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)

Immunologic mechanisms of proteinuria were investigated in guinea pigs (GP) injected with sheep antiserum (NTS) to GP glomerular basement membrane (GBM). Linear deposition of sheep gamma 1 and gamma 2 IgG led to a prompt but transient (36 hr) increase in albumin excretion from control values of 0.026 +/- 0.013 mg/hr to maximal values of 26+/-12.1 mg/rh at six hours without detectable histologic or electron microscopic changes except for decreased staining for glomerular polyanion and epithelial cell foot process fusion. GBM permeability to anionic ferritin was not increased during proteinuria. Anti-GBM antibody deposits did not fix GP C3 or C4 in vivo or in vitro. NTS-induced proteinuria was the same in guinea pigs that were normal, greater than 95% depleted of C3 through C9, genetically deficient in C4, and depleted of circulating polymorphonuclear leukocytes (PMN). Prior administration of antihistamines, steroids, azathioprine, colchicine, indomethacin, heparin, aprotinin (Trasylol), and niridazole also failed to reduced proteinuria. Initial proteinuria subsided by 36 hr, did not recur despite linear deposition of GP gemma 1 and gemma 2 after day seven, and antibody to GMB-bound sheep globlin. In the GP nephrotoxic nephritis model, anti-GBM antibody deposits apparently mediate increased permeability to albumin by a currently undefined mechanism which is independent of complement, PMN, and other know mediators of inflammation.
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PMID:Complement-independent nephrotoxic nephritis in the guinea pig. 1 57

Mice undergoing prolonged (5 to 8 weeks) immunization with cadium-free feeritin were studied 1 to 32 days following the last ferritin injection. Urine protein was measured and renal tissue examined by light, immunofluorescence, and electron microscopy. Immunized animals developed significant proteinuria and circulating antibody to ferritin.by light microscopy, proetinuric animals had a proliferative glomerular lesion with mesangial hypercellularity and martrix increase, focal and segmental necrosis, fibrin deposits, and occasional crescents. Iron stains revealed prominent mesangial iron deposition. In immunized animals, IgG and C3 deposits were localized mainly in the mesanglium. Electron microscopic studies revealed marked deposition of ferratin complexesexpanded mesangial matrix and mesangial interposition. Ferratin immune complexes were also visualized in epithelial spaces. In the latter location ferritin immune complexes occasionally formed characteristic electron-dense subepithelial deposits. In this model, mesangial and subepithelial localization of autologous ferritin immune complexes is associated with development of glomerulonephritis and characteristic mesangial lesions resembling those seen in some types of human glomerulonephritis.
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PMID:Experimental glomerulonephritis in the mouse associated with mesangial deposition ofautologous ferritin immune complexes. 12 61

Nephrotoxic nephritis was induced in Sprague-Dawley and Munich-Wistar rats by the injection of rabbit antirat kidney serum. A biphasic pattern of proteinuria was induced: the heterologous phase with a peak of proteinuria occurring at 10 to 16 hours, and the autologous phase with a peak at 10 to 15 days. For morphologic studies, glomeruli were fixed by perfusion, or by drip-fixation during good blood flow. In the heterologous phase, glomerular endothelial detachment or loss and leukocytic infiltration were prominent. In the autologous phase, focal detachment of glomerular endothelium and epithelium was commonly found. At sites of endothelial loss, in both phases, endogenous albumin (demonstrated by an ultrastructural immunoperoxidase technique), but not intravenously injected ferritin, showed abnormally deep penetration into the glomerular basement membrane. At sites of epithelial loss, found in the autologous phase, both albumin and ferritin were detected throughout the glomerular basement membrane. It is proposed that, in glomerular disease, leakage of plasma proteins may occur across the glomerular basement membrane at sites of endothelial or epithelial detachment.
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PMID:An ultrastructural study of the mechanisms of proteinuria in rat nephrotoxic nephritis. 32 69

Mice injected intraperitoneally with 20 mg of ferritin twice weekly for more than 4 weeks developed proteinuria due to the deposition of ferritin-antiferritin antibody complexes in renal glomeruli. Deposits of ferritin, immunoglobulin G (IgG) and third complement component (C3) also accumulated in the perivascular, extracellular space of the choroid plexus as demonstrated by immunofluorescence and electron microscopy. The findings confirm previous observations on immune complex deposits in the choroid plexus in spontaneous autoimmune disease and persistent viral infections. The occurrence of similar deposits in the human choroid plexus and the possibility of an associated disturbance of the blood-spinal fluid barrier are discussed.
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PMID:Ferritin immune complex deposits in the choroid plexus. 32 48

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.
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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.
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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

Humoral immune processes mediate alterations in glomerular basement membrane (GBM) permeability by two mechanisms. One requires complement and polymorphonuclear leukocytes and the second is complement- and polymorphonuclear leukocyte-independent. The structural basis for enhanced GBM permeability induced by anti-GBM antibody is not clear. Experimental anti-GBM glomerulopathy was induced in guinea pigs by immunization with human GBM in complete Freund's adjuvant. Control animals received injections of complete Freund's adjuvant alone. Light, immunofluorescent, and electron microscopic studies were done on eight heavily proteinuric animals, four immunized nonproteinuric animals, three controls, and two normal animals. All animals that received injections of GBM had intense linear deposits of gamma2 anti-GBM antibody. Complement deposition was not demonstrable in vivo, and anti-GBM antibody deposits did not fix complement in vitro. Histologic abnormalities in proteinuric animals were confined to the GBM, which was of variable density and had a characteristic beaded thickening, with numerous areas of electron lucency most prominent in the outer aspect of GBM in peripheral portions of capillary loops. The inner margin and endothelium were normal. Ultrastructural tracer studies with ferritin demonstrated increased permeability confined to portions of GBM demonstrating ultrastructural lesions. The urine protein excreted by animals with ultrastructural GBM lesions was largely albumin. The absence of complement deposition accompanying anti-GBM antibody deposits in vivo and the unique GBM lesion in this model differ from the findings in nephritis induced by most heterologous nephrotoxic antibodies and suggest that GBM injury in this model is mediated by autologous antibody through complement-independent mechanisms. The selective proteinuria and ultrastructural lesions suggest a derangement in glomerular permeability functionally localized to the epithelial side of the GBM and could reflect an antibody-mediated abnormality in GBM biosynthesis.
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PMID:Experimental glomerulonephritis in the guinea pig. II. Ultrastructural lesions of the basement membrane associated with proteinuria. 108 38

Sprague-Dawley rats injected i.v. with a single dose of puromycin aminonucleoside (PAN) developed massive proteinuria five days later. Electron microscopic studies of perfusion-fixed glomeruli showed that loss of epithelial foot processes and their replacement by flattened expanses of epithelial cytoplasm began at two days and was extensive by four days after the injection of PAN. At and after five days (correlating with the onset and persistence of massive proteinuria), areas of focal loss of the epithelial covering on the outside of the glomerular basement membrane (GBM) were observed in 30% of glomeruli. Intravenously administered ferritin was distributed normally in most sections of the GBM of nephrotic animals, but abnormally deep penetration of particles was observed in GBM segments that lacked an external covering of epithelium. The same changes were found following in situ fixation of superficially placed glomeruli of Munich-Wistar rats with PAN nephrosis. We propose that the massive, early proteinuria in PAN nephrosis may be primarily due to a glomerular epithelial lesion, leading to scattered focal defects in the external covering of the GBM. Increased bulk flow of glomerular filtrate across the GBM in such areas may explain the highly selective proteinuria found in this form of the nephrotic syndrome.
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PMID:An ultrastructural study of the mechanisms of proteinuria in aminonucleoside nephrosis. 110 66

The relationship between iron status and degree of infection by Schistosoma haematobium was examined in 174 schoolchildren from Niger in an area endemic for urinary schistosomiasis. Iron deficiency was defined by a combination of 3 reliable indicators: a low serum ferritin level combined with a low transferrin saturation, a high erythrocyte protoporphyrin level, or both. Hematuria and proteinuria were seen in 76.4% and 79.9% of the children, respectively, while 95.4% excreted eggs (geometric mean egg count of 31.5 eggs/10 ml of urine). Anemia was seen in 59.7% of the subjects. The prevalence of iron deficiency was 47.1%. Anemia was associated with iron deficiency in 57.7% of the cases. Hemoglobin level and transferrin saturation decreased significantly when the degree of hematuria increased, while prevalence of anemia and iron deficiency increased significantly. The hemoglobin level and hematocrit were negatively correlated with egg count, while anemia prevalence increased with increasing egg count. This inverse relationship between degree of infection by s. haematobium and iron status shows a deleterious consequence of urinary schistosomiasis on nutrition and hematopoietic status, which should be considered in the design of nutrition intervention programs.
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PMID:Consequences of Schistosoma haematobium infection on the iron status of schoolchildren in Niger. 152 42

Serum sickness nephritis was induced in male Fisher rats by immunization with egg albumin (EA). Correlations of subepithelial deposits (SD) with size and charge barriers of the glomerular filter were investigated using native (NF) and cationized (CF) ferritin as tracer probes. In proteinuric animals large numbers of NF molecules perfused from the abdominal aorta were observed to cross the glomerular basement membrane (GBM) and enter SD. The concentration of NF molecules was higher in GBM segments with SD than in GBM segments without SD, and the concentration of these molecules was higher within SD than in the intervening GBM. In contrast, CF clusters were fewer in number in the lamina rara externa (LRE) of GBM segments with SD than in the GBM segments without SD. CF particles could not be observed within SD, even in the areas of podocyte detachment. It is suggested that permeability in GBM segments with SD increases and that the development of proteinuria in this model can be attributed to alterations in both charge- and size-selective barriers to glomerular filtration.
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PMID:Influence of subepithelial deposits on permeability of the glomerular capillary wall in serum sickness nephritis in the rat. 180 51


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