Course of transplanted Heymann nephritis kidney in normal host. Implications for mechanism of proteinuria in membranous glomerulonephropathy

Sudesh P Makker, J. J. Kanalas

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Abstract

Heymann nephritis [model of membranous glomerulonephropathy (MGN)] kidneys (n = 20) with proteinuria were transplanted into unilaterally nephrectomized normal syngeneic Lewis recipient rats to study the course of established MGN lesion in normal milieu. Concurrent with the loss of C3 staining from the MGN lesion at 2 to 4 wk after transplantation, the proteinuria decreased from the transplanted kidney (p < 0.02). Thereafter, from 2 to 28 wk no further decrease was noted in proteinuria which stabilized at a lower but still abnormal level. No appreciable decrease in IgG deposits in MGN lesion was noted up to 12 wk but at 28 wk the deposits had decreased significantly (p < 0.005). However, the deposits did not resolve completely even at 40 wk. The results indicate that in GMN one component of proteinuria is due to ongoing activation of C with the deposition of new antibody and the other is perhaps due to structural damage to glomerular filter. The former appears reversible and the later irreversible. Although the resolution of IgG deposits in the lesion is very slow significant improvement can occur with time (several months).

Original languageEnglish (US)
Pages (from-to)3406-3410
Number of pages5
JournalJournal of Immunology
Volume142
Issue number10
StatePublished - 1989
Externally publishedYes

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Membranous Glomerulonephritis
Proteinuria
Kidney
Immunoglobulin G
Transplantation
Staining and Labeling
Antibodies

ASJC Scopus subject areas

  • Immunology

Cite this

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title = "Course of transplanted Heymann nephritis kidney in normal host. Implications for mechanism of proteinuria in membranous glomerulonephropathy",
abstract = "Heymann nephritis [model of membranous glomerulonephropathy (MGN)] kidneys (n = 20) with proteinuria were transplanted into unilaterally nephrectomized normal syngeneic Lewis recipient rats to study the course of established MGN lesion in normal milieu. Concurrent with the loss of C3 staining from the MGN lesion at 2 to 4 wk after transplantation, the proteinuria decreased from the transplanted kidney (p < 0.02). Thereafter, from 2 to 28 wk no further decrease was noted in proteinuria which stabilized at a lower but still abnormal level. No appreciable decrease in IgG deposits in MGN lesion was noted up to 12 wk but at 28 wk the deposits had decreased significantly (p < 0.005). However, the deposits did not resolve completely even at 40 wk. The results indicate that in GMN one component of proteinuria is due to ongoing activation of C with the deposition of new antibody and the other is perhaps due to structural damage to glomerular filter. The former appears reversible and the later irreversible. Although the resolution of IgG deposits in the lesion is very slow significant improvement can occur with time (several months).",
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T1 - Course of transplanted Heymann nephritis kidney in normal host. Implications for mechanism of proteinuria in membranous glomerulonephropathy

AU - Makker, Sudesh P

AU - Kanalas, J. J.

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N2 - Heymann nephritis [model of membranous glomerulonephropathy (MGN)] kidneys (n = 20) with proteinuria were transplanted into unilaterally nephrectomized normal syngeneic Lewis recipient rats to study the course of established MGN lesion in normal milieu. Concurrent with the loss of C3 staining from the MGN lesion at 2 to 4 wk after transplantation, the proteinuria decreased from the transplanted kidney (p < 0.02). Thereafter, from 2 to 28 wk no further decrease was noted in proteinuria which stabilized at a lower but still abnormal level. No appreciable decrease in IgG deposits in MGN lesion was noted up to 12 wk but at 28 wk the deposits had decreased significantly (p < 0.005). However, the deposits did not resolve completely even at 40 wk. The results indicate that in GMN one component of proteinuria is due to ongoing activation of C with the deposition of new antibody and the other is perhaps due to structural damage to glomerular filter. The former appears reversible and the later irreversible. Although the resolution of IgG deposits in the lesion is very slow significant improvement can occur with time (several months).

AB - Heymann nephritis [model of membranous glomerulonephropathy (MGN)] kidneys (n = 20) with proteinuria were transplanted into unilaterally nephrectomized normal syngeneic Lewis recipient rats to study the course of established MGN lesion in normal milieu. Concurrent with the loss of C3 staining from the MGN lesion at 2 to 4 wk after transplantation, the proteinuria decreased from the transplanted kidney (p < 0.02). Thereafter, from 2 to 28 wk no further decrease was noted in proteinuria which stabilized at a lower but still abnormal level. No appreciable decrease in IgG deposits in MGN lesion was noted up to 12 wk but at 28 wk the deposits had decreased significantly (p < 0.005). However, the deposits did not resolve completely even at 40 wk. The results indicate that in GMN one component of proteinuria is due to ongoing activation of C with the deposition of new antibody and the other is perhaps due to structural damage to glomerular filter. The former appears reversible and the later irreversible. Although the resolution of IgG deposits in the lesion is very slow significant improvement can occur with time (several months).

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