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J Am Soc Nephrol 10:499-506, 1999
© 1999 American Society of Nephrology

REGULAR ARTICLES

Prominence of Cell-Mediated Immunity Effectors in "Pauci-Immune" Glomerulonephritis

MALCOLM A. CUNNINGHAM*, XIAO RU HUANG*, JOHN P. DOWLING{dagger}, PETER G. TIPPING* and STEPHEN R. HOLDSWORTH*

* Centre for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
{dagger} Department of Pathology, Monash University, Alfred Hospital, Prahran, Victoria, Australia.

Correspondence to Dr. Malcolm Cunningham, Centre for Inflammatory Diseases, Department of Medicine, 5th Floor Block E, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria, 3168, Australia. Phone: 613 9550 5544; Fax: 613 9550 5524; E-mail: malcolmc{at}mmcc1.cc.monash.edu.au

Abstract. The majority of patients with rapidly progressive crescentic glomerulonephritis show histologic features of extensive necrosis and focal and segmental proliferation with fibrin production, but little or absent Ig deposition in the glomerulus. This subcategory of the disease, labeled "pauci-immune" glomerulonephritis, has recently been shown to be associated with the presence of antineutrophil cytoplasmic antibody in the patient's circulation (but not within the glomerulus). The absence of the effectors of humoral immunity at the site of renal injury led to this investigation of the contribution of cell-mediated immunity to the glomerular injury in this form of glomerulonephritis. In 15 patients presenting acutely with pauci-immune glomerulonephritis, CD3-positive T cells (3.7 ± 2.5 [mean ± SD] cells per glomerular cross section, [c/gcs]), CD45RO-positive T cells (2.7 ± 1.9 c/cgs), macrophages (7.3 ± 6.1 c/gcs), fibrin (3+), and endothelial-associated tissue factor were demonstrated to be prominent in glomeruli. These mediators were absent in a group of 12 patients with thin basement membrane disease and only occasionally observed in a group of eight patients with "humorally mediated" (noncrescentic) glomerulonephritis. Thus, in pauci-immune glomerulonephritis, there is the development of significant cell-mediated immunity with activated T cells, macrophages, tissue factor, and fibrin at the site of glomerular injury, suggesting that this glomerular disease is most likely a manifestation of T cell-directed cognate immune injury.




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