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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Pty
    Nephrology 7 (2002), S. 0 
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY: IgA nephropathy (IgAN) is characterized by the mesangial deposition of polymeric IgA1 (pIgA1). The original view that this pIgA1 is derived from the mucosal immune system can no longer be sustained. Studies of duodenal mucosa and marrow indicate increased production of pIgA1 in the marrow and decreased production in the mucosa. These changes are consistent with immunization studies showing exaggerated and prolonged pIgA responses to systemic immunization, and reduced mucosal responses to mucosal neoantigens. However, the IgA1 and IgG systemic responses to mucosal antigen are increased in IgAN, a finding consistent with impairment in oral tolerance, the process by which systemic immune responses to mucosal antigen challenge are normally suppressed. Both IgA1 production and the induction of oral tolerance are under T-cell control. T-cell populations involved in these processes include γδ T cells, Tr cells and T-helper (Th)3 cells; cytokines with a key role in the control of IgA production include interleukin (IL)-10 and transforming growth factor (TGF)-β. There is evidence of abnormal γδ T-cell V region usage in both mucosa and marrow in IgAN. Increased expression of relevant cytokines has also been reported in circulating T cells in IgAN. The increased O-glycosylation of circulating IgA1 in IgAN may also be further evidence of a shift in the production of mucosal-type pIgA1 from the mucosa to marrow. These findings suggest that the specific lymphocyte homing mechanisms that normally maintain oral tolerance and control the site of IgA production require further study in IgAN.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Nephrology 7 (2002), S. 0 
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY: IgA nephropathy (IgAN) is characterized by the mesangial deposition of polymeric IgA1 (plgA1). the original view that this plgA1 is derived from the mucosal immune system can no longer be sustained. Studies of duodenal mucosa and marrow indicate increased production of plgA1 in the marrow and decreased production in the mucosa. These changes are consistent with immunization studies showing exaggerated and prolonged plgA responses to systemic immunization, and reduced mucosal responses to mucosal neoantigens. However, the IgA1 and IgG systemic responses to mucosal antigen are increased in IgAN, a finding consistent with impairment in oral tolerance, the process by which systemic immune responses, to mucosal antigen challenge are normally suppressed. Both IgA1 production and the induction of oral tolerance are under T-cell control. T-cell populations involved in these processes include γδ T cells, Tr cells and T-helper (Th)3 cells; cytokines with a key role in the control of IgA production include interleukin (IL)-10 and transforming growth factor (TGF)-β. There is evidence of abnormal γδ T-cell V region usage in both mucosa and marrow in IgAN. Increased expression of relevant cytokines has also been reported in circulating T cells in IgAN. the increased O-glycosylation of circulating IgA1 in IgAN may also be further evidence of a shift in the production of mucosal-type plgA1 from the mucosa to marrow. These findings suggest that the specific lymphocyte homing mechanisms that normally maintain oral tolerance and control the site of IgA production require further study in IgAN.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    ISSN: 1432-198X
    Keywords: IgA nephropathy ; Haematuria ; Circulating immune complexes ; Food antigens ; Ovalbumin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The response of circulating immune complexes (CIC) to food challenge was assessed in 15 subjects with IgA nephropathy (IgAN) and recurrent macroscopic haematuria. CIC were measured by solid-phase C1q binding assay (SP-C1q), immunoglobulin class-specific polyethylene glycol (PEG) precipitation assays (PEG-G, PEG-A, PEG-M) and by an antigen (ovalbumin)-specific radioimmunoassay after acid dissociation (OA-IC). CIC were measured when the subjects were fasting and hourly for 6 h after a test meal containing eggs. All 15 subjects were tested while clinically quiescent (remission) and 6 were tested again during episodes of macroscopic haematuria (relapse). The PEG-A CIC response to food challenge was significantly exaggerated in IgAN remission compared with controls at 3–6 h after food. There were also non-significant increases in PEG-G, though not in PEG-M. Paired data showed further exaggeration of PEG-G, PEG-A and PEG-M responses to food during IgAN relapse, but significance was not attained if the findings in 1 subject were separated. In this individual a florid clinical relapse with transient decline in renal function was associated with very high levels of PEG-IC, and only in this patient in relapse was OA-IC detectable, confirming that some PEG-precipitated material represented antigen-antibody complexes containing food antigen.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2277
    Keywords: Nifedipine, CyA, renal transplantation ; CyA, nifedipine, renal transplantation ; Renal transplantation, nifedipine, CyA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to test the hypothesis that nifedipine will improve graft survival in cyclosporin A (CyA)-treated renal transplant recipients. One hundred and forty-seven patients were randomised to one of three regimens. Group A received CyA, 7 mg/kg per day, and prednisolone; group B followed the same regimen as group A plus oral nifedipine and group C received CyA, 4 mg/kg per day, prednisolone and azathioprine. Calcium channel blockers were avoided in groups A and C. The crude 2-year (P=0.0223) and 4-year (P=0.0181) graft survival was significantly better in group B (86% and 81%, respectively) than in group A (75% and 63%, respectively). Delayed initial function was seen least frequently in group B (10.2%) compared to groups A (31%) and C (28%; P〈0.01). Group B also experienced fewer rejection episodes than groups A and C (P〈0.05). We conclude that the combination of oral nifedipine and CyA significantly improves initial graft function, rejection frequency and long term graft survival.
    Type of Medium: Electronic Resource
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