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)

A controlled, prospective study compared the effectiveness of oral ferrous sulfate to intravenous iron dextran, each with and without concurrent intramuscular androgen for therapy of iron deficiency anemia in patients with chronic renal failure treated with maintenance hemodialysis. During the 12-week period of therapy, the patients who received oral ferrous sulfate and androgens showed an increment in their mean hematocrit of 16.3% and those who received oral ferrous sulfate alone had an increase of 8.3%. Patients treated with intravenous iron dextran androgens showed an increment in their mean hematocrit of 9.4% and those given iron dextran alone showed an increase of 3.5%. Serum ferritin levels increased with iron repletion but correlated inversely with the erythropoietic response. The serum ferritin assay provides a simple and reliable method to demonstrate iron repletion, and oral ferrous sulfate is the preferred method of iron repletion in compliant patients.
Nephron 1979
PMID:Therapy of iron deficiency anemia in patients on maintenance dialysis. 47 Nov 41

In order to study the effects of the protein moiety independent of the protein-iron complex in the development of ferritin-induced glomerulonephritis, we compared the effects of ferritin, equimolar amounts of apoferritin, and equimolar amounts of iron dextran in Swiss albino mice. The results were compared to both saline-injected and non-injected controls. Ferritin resulted in a glomerulonephritis associated with predominantly mesangial deposition of immune complexes. Tubulo-interstitial changes occurred as well. Iron dextran resulted in similar but less severe tubulo-interstitial changes and evoked no glomerular alterations. Apoferritin resulted in an immune complex glomerulonephritis usually associated with membranous deposits. No tubular or interstitial changes occurred. Proteinuria developed in animals receiving apoferritin. Since the protein-iron complex caused tubular and interstitial damage, apoferritin may provide a more suitable model of immune-complex-mediated glomerulonephritis.
Nephron 1979
PMID:Ferritin- and apoferritin-induced immune complex glomerulonephritis in mice. 49 22

The morphologic basis of proteinuria in experimental chronic serum sickness glomerulonephritis in rabbits was studied by light and electron microscopy using horseradish peroxidase (effective radius 30 A; mol. wt. 40,000) and ferritin (effective radius 60 A; mol. wt. 480,000) as protein tracers. It was found that more ferritin, but paradoxically, less horseradish peroxidase gained access to the urinary space. Observations made by electron microscopy appeared to indicate a decreased permeability of most part of the damaged glomerular capillary wall to both tracers. These results favor the interpretation that proteinuria in chronic serum sickness glomerulonephritis is the result of focal rather than diffuse increase in permeability of the glomerular capillary wall. Lesions of segments of the nephron other than the glomerular capillary wall, may contribute to the leakage of proteins to the urinary space.
Nephron 1978
PMID:The morphologic basis of proteinuria in experimental chronic serum sickness glomerulonephritis. A light and electron microscopic study using horseradish peroxidase and ferritin as tracers. 66 50

The dose of recombinant human erythropoietin (r-HuEpo) required to correct anemia of end-stage renal disease varies among patients. The possible factors that interfere with the responsiveness to r-HuEpo were not completely known. In 32 patients on regular hemodialytic treatment with marked anemia (Hb 5.6 +/- 0.7 g/dl), we evaluated circulating erythroid progenitor cells [burst-forming-unit erythroid (BFU-E)], erythropoietin, ferritin, folate and 1-84-parathormone levels before r-HuEpo therapy. In 12 patients, the aluminum levels after deferoxamine were also evaluated. The possible correlation between these factors and the response to r-HuEpo therapy was then evaluated. The number of circulating (c) BFU-E was highly variable (521 +/- 447 colonies/ml of blood; normal level 742 +/- 192) and does not correlate with erythropoietin, ferritin, folate, 1-84-parathormone or aluminum levels. A direct correlation between basal cBFU-E and the responsiveness to r-HuEpo therapy was recorded while no correlation was found with the other analyzed parameters. We hypothesized that low basal cBFU-E (interleukin-3 deficiency?) could reduce the response to r-HUEpo because of failure of this hematopoietic stem cell compartment to replenish the pool of more mature erythropoietic progenitor cells during the phase of accelerated maturation induced by r-HuEpo.
Nephron 1992
PMID:Circulating burst-forming-unit erythroid and the responsiveness to recombinant human erythropoietin in patients on regular hemodialytic treatment. 143 6

Nephrogenic ascites associated with maintenance hemodialysis is a complex problem with poorly understood pathophysiology. We report 4 pediatric patients investigated between 1986 and 1990. All the patients treated with maintenance hemodialysis required multiple blood transfusions. Each patient was carefully evaluated for factors potentially relevant to ascites, and serum ferritin levels were found to be extremely high. Peritoneoscopy which was utilized in all patients led to a specific diagnosis of hemosiderosis in the peritoneum and liver biopsies. In 1 patient, lymph node biopsy also showed iron deposition. We believe that iron deposition played a role in changing the permeability of the peritoneum and is presumed to be a pathogenetic factor in nephrogenic ascites.
Nephron 1992
PMID:Peritoneal hemosiderosis in pediatric patients with nephrogenic ascites. 143 41

278 azathioprine and methylprednisolone (AZA)-treated and 406 ciclosporin (CS) treated patients with a kidney graft functioning for more than 1 year were investigated for the presence of chronic liver disease (CLD), defined as an increase in transaminases of 1.5 times the upper normal limits for a period of at least 12 months. The prevalence of CLD was 36 and 27% in the two groups, respectively. The univariate analysis showed that male sex, alcohol abuse and HBsAg positivity correlated with CLD onset in the AZA group while blood transfusions, length of dialysis treatment, pretransplantation CLD, HBsAg positivity and ferritin levels over 800 ng/ml correlated with CLD onset in CS. The multivariate analysis identified male sex and HBsAg positivity in the AZA group and age over 18 years, high ferritin levels and HBsAg positivity in the CS group as risk factors predictive of CLD onset. Liver failure represented the 4th cause of death in the AZA group but 1 of the 2 most important causes of death in CS in the long term. However, these drawbacks were overcome by the overall low mortality rate in CS. Therefore, renal transplantation should not be refused to patients positive for HBsAg and/or with preexisting liver disease.
Nephron 1992
PMID:Renal transplant recipients and chronic liver disease: statistical evaluation of predisposing factors. 150 27

To achieve a rational basis for the use of deferoxamine (DFO) in aluminum (AL) -and iron (Fe)-overloaded uremic patients, important insights may be provided by the recently available micromethods to determine DFO and its metallochelates aluminoxamine (AlA) and feroxamine (FeA). With this procedure, AlA and FeA plasma kinetics were evaluated in a pilot study in 10 uremic patients during a whole week after a single DFO infusion performed during the first hour of the first standard bicarbonate hemodialysis (HD) of the week. Patients were divided into normal (n = 6) and high (n = 4) ferritin groups (1 and 2 respectively). Baseline Al concentrations were greater than 2 less than 6 in group 1 and less than 1.5 mumol/l in group 2. DFO was given at doses of 40, 20 and 10 mg/kg. AlA and FeA showed substantially different kinetics. AlA kinetics were similar in group 1 and 2: they reached their peak at the beginning of the 2nd HD, decreased during the 2nd and 3rd HD, and with the highest DFO dose still increased between the 2nd and 3rd HD. At similar pre-DFO Al values (greater than 2 less than 3.3 mumol/l), increased DFO doses produced increased AlA concentrations ranging from 95 to 40% of total plasma Al for all the week. At higher pre-DFO Al values (greater than 3.5 less than 6 mumol/l), even a DFO dose as low as 10 mg/kg was sufficient to form consistent AlA amounts (from 80 to 15% of total Al).(ABSTRACT TRUNCATED AT 250 WORDS)
Nephron 1992
PMID:Kinetics of aluminoxamine and feroxamine chelates in dialysis patients. 158 15

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

Alterations of tubules and glomerules have been reported previously in kidneys of rat neonates after aminoglycosides were given to the mother during gestation. Here, we have studied the effects of gentamicin on the development of the glomerular basement membrane (GBM). Pregnant Wistar female rates were treated with gentamicin. Deliveries occurred normally. Using electron microscopy, we looked at the deepest glomerules of the kidneys of 1-day-old neonates: myeloid bodies were found in podocytes, and the GBM appeared thicker and denser than in controls. Anionic ferritin, injected intravenously crossed the GBM in prenatally gentamicin-exposed animals, but not in controls. Furthermore, urine electrophoresis showed the presence of proteins normally found only in the urine of fetuses 2 days before birth. We suggest then, that in utero exposure to gentamicin leads to a delay of renal maturation and that the GBM is altered in juxtamedullary nephrons while it is normally differentiated and functioning in controls. Thus exposure to drugs before birth could be harmful to the GBM.
Nephron 1991
PMID:Glomerular alterations in rat neonates after transplacental exposure to gentamicin. 176 3

To determine whether the chelation of aluminium enhances the haemopoietic response to recombinant human erythropoietin (r-HuEPO), desferrioxamine (DFO) at a dose of 20-30 mg/kg was given to 7 of 17 transfusion-dependent haemodialysis patients treated with r-HuEPO (40 units/kg/dialysis i.v.). The two randomly allocated groups did not differ in age, initial haemoglobin, plasma aluminium, plasma aluminium after DFO challenge, and ferritin, but, by chance, dialysis time was longer in the DFO group (69 vs. 32 months; p = 0.02). DFO was administered for 16 +/- 4 (SE) dialyses. During this period, Hb rose faster in the DFO group, in relation to time (0.61 vs. 0.29 g/l day; p less than 0.05) and r-HuEPO dose (3.35 vs. 1.88 g/l/100 units r-HuEPO/kg; p less than 0.05). However, in the DFO group, there was a high incidence of side effects, especially visual toxicity. It is concluded that DFO enhances the effectiveness of r-HuEPO in correcting the anaemia of chronic renal failure, but the combination of DFO and r-HuEPO is unsafe under the conditions described.
Nephron 1991
PMID:Desferrioxamine enhances the haemopoietic response to erythropoietin, but adverse events are common. 185 80


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