Clinical Investigation

Kidney International (1974) 5, 292–299; doi:10.1038/ki.1974.39

Participation of immunoglobulin E (IgE) in immune-mediated glomerulonephritis

John J McPhaul Jr, Richard W Newcomb, James D Mullins, Alfred L Thompson Jr, Robert E Lordon and Phillip W Rogers

Departments of Medicine and Pathology and the Clinical Research Laboratory, Wilford Hall United States Air Force Medical Center (AFSC), Lackland Air Force Base, Texas, Childrens Asthma Research Institute and Hospital, Denver, Colorado, and Brooke General Hospital, Brooke Army Medical Center, San Antonio, Texas

Correspondence: Col. John J McPhaul Jr, USAF, MC, Aerospace Medical Laboratory (Clinical), (SGS), Wilford Hall USAF Medical Center, Lackland AFB, Texas 78236, U.S.A.

Received 3 October 1973; Revised 12 November 1973.

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Abstract

Participation of immunoglobulin E in immune-mediated glomerulonephritis. Renal biopsy specimens from 146 consecutive patients were studied by direct immunofluorescent tests for immunoglobulins G, M, A, D, E, third component of complement and fibrinogen; 46 of the patients had nephrotic syndrome. Glomerular-bound Ig was detected in glomeruli of 85 patients, and significant immunoglobulin E (IgE) in 22 of them. The granular glomerular deposits of six of the 22 patients comprised IgE as the dominant or codominant Ig class; in one patient it was the only Ig seen. In all other instances IgE was a relatively less obvious Ig component of glomerular deposits. No correlation was detected between serum IgE concentrations and glomerular IgE deposits. The six patients with notable IgE deposits had persistent disease clinically and generalized glomerular disease immunohistochemically; two of the six patients had rapidly progressive glomerulonephritis. Clinical data implicated the beta-hemolytic streptococcus as etiologic agent in three of the six patients, and suggested it in another.

Participation de l'immunoglobuline E (IgE) à la glomérulonéphrite immune. Les biopsies rénales de 146 malades ont été étudiées en immunofluorescence directe pour les immunoglobulines G, M, A, D, E, pour le torisième facteur du complément et le fibrinogène. 46 malades avaient un syndrome néphrotique. Les dépôts glomérulaires d'immunoglobulines ont été observés chez 85 malades et d'IgE chez 22 d'entre eux. Les dépôts glomérulaires granulaires de 6 des 22 malades comportaient l'IgE comme immunoglobuline dominante ou codominante. Chez un malade c'était la seule immunoglobuline observée. Dans tous les autres cas la participation de l'IgE aux dépôts glomérulaires était beaucoup moins importante. Les six malades ayant des dépôts importants d'IgE avaient une symptomatologie clinique persistante et une atteinte glomérulaire immunohistochimique généralisée; deux de ces six malades ont eu une glomérulonéphrite rapidement progressive. Les arguments cliniques impliquaient le streptocoque beta hémolytique comme agent étiologique trois de ces six malades et le suggéraient chez un autre.

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