factors contribute to the pathogenesis of anemia due to renal failure. Hypoproliferation of red cell progenitors may be caused partially by an inhibitory effect of some 'uremic toxins' whose existence certainly is very controversial. Iron deficiency due to gastrointestinal and dialysis-related blood losses and occasionally aluminum intoxication may interfere with the maturation of the erythron. Moderate hemolysis with shortening of red cell survival to some 50% of normal may be an additional factor. The main cause of anemia is, however, inadequate production of erythropoietin by the diseased kidney. This latter factor has now become amenable to treatment.
Nephron 1989
PMID:[Pathogenesis of anemia due to kidney disease]. 264 77

The accurate radioimmunological measurement of serum erythropoietin (EPO) levels has only been possible since the development of highly specific antibodies directed against recombinant human EPO. In the present study, we determined the serum EPO levels in 100 healthy volunteers and in over 300 patients with anemias and hyperglobulinemia of various causes. In the healthy group, the females had levels of 11.3 +/- 3.4 mU/ml, while the males had levels of 8 +/- 3.2 mU/ml. The serum EPO concentrations were inversely related to the degree of anemia in patients with nonrenal anemias, while predialysis patients with renal anemias showed only partially such a tendency. Hemodialysis patients exhibited EPO-levels that were inadequately low relative to the degree of anemia. Patients with hyperglobulinemia had significantly higher serum EPO-levels than healthy individuals and polycythemia vera patients, the latter having particularly low serum EPO levels. Our results show that the determination of serum EPO levels can be of value in the differential diagnosis of hyperglobulinemia. Finally, sequential measurements document fluctuating serum EPO-levels after gastrointestinal hemorrhages and in patients with iron deficiency anemias receiving iron substitution. The probable reason for this phenomenon seems to be the intermittent utilisation of the hormone by EPO-sensitive erythropoietic precursor cells.
Nephron 1989
PMID:[Serum erythropoietin levels in several diseases]. 291 82

Norepinephrine turnover and energetic efficiency studies were conducted in three groups of male Sprague-Dawley rats placed on low iron diets for 5 weeks on weaning. Iron-deficient rats had significant anemia (hematocrit less than 20%) and growth retardation relative to pair-fed and ad libitum fed controls who received the same diet plus weekly iron dextran injections. Energetic efficiency over a 7-day period was nearly 30% less in anemic animals. This was associated with significantly higher rates of norepinephrine turnover in brown adipose tissue (110%) and heart (330%) with significant hypertrophy in both tissues. There was no difference in body composition in ad libitum groups. Plasma triiodothyronine and thyroxine were reduced by 37% in iron deficients compared to controls. Thus 39% increase in caloric requirements in iron deficiency is associated with increased sympathetic and perhaps thermogenic activity in brown adipocytes.
 ...
PMID:Feed efficiency and norepinephrine turnover in iron deficiency. 382 10

It appears well established that a microcytic, hypochromic anaemia is present in patients receiving regular haemodialysis treatment, who also suffer from chronic aluminium intoxication. This characteristic anaemia is slightly improved following deionization or reverse-osmosis treatment of dialysate water. Iron deficiency has been tentatively excluded as a cause of this anaemia by measurement of serum ferritin levels. The exact mechanisms involved in the pathogenesis of this anaemia are still to be fully elucidated but a disturbance in haem synthesis and porphyrin metabolism seems probable, and secondary effects of PTH in the bone marrow may be involved. Evidence has accumulated that aluminium is the most likely ion responsible for this anaemia but other ions, trace metals in excess or deficiency and potentially toxic substances cannot be excluded yet.
Nephron 1985
PMID:Aluminium-induced anaemia in haemodialysis patients. 396 84

The diagnostic usefulness of bone marrow hemosiderin, serum ferritin, transferrin saturation, mean corpuscular volume (MCV) and red cell protoporphyrin (EPP) in the evaluation of iron status in patients on chronic hemodialysis was studied in 39 subjects. The correlation between serum ferritin and the number of transfusions received per month was slightly higher (r = 0.717; p less than 0.001) than the correlation between bone marrow hemosiderin and transfusions (r = 0.685; p less than 0.01). Serum ferritin was useful in identifying subjects with both increased or reduced iron stores. In contrast, transferrin saturation could only be used for indicating iron overload. MCV for indicating iron deficiency, and EPP was not useful in either case. The abnormal increase of EPP in chronic uremia has not been previously described. It is unrelated to iron deficiency and is most probably explained by the known reduction in red cell ferrochelatase activity associated with chronic uremia. Serum ferritin is clearly the most useful diagnostic aid for assessing iron stores in patients on chronic hemodialysis. Whether ferritin is also the best predictor of response to iron therapy, cannot be determined on the basis of the present data.
Nephron 1983
PMID:Evaluation of iron status in patients on chronic hemodialysis: relative usefulness of bone marrow hemosiderin, serum ferritin, transferrin saturation, mean corpuscular volume and red cell protoporphyrin. 663 60

Various haematological, ferrokinetic and iron absorption measurements were carried out on 15 patients with chronic renal failure who were undergoing regular haemodialysis. There was no evidence that the rate of iron absorption was impaired significantly by the depressed erythropoietic activity present in these patients. In contrast, there was a significant inverse correlation between the rate of iron absorption and the serum ferritin concentration, which has been shown to be an index of the size of the iron stores. This relationship, which was shown with both small (3 mg) and large (50 mg) doses of ferrous iron, was no different from that previously noted in subjects with normal renal function. These results suggest that iron deficiency in patients with chronic renal failure undergoing regular haemodialysis can be adequately prevented or treated with oral iron therapy, since the absorptive mechanism for iron appears to be normal.
Nephron 1981
PMID:Iron absorption in patients on regular dialysis therapy. 731 83


1 2 3 Next >>