Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anemia is one of the complications of terminal chronic renal failure that may worsen with periodical hemodialysis because of residual blood losses in the dialyzers that may be significant if clotting occurs within the circulation system. The potential iron deficiency component of the anemia has been studied in 86 patients submitted to periodic hemodialysis by measurement of hemoglobin, serum iron, transferrin saturation, total iron binding capacity, and ferritin. The following correlations were investigated: degree of anemia and type of renal disease, months on hemodialysis and hemoglobin, months on hemodialysis and serum ferritin, and liters of blood transfused and serum ferritin. Statistically significant correlations were found between months on hemodialysis and hemoglobin, and between liters of blood transfused and serum ferritin. From the correlation between serum iron and ferritin the patients could be classified in three groups: 1, with either normal or low serum iron and ferritin, candidates to iron therapy; 2, with elevated serum iron and ferritin, needing no iron treatment; and 3, with unequal changes of serum iron and ferritin, in whom iron kinetic studies are indicated in order to discover the patents that may benefit from iron therapy.
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PMID:[A study of anemia in 86 patients on hemodialysis (author's transl)]. 724 64

The distribution of stainable iron stores was investigated in various organs of 50 hemodialysis patients with chronic renal disease. Massive iron deposits were found in the liver and spleen. Among 18 patients with severe hepatosplenic siderosis, iron deposits were abundant in the adrenal glands, lymph nodes, and lungs and were sparse in the heart, kidneys, and pancreas. There was an absence or scarcity of stainable iron in bone marrow of 19 pats. In five of these marrow-iron-depleted patients, serum concentrations of ferritin were high. In long-term hemodialysis patients, a variety of factors make massive iron overloads of various organs a likely occurrence, severe hepatosplenic siderosis may occur in marrow-iron-depleted patients, and serum ferritin levels in this setting may not always accurately reflect the status of marrow iron store.
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PMID:Hemosiderosis in hemodialysis patients. An autopsy study of 50 cases. 739 25

Hypoalbuminemia is the most powerful predictor of mortality in end-stage renal disease. Since protein-calorie malnutrition can decrease albumin synthesis it is assumed that hypoalbuminemia results principally from malnutrition in these patients, but albumin synthesis may also be decreased as part of the acute-phase response, and hypoalbuminemia can also result from redistribution of albumin pools or from albumin losses. We measured albumin synthesis, fractional catabolic rate, and distribution from the turnover of [125I] human albumin in six hemodialysis patients with plasma albumin less than 35 mg/ml and in six patients with plasma albumin greater than 40 mg/ml. Patients with liver disease, HIV, or other infection were excluded. Both groups were maintained with high-flux polysulfone dialyzers for more than three months. Kt/Vurea and PCR were measured during each dialysis (N = 12 to 18/patient). A four-day calorie and protein intake was determined by dietary history and long-term nutritional status was determined anthropometrically. Measured variables included serum urea, creatinine, transferrin, and the positive acute-phase proteins alpha 2- macroglobulin, C-reactive protein, ferritin, and IGF-1. Albumin synthesis was significantly reduced in the low albumin group. There were no differences in dietary intake, body composition, PCR, BUN, creatinine, or Kt/Vurea. Plasma albumin concentration correlated negatively with ferritin, C-reactive protein and alpha 2-macroglobulin. Albumin synthesis rate correlated negatively with both alpha 2-macroglobulin and Kt/Vurea. Both plasma albumin concentration and synthesis rate correlated positively with IGF-1, and both were independent of PCR and all other nutrition-related variables.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of hypoalbuminemia in hemodialysis patients. 756 20

Adriamycin, a commonly used antineoplastic antibiotic, induces glomerular lesions in rats, resulting in persistent proteinuria and glomerulosclerosis. We studied the effects of dietary protein and of an angiotensin I converting enzyme inhibitor on the progression of this nephropathy and the evolution of the histological lesions, as well as mesangial macromolecule flow. Adriamycin nephropathy was induced by injecting a single iv dose of adriamycin (3 mg/kg body weight) into the tail vein of male Wistar rats (weight, 180-200 g). In Experiment I animals with adriamycin-induced nephropathy were fed diets containing 6% (Low-Protein Diet Group = LPDG), 20% (Normal-Protein Diet Group = NPDG) and 40% (High-Protein Diet Group = HPDG) protein and were observed for 30 weeks. In Experiment II the rats with adriamycin nephropathy were divided into 2 groups: ADR, that received adriamycin alone, and ADR-ENA, that received adriamycin plus enalapril, an angiotensin I converting enzyme inhibitor. The animals were sacrificed after a 24-week observation period. Six hours before sacrifice the animals were injected with 131I-ferritin and the amount of 131I-ferritin in the glomeruli was measured. In Experiment III, renal histology was performed 4, 8 and 16 weeks after adriamycin injection. At the end of Experiment I the tubulointerstitial lesion index was 2 for LPDG, 8 for NPDG, and 7.5 for HPDG (P < 0.05); the frequency of glomerulosclerosis was 19 +/- 6.1% in LPDG, 42.6 +/- 6% in NPDG, and 54 +/- 9% in HPDG (P < 0.05); and proteinuria was 61.1 +/- 25 mg/24 h in LPDG, 218.7 +/- 27.5 mg/24 h in NPDG, and 324.5 +/- 64.8 mg/24 h in HPDG (P < 0.05). In Experiment II, at sacrifice, 24-h proteinuria was 189 +/- 16.1 mg in ADR, and 216 +/- 26.1 mg in ADR-ENA (P > 0.05); the tubulointerstitial lesion index was 5 for ADR, and 5 for ADR-ENA (P > 0.05); the frequency of glomerulosclerosis was 40 +/- 5.2% in ADR and 44 +/- 6% in ADR-ENA (P > 0.05); the amount of 131I-ferritin in the mesangium was 214.26 +/- 22.71 cpm/mg protein in ADR and 253.77 +/- 69.72 cpm/mg protein in ADR-ENA (P > 0.05). In Experiment III, sequential histological analysis revealed an acute tubulointerstitial cellular infiltrate at week 4, which was decreased at week 8. Tubular casts and dilatation were first seen at week 8 and increased at week 16 when few glomerular lesions were found.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of dietary protein, angiotensin I converting enzyme inhibition and mesangial overload on the progression of adriamycin-induced nephropathy. 758 Oct 27

In the absence of a specific marker for renal cell carcinoma (RCC), we evaluated the tumour-associated trypsin inhibitor (TATI) in patients with RCC. Between November 1990 and November 1993, 63 patients with RCC and 23 patients with benign renal disease underwent a competitive radioimmunoassay of TATI. The cutoff value was defined on a series of serum samples of 96 healthy subjects (normal n < 20 micrograms/l, then 25 micrograms/l after April 1993). We related the value of TATI to the tumour stage and compared the sensitivities of TATI and other markers (CEA, CA 15-3, CA 125, CA 19-9, ferritin). In 24 patients the TATI assay was repeated 3-12 months after radical nephrectomy. 15 patients with benign disease had a normal value of TATI (specificity: 65%). 44 of the 63 patients had a value of TATI above the cutoff point (sensitivity: 69%). Sensitivities of CEA, CA 15-3, CA 125, CA 19-9 and ferritin were 5, 10, 13, 5, 35%, respectively. The TATI value was correlated with the stage of the disease. Among the 15 patients without metastasis, the mean preoperative value was 112 micrograms/l (14-760) versus 46 micrograms/l (24-180) postoperatively. In the 9 patients with metastasis, the preoperative mean value was 100 micrograms/l (20-434) versus 240 micrograms/l (22-544) postoperatively. TATI showed a better sensitivity than other markers for RCC but its specificity is limited. Nevertheless it can be useful for a postoperative follow-up. TATI remains one of the best serum markers for RCC.
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PMID:Tumour-associated trypsin inhibitor and renal cell carcinoma. 760 Nov 86

Serum ferritin concentration correlates with tissue iron stores in humans, horses, calves, dogs, and pigs but not in rats. Because serum iron and total iron-binding capacity can be affected by disorders unrelated to iron adequacy (such as hypoproteinemia, chronic infection, hemolytic anemia, hypothyroidism, and renal disease), serum ferritin is probably the most reliable indicator of total body iron stores in larger species. To test the hypothesis that serum ferritin might be correlated with tissue iron levels in cats, we developed a quantitative enzyme-linked immunosorbent assay that uses two monoclonal antibodies in a sandwich arrangement to measure feline serum ferritin. The recovery of purified ferritin added to feline sera ranged from 94% to 104%; the within-assay coefficient of variability was 8.4%, and the assay-to-assay variability was 13.2%. Mean serum ferritin from 40 apparently healthy cats was 76 ng/ml (SD = 24 ng/ml). Serum ferritin concentration was significantly correlated (P < 0.001, n = 101, r = 0.365) with the nonheme iron in the liver and spleen (expressed as milligrams of iron per kilogram of body weight), as determined by Pearson product-moment correlation analysis. Because serum iron can decrease in diseases other than iron deficiency, the combination of serum iron and serum ferritin should provide sufficient evidence to differentiate anemia of chronic inflammation from anemia of iron deficiency in the cat.
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PMID:Enzyme-linked immunosorbent assay to measure serum ferritin and the relationship between serum ferritin and nonheme iron stores in cats. 786 83

The optimal method for diagnosing iron deficiency in end-stage renal disease is an area of controversy. This study compared the use of zinc protoporphyrin (ZPP) with the use of conventional tests for determination of iron deficiency when evaluating the need for intravenous iron therapy in hemodialysis patients maintained on erythropoietin (EPO). A baseline survey was performed in all hemodialysis patients at the Baumritter Kidney Center (Bronx, NY), measuring ZPP, ferritin, transferrin saturation (TSAT), mean corpuscular volume, and hematocrit. Patients with ZPP > or = 90 mumol/mol heme or ferritin less than 100 ng/mL were considered likely to be iron deficient and were treated with 1,000 mg of intravenous iron dextran over 10 hemodialysis treatments. The positive predictive values of ferritin and ZPP for predicting a response to intravenous iron dextran were similar (73% v 83%, respectively; two-tailed, P = 0.48). To determine the sensitivity and specificity of the tests, patients were divided into two groups at the end of the study period: those in whom iron therapy was required (n = 23) (patients treated with intravenous iron dextran who had a 5% increase in hematocrit or a decrease in erythropoietin dose of > or = 2,000 U/treatment) and those in whom iron therapy was not required (n = 24) (patients either treated with intravenous iron dextran without a response [n = 9] or patients whose initial ZPP and ferritin levels were not suggestive of iron deficiency and who maintained a stable hematocrit and erythropoietin dose during the study period [n = 15]).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The utility of zinc protoporphyrin for predicting the need for intravenous iron therapy in hemodialysis patients. 787 20

Anemia is rapidly corrected by r-HuEPO in the majority of patients with end-stage renal disease provided that iron stores are carefully assessed. Serum ferritin, transferrin saturation and hypochromic red cells are parameters in evaluating the patients' iron status. Replenishment of diminished iron stores may be achieved using oral or intravenous iron. Vigorous iron substitution in r-HuEPO treated patients seems to be mandatory concerning public economy. The intravenous route is the way of choice in delivering sufficient iron supplementation not only in patients felt to be insensitive to standard r-HuEPO dose in therapy. The strategy for the most effective preservation of the iron storage pool and the optimal parameters for monitoring iron demand remains to be elucidated.
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PMID:Iron metabolism and iron substitution during erythropoietin therapy. 795 Jan 65

In order to study the relationship between erythropoiesis and serum ferritin (SF) during erythropoietin (rHuEPO) therapy in the anaemia of end-stage renal disease (ESRD), 19 patients were followed without iron supplementation and at a fixed dose of the drug (40 U/kg). Twelve patients failed to attain the target haemoglobin (Hb) value, 7 of whom due to the appearance of iron deficiency. Erythropoiesis, as measured by the serum transferrin receptor concentration, increased from 12 to 120% of the basal value. This increment was not constantly associated with a proportional rise of Hb or reticulocyte count. SF decreased exponentially from a median value of 221 micrograms/dl (range 42-470) to a median value of 54 micrograms/dl (range 20-172). Halving of the basal SF value (SF-T50) was reached at the 18th-95th day of therapy (median = 43), representing a iron shift of 3.4-11.6 mg/day (median = 5.4). SF-T50 was not correlated with the Hb increase, but with that of erythropoiesis (r = 0.78; p = 0.003). The minimum SF (MSF) value attained was not correlated with the appearance of iron deficiency. The conclusion is that the rate of SF decrease during rHuEPO in ESRD is a reliable measure of iron mobilisation for erythropoiesis, but not for haematologic response. The MSF value reached during therapy is not representative of available iron for erythropoiesis.
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PMID:Variations in erythropoiesis and serum ferritin during erythropoietin therapy for anaemia of end-stage renal disease. 823 68

Twenty-seven transfusion dependent patients with end-stage renal disease on long-term dialysis had blood cell counts, serum chemistries, blood pressure, and whole blood viscosity measured, as well as having transfusion requirements assessed. Three months after the institution of recombinant human erythropoietin (rHU-EPO) (75 u per kg per wk), there was an 88 percent fall in transfusion requirement. After four months, the hematocrit increased from 24 +/- 3.8 to 25.6 +/- 4.2 percent, mean corpuscular volume from 93 +/- 4.9 to 97 +/- 6.6 fl, 2-3-diphosphoglycerate (2,3-DPG) from 13.2 +/- 3.2 to 15.6 +/- 4.3 microM per g of Hb. Whole blood viscosity fell from 14.1 +/- 2.1 to 12.7 +/- 2.3 seconds, and ferritin levels fell from 3282 +/- 3889 to 2131 +/- 2441 ng per ml. In eight patients in whom the dose of rHU-EPO was further increased by up to 50 units per kg three times weekly for three months, the hematocrit rose further to 29.3 +/- 3.0 percent and the rise in hematocrit was accompanied by a further increase in 2,3-DPG to 17.9 +/- 2.8 microM per g of Hb (p < 0.03). There were no major side effects or vascular complications.
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PMID:Blood rheology and 2,3-diphosphoglycerate levels after erythropoietin treatment. 843 Sep 97


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