1508 gliadin-induced hypocomplementemic membranous glo-merulonephritis

1508 gliadin-induced hypocomplementemic membranous glo-merulonephritis

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ABSTRACT A 13-month-old presented with intractable diarrhea, marked proteinuria (8 g/24 hrs) and severe nephrotic syndrome. Small bowel biopsy showed celiac disease. Renal biopsy demonstrated epimembranous glomerulonephritis with deposition of IgG, IgA, C3, properdin and substantial amounts of gliadin. Serum complement studies showed marked depression of CH50 titers and classical pathway (CP) proteins C1, C2, C3 and C3-C9. Alternative pathway (AP) proteins factor B, properdin, β1H and C3bINA were equally depressed as was the lysis of unsensitized rabbit erythrocytes by the patient's serum. In all cases, values were more than 3 S.D. from the age-corrected mean. No C3NeF or circulating immune complexes by Raji cell assay were detectable. Treatment with prednisone, restricted diet, and hyperalimentation allowed for a reduction in diarrhea and proteinuria (400 mg/24 hrs) as well as an increase in all CP proteins within 2 months. Serum levels of β1H and C3bINA also rose but the remainder of the AP abnormalities persisted for several more months before returning to normal. These data suggest that gliadin, adsorbed via the GI tract and deposited within the glomerulus, may have induced the development of membranous glomerulonephritis in this child. Further, the bound gliadin may also have been responsible for the IgG-mediated CP activation and, either alone or with IgA, the more persistent AP activation. ARTICLE PDF AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Departments of Medicine and Pediatrics, SUNY, Upstate Medical Center, Syracuse, NY. Nancy B Jermanovitch, Roger E Spitzer & Judith M Sondheimer Authors * Nancy B Jermanovitch View author publications You can also search for this author inPubMed Google Scholar * Roger E Spitzer View author publications You can also search for this author inPubMed Google Scholar * Judith M Sondheimer View author publications You can also search for this author inPubMed Google Scholar RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Jermanovitch, N., Spitzer, R. & Sondheimer, J. 1508 GLIADIN-INDUCED HYPOCOMPLEMENTEMIC MEMBRANOUS GLO-MERULONEPHRITIS. _Pediatr Res_ 15 (Suppl 4), 694 (1981). https://doi.org/10.1203/00006450-198104001-01531 Download citation * Issue Date: 01 April 1981 * DOI: https://doi.org/10.1203/00006450-198104001-01531 SHARE THIS ARTICLE Anyone you share the following link with will be able to read this content: Get shareable link Sorry, a shareable link is not currently available for this article. Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative

ABSTRACT A 13-month-old presented with intractable diarrhea, marked proteinuria (8 g/24 hrs) and severe nephrotic syndrome. Small bowel biopsy showed celiac disease. Renal biopsy


demonstrated epimembranous glomerulonephritis with deposition of IgG, IgA, C3, properdin and substantial amounts of gliadin. Serum complement studies showed marked depression of CH50 titers


and classical pathway (CP) proteins C1, C2, C3 and C3-C9. Alternative pathway (AP) proteins factor B, properdin, β1H and C3bINA were equally depressed as was the lysis of unsensitized rabbit


erythrocytes by the patient's serum. In all cases, values were more than 3 S.D. from the age-corrected mean. No C3NeF or circulating immune complexes by Raji cell assay were


detectable. Treatment with prednisone, restricted diet, and hyperalimentation allowed for a reduction in diarrhea and proteinuria (400 mg/24 hrs) as well as an increase in all CP proteins


within 2 months. Serum levels of β1H and C3bINA also rose but the remainder of the AP abnormalities persisted for several more months before returning to normal. These data suggest that


gliadin, adsorbed via the GI tract and deposited within the glomerulus, may have induced the development of membranous glomerulonephritis in this child. Further, the bound gliadin may also


have been responsible for the IgG-mediated CP activation and, either alone or with IgA, the more persistent AP activation. ARTICLE PDF AUTHOR INFORMATION AUTHORS AND AFFILIATIONS *


Departments of Medicine and Pediatrics, SUNY, Upstate Medical Center, Syracuse, NY. Nancy B Jermanovitch, Roger E Spitzer & Judith M Sondheimer Authors * Nancy B Jermanovitch View author


publications You can also search for this author inPubMed Google Scholar * Roger E Spitzer View author publications You can also search for this author inPubMed Google Scholar * Judith M


Sondheimer View author publications You can also search for this author inPubMed Google Scholar RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE


Jermanovitch, N., Spitzer, R. & Sondheimer, J. 1508 GLIADIN-INDUCED HYPOCOMPLEMENTEMIC MEMBRANOUS GLO-MERULONEPHRITIS. _Pediatr Res_ 15 (Suppl 4), 694 (1981).


https://doi.org/10.1203/00006450-198104001-01531 Download citation * Issue Date: 01 April 1981 * DOI: https://doi.org/10.1203/00006450-198104001-01531 SHARE THIS ARTICLE Anyone you share the


following link with will be able to read this content: Get shareable link Sorry, a shareable link is not currently available for this article. Copy to clipboard Provided by the Springer


Nature SharedIt content-sharing initiative