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)

The effects of increasing two dietary polyunsaturated fatty acids, eicosapentaenoic and linoleic, on the glomerulonephritis induced by repeated injections of apoferritin in the mouse were studied. Urinary protein excretion was measured serially; serum creatinine, aortic and renal production of eicosanoids and kidney histology were measured at sacrifice at 8 weeks. Both high EPA and LA feedings were associated with lesser proteinuria, normalization of renal function and profound changes in the tissue production of prostaglandin and thromboxane, which may explain their protective effect in this model of renal disease.
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PMID:Protective effect of polyunsaturated fatty acid supplementation in apoferritin induced murine glomerulonephritis. 301 61

The ability of magnetic resonance imaging (MRI) to detect iron overload in children with end-stage renal disease (ESRD) was studied in 18 multiply transfused patients, aged 15.5 +/- 4.8 years, and 5 nontransfused children without evidence of renal disease. In the transfused patients, the serum ferritin (SF) level was compared to (a) a subjective rating of signal intensity of MRI images (scale of 0-10), (b) mean T1 values of liver and spleen, and (c) computer-assisted measurements of spin echo intensity (SEI) of liver, spleen, muscle and fat tissue. On subjective evaluation, the mean signal intensity was significantly lower in transfused patients than in controls and a significant correlation with the SF levels was observed for ratings of both liver and spleen. Mean T1 values of liver and spleen did not correlate with the SF levels. On computer analysis, the ratios of SEI of fat/liver, fat/spleen, muscle/liver and muscle/spleen were significantly correlated with the SF levels as well as the subjective evaluation sources. These data indicate that MRI is a suitable technique of documenting the presence and degree of iron overload in multiply transfused children with ESRD.
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PMID:Magnetic resonance imaging of iron overload in children treated with peritoneal dialysis. 322 57

During a 19-month period we determined the incidence of bacterial infection among 39 patients treated with desferrioxamine who had end-stage renal disease and were undergoing maintenance hemodialysis. Twenty-three received desferrioxamine because of aluminum-related bone disease, and 16 because of iron overload. A control group of 193 patients on maintenance hemodialysis but without desferrioxamine was used. No difference was found in the incidence of septicemia or of all bacterial infections between the patients with aluminum-related bone disease treated with desferrioxamine and the control patients (0.12 vs. 0.12 septicemia per patient-therapy-year, p greater than 0.05; 0.23 vs. 0.26 bacterial infections per patient-therapy-year, p greater than 0.05). The incidence of septicemia in patients treated with desferrioxamine for iron overload, however, was almost three times that in the control patients (0.36 vs. 0.12 septicemia per patient-therapy-year, p less than 0.01). To assess the effect of iron overload itself, we determined the frequency of bacterial infection in patients on regular hemodialysis who have never received desferrioxamine. These were subdivided into three groups according to serum ferritin level which indicated normal or low iron stores (Group I: serum ferritin 10-330 micrograms/l, n = 125), moderate (Group II: serum ferritin 331-1000 micrograms/l, n = 49) or more advanced iron overload (Group III: serum ferritin 1001-2000 micrograms/l, n = 10). Compared to patients with normal or low serum ferritin levels (Group I), we found a significantly higher rate of bacterial infection among patients in Group II compared with Group I (0.18 vs. 0.34 infections per patient-therapy-year, p less than 0.05) and Group III compared with Group I (0.18 vs. 0.58 infections per patient-therapy-year, p less than 0.01). These results suggest that treatment with desferrioxamine does not favour the development of septicemia or bacterial infection independently of iron overload and that iron overload itself may predispose patients on regular hemodialysis to bacterial infection.
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PMID:Iron overload, but not treatment with desferrioxamine favours the development of septicemia in patients on maintenance hemodialysis. 345 53

To study the nephropathy associated with sickle-cell disease (SCD), spin-echo magnetic resonance (MR) imaging of the kidneys was performed in 19 SCD patients, six with beta-thalassemia major (BTM), and ten healthy individuals as controls. Eleven SCD patients had decreased relative cortical signal, most evident on T2-weighted images. No correlation with serum ferritin, urine-concentrating ability, serum blood urea nitrogen, or creatinine levels was established. Iron deposition in the renal cortices of sickle-cell nephropathy patients may, at least in part, be responsible for the relatively diminished cortical signal intensity. No BTM patients, all of whom were clinically and biochemically in iron overload from frequent transfusions, demonstrated diminished renal cortical signal intensity. This suggests that renal changes in SCD seen on MR images are not due simply to systemic iron overload per se but perhaps reflect abnormalities of iron metabolism in the renal cortex peculiar to SCD nephropathy.
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PMID:Sickle-cell nephropathy: MR imaging. 394 63

1. Kidney biopsies from 4 cases of severe acute glomerulonephritis were obtained 11 to 25 days after the onset of clinical manifestations of the disease. These tissues were treated with ferritin-conjugated antibodies to 7S gamma-globulin, beta(1C), and Type 12 streptococcal products. Adjacent pieces of the biopsied material were treated with control ferritin-labeled antisera or with ferritin alone. As further controls, normal renal tissue and renal tissue from patients with other kidney diseases were treated with the same antisera. The 3 antisera to 7S gamma-globulin, beta(1C) and Type 12 streptococcus were specifically bound in electron-opaque foreign material in the following renal areas: (a) the lumen of glomerular capillaries; (b) medullary arteriolar walls (2 cases); (c) pinocytic vacuoles and absorption droplets of endothelial or mesangial cells; (d) canals between proliferating mesangial or endothelial cells which connect the capillary lumen with the deep mesangial region or with the endothelial side of the basement membrane; (e) basement membrane proper; (f) subendothelial and certain subepithelial deposits; and (g) Bowman's space. 2. None of the 3 ferritin-conjugated antisera listed above were bound to the nuclei of glomerular cells or to portions of the cytoplasm other than those specified. 3. Ferritin-conjugated antisera to pneumococcus Type II and vaccinia virus and ferritin alone were not bound to any structures in the glomerular tissue. 4. None of the ferritin-conjugated antisera bound to normal renal tissue or to kidney tissue from other renal disease. 5. The data obtained are compatible with the following working hypothesis: Antigen-antibody aggregates of Type 12 streptococcal products, gamma-globulin, and complement are present in the circulating blood of patients with severe acute glomerulonephritis. Large amounts of the complexes are caught in the filtering system of the glomeruli. The inflammatory reactions seen in the glomerular structures result from the presence of the immune complexes and of the polymorphonuclear leukocytes which conjointly may be responsible for the disease.
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PMID:Electron microscopic studies of human glomerulonephritis with ferritin-conjugated antibody. Localization of antigen-antibody complexes in glomerular structures of patients with acute glomerulonephritis. 532 24

In RDT hemosiderosis appears to be an inevitable complication only in the small number of patients in need of frequent transfusions. To prevent clinical consequences (e.g. cardiomyopathy) known from polytransfused patients without renal disease, transplantation should be considered in RDT patients in need of frequent transfusions. Iron substitution - preferably oral - to replace dialysis-related iron loss does not cause clinically significant hemosiderosis provided iron stores are monitored adequately. A sufficient method of controlling iron stores in RDT patients under iron substitution or regular transfusion therapy is a twice annual determination of serum ferritin concentration. The treatment of choice for hemosiderosis in nontransfused RDT patients is discontinuation of iron substitution. When polytransfused RDT patients with severe hemosiderosis cannot be transplanted and submitted consecutively to phlebotomy, DFO treatment is indicated. Quantitative data regarding optimal dosage and application of DFO in RDT patients are not yet available. Constant infusion of DFO during hemodialysis may be superior to bolus application.
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PMID:Therapy and monitoring of hypersiderosis in chronic renal insufficiency. 671 93

Levels of testosterone, free testosterone, oestrogen, LH, FSH, prolactin were measured in 39 dialysed men. A LHRH stimulation test was performed. This study was analysed in function of the underlying renal disease, the duration of hemodialysis, and serum ferritin levels. In chronic glomerulonephritis serum gonadotrophins concentrations were significantly higher than in chronic interstitial nephritis or polycystic disease. A correlation between prolactin and ferritin was found, which may reflect the pituitary iron overload. Free testosterone levels were significantly lower in patients with gynecomastia (23-29 patients). In fact, the most direct relationship that we found with gynecomastia in dialysed men was with the free testosterone/oestrogen ratio.
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PMID:[Anomalies of human gonadal function in periodic hemodialysis: role of the etiology of kidney failure and the role of iron overload]. 687 81

Forty-three spinal cord injured patients with endstage renal disease (ESRD) maintained on hemodialysis were studied. The most prevalent renal lesions consisted of chronic pyelonephritis and amyloidosis while the main renal functional features included nephrotic range proteinuria, high urine output and relatively low serum creatinine for the degree of renal insufficiency. Normocytic, normochromic anemia with low reticulocyte response, low serum iron and iron binding capacity and high transfusion requirement and serum ferritin were noted. Various cardiovascular, pulmonary and gastrointestinal abnormalities were found with considerable frequencies. The incidence of amyloidosis was much higher than that reported previously. This is thought to be due to continued progression of amyloidosis occasioned by longer survival in the present series.
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PMID:Clinicopathological characteristics of dialysis patients with spinal cord injury. 688 88

Radio-iron kinetic tests were performed in 7 patients with end-stage renal disease treated by hemodialysis; the study could be completed in 6 patients. The incorporation of radio-iron into the erythrocytes was 21% on average in patients with acute anemia. The red cell life-span determined in 4 patients became significantly shorter in 3 patients. Iron turnover in the bone marrow was significantly lower than normal, the rate of ineffective erythropoiesis being higher. Serum ferritin levels were significantly higher, and tissue and extravascular iron turnover was found to be enhanced compared to normal. At the same time, serum iron level was normal. The data on iron turnover indicated deficient hemopoiesis in the bone marrow, due partly to the lack of erythropoietin and partly to the insufficiency of the BFU-E (burst forming units) and CFU-E (colony-forming units) reserves. Undoubtedly, this was a consequence of the uremia.
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PMID:Iron turnover in patients with chronic uraemia treated with hemodialysis. 718 45

Serum ferritin, measured by radioimmunoassay in 65 dialysis patients (mean time of dialysis 38.9 months), was significantly higher (247.9 +/- 224.5 ng/ml) than in controls (p less than 0.001), inversely correlated with dialytic age (p less than 0.05), and had no difference as far as sex or underlying nephropathy were concerned. With regard to the other hematological parameters, serum ferritin correlated inversely with total transferrin and directly with percentage of total transferrin only. In 28 patients, an intravenous iron load (0.6 g in one month) induced a further increase in serum ferritin (p less than 0.001), rather disomogenous and not clearly correlated with initial levels. The change in hemoglobin concentration after iron administration was in close relationship with initial serum ferritin levels (r = -0,72, p less than 0.001). A significant increase in hemoglobin could be detected in all the patients with serum ferritin less than 65 ng/ml and in most patients with serum ferritin less than 160 ng/ml, while hemoglobin change was negligible when serum ferritin levels in dialysis exceeded this value. Thus, although serum ferritin levels in dialysis patients may reflect not only iron overload but also an abnormal metabolism, serum ferritin measurement remains a reliable guide to iron requirement. We suggest maintaining serum ferritin levels between 65 and 160 ng/ml, to avoid iron stores depletion and on the contrary, iron overload.
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PMID:[Serum ferritin and iron therapy in patients treated with periodic hemodialysis]. 718 48


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