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)

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

Genetically disparate inbred mouse strains mounting quantitatively different immune responses to a potentially nephritogenic heterologous protein had varied development of glomerulonephritis (GN) dependent upon the interaction between level of antibody response and antigen dose. High responder BALB/c mice given high doses of horse apoferritin developed a severe necrotizing GN. BALB/c mice given low dose horse apoferritin developed less severe GN, or when antibodies were in extreme excess, no GN. Low responder C3H mice given high dose horse apoferritin were in extreme antigen excess and developed no GN. C3H mice given low dose horse apoferritin developed a glomerulopathy characterized by capillary loop immune deposits. Interstrain differences in immune clearance and avidity did not account for this varied nephritogenicity, although avidity did relate to glomerular site of immune deposits in the BALB/c model. In the models under consideration susceptibility to heterologous antigen-induced glomerular injury was a function of the magnitudes of both the antibody response and the antigenic challenge.
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PMID:Interaction of antigen load and antibody response in determining heterologous protein nephritogenicity in inbred mice. 634 22

In the present work general characteristics and occurrence of TLR receptors have been presented. The participation of TLR receptors in kidney pathology in experimental models in the course of urinary system infection, acute renal failure and interstitial fibrosis has been discussed. In addition, the importance of TLRs in various forms of glomerular nephritis and in haemodialytic patients as well as in postrenal-transplant patients has been shown. It is believed that in lipopolysaccharide-induced renal failure in the course of infections caused by Gram negative bacteria TLR4 plays a fundamental role. In the event of damage of renal tubular epithelial cells by mechanical, toxic, or ischemic factors activation of TLRs induces inflammatory processes leading to acute renal failure. In the course of progressive fibrosis of renal interstitial tissue TLR 2 and 4 receptors are stimulated, which results in the fact that immunological and structural cells of renal tissue release chemokines and cytokines, which causes increased inflow of leucocytes and intensification of interstitial nephritis and progressive fibrosis. The study on experimental models on mice MLR (mixed lymphocyte reaction) with genetically conditioned lupus-like disease showed that, CpG-DNA stimulation as a TLR 9 specific agonist intensifies inflammatory symptoms in mice. Similarly in apoferritin induced glomerulopathy (model of immune complex disease) CpG-DNA nucleotide increased glomerulopathy symptoms. It has been proved that activation of mechanisms of inherent immunity through TLR4 receptors affects the frequency and intensity of acute rejections in human organ transplantations. Incidence of acute kidney and lung [transplant rejections was significantly lower in recipients with mutated variants of Toll-like receptor 4 (TLR-4 Asp 299Gly and TLR-4-Tyr399-IIe).
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PMID:[Toll-like receptors (TLR) in the pathogenesis of kidney diseases]. 1836 25

We present an interesting case of a 37-year old man with acute renal failure following a febrile illness. Laboratory results showed features of macrophage activation syndrome (MAS) with anemia, thrombocytopenia, hypofibrinogenemia and elevated ferritin levels. Renal biopsy was then done to determine the cause of renal failure and showed unique glomerular findings with massive histiocytic infiltration ('histiocytic glomerulopathy') and evidence of endothelial injury. Recognizing that the histiocytic infiltrate and endothelial injury is a part of MAS is important because early recognition and treatment is of utmost importance since the disease can be fatal.
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PMID:Histiocytic glomerulopathy associated with macrophage activation syndrome. 2581 71