Circulating Anti-Tubular Basement Membrane Antibody in a Variety of Human Renal Diseases

Cattran, Daniel C.

doi:10.1159/000181943

Cited by 14 publications

(5 citation statements)

References 16 publications

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“…TBM deposition is not common in anti-GBM nephritis [22]. We suggested that the high detection rate of IgG deposits along TBM may be due to the high sensitivity of immunohistochemistry used in the current study.…”

Section: Discussionmentioning

confidence: 82%

The distribution of IgG subclass deposition on renal tissues from patients with anti-glomerular basement membrane disease

Cui

Liu

et al. 2013

BMC Immunol

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BackgroundRenal injury of anti-glomerular basement membrane (GBM) disease is defined by the linear deposition of IgG along GBM and rapidly progressive glomerulonephritis. To date, the distribution of anti-GBM IgG subclasses on renal tissue is still unclear. In the current study, we investigated the deposition of the four IgG subclasses using immunohistochemistry in the renal biopsy specimens from 46 patients with anti-GBM disease.ResultsAll four IgG subclasses can be detected within the GBM. Anti-GBM IgG3 was detected in all patients (100%), with 39 (84.8%) patients presenting with weak segmental staining and 7 (15.2%) patients with strong linear deposition. Anti-GBM IgG2 was detected in 22 (47.8%) patients, with 20 (90.9%) patients having weak segmental deposition and 2 (9.1%) patients presenting strong linear staining. Anti-GBM IgG1 and IgG4 were detected in 9 (19.6%) and 7 (15.2%) patients, respectively. IgG deposition along tubular basement membrane (TBM) was also detected in 31 (67.4%) patients. Among them, the IgG subclass distribution was similar to that of the deposition within the GBM: IgG1 6.5% (2/31), IgG2 45.2% (14/31), IgG3 100% (31/31) and IgG4 9.7% (3/31). We observed increased inflammatory cell infiltration into the interstitium in patients with increased anti-TBM IgG3 deposits (P=0.031).ConclusionsAnti-GBM IgG3 predominantly deposits along GBM and TBM on renal biopsy specimens from patients with anti-GBM disease, which may be involved in the development of renal injury of the disease.

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Section: Discussionmentioning

confidence: 82%

The distribution of IgG subclass deposition on renal tissues from patients with anti-glomerular basement membrane disease

Cui

Liu

et al. 2013

BMC Immunol

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“…Test results were read from the standard curve with a range of 0-100 units. Free antibody was determined by two methods: indirect immunofluorescence (IFF) using normal rat kidney as a target with counterstaining by goat antirat IgG and by hemaggluti nation assay (HA) (20).…”

Section: Methodsmentioning

confidence: 99%

“…A positive control for HA consisted of sensitized cells plus rabbit antirat FXIA [20] in serial dilution and a negative control was normal rat serum as well as test rat serum against unsensitized cells plus diluent and phosphate-buffered saline. All rats were bled serially every 1-2 weeks, in order to compare CIC and Ab changes over time.…”

Section: Methodsmentioning

confidence: 99%

Effect of Ciclosporin on Active Heymann Nephritis

Cattran¹

1988

Nephron

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The effects of ciclosporin on active Heymann’s nephritis starting at different times after induction was studied. When given at the time of antigen injection, ciclosporin blocked both free antibody and circulating immune complex formation. Immunopathology and renal function tests remained normal in this group despite a rise in both these parameters to control values after ciclosporin was discontinued. When given at a later stage of the disease process, despite suppression of both antibody and complex formation, neither pathology nor functional parameters were modified. This suggests either a limited time frame for immunologically mediated injury in Heymann’s nephritis or that early treatment with ciclosporin may permanently alter a vital primary step in the immunopathogenesis.

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“…Human and rat FX1A fraction against rabbit anti-FX1A was used as a positive control with a negative control normal rat sera against the anti-FXIA antibody. Free Ab was determined by two methods: IIF using normal human kidney as a target with counterstaining by goat antirat IgG and by hemagglutination assay (HA) [2]. A positive control consisted of sensitized cells plus rabbit anti-FXIA in serial dilution and a negative control was normal rat serum as well as test rat serum against unsensitized cells plus diluent and PBS.…”

Section: Immune Complex Determinationmentioning

confidence: 99%

Experimental Membranous Glomerulonephritis

Cattran¹,

Chodirker²

1982

Nephron

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Active Heymann’s nephritis was induced in Wistar rats by a single injection of human renal tubular epithelial antigen (FXIA) and the animals were followed for 1 year. Correlations were made between circulating anti-FXIA antibody, circulating immune complexes (CIC) and pathology. The disease progressed pathologically through all stages of membranous nephropathy associated with a high level of free antibody but without significant detectable CIC, suggesting that the dominant disease mechanism may be the reaction between circulating free antibody and a fixed glomerular antigen rather than the deposition of CIC.

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Circulating Anti-Tubular Basement Membrane Antibody in a Variety of Human Renal Diseases

Cited by 14 publications

References 16 publications

The distribution of IgG subclass deposition on renal tissues from patients with anti-glomerular basement membrane disease

The distribution of IgG subclass deposition on renal tissues from patients with anti-glomerular basement membrane disease

Effect of Ciclosporin on Active Heymann Nephritis

Experimental Membranous Glomerulonephritis

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