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Research Article Free access | 10.1172/JCI107686

Immunofluorescent Localization of Antihemophilic Factor Antigen and Fibrinogen in Human Renal Diseases

John R. Hoyer, Alfred F. Michael, and Leon W. Hoyer

Department of Pediatrics, University of Minnesota School of Medicine, Minneapolis, Minnesota 55455

Department of Medicine, University of Connecticut School of Medicine, Farmington, Connecticut 06032

Find articles by Hoyer, J. in: PubMed | Google Scholar

Department of Pediatrics, University of Minnesota School of Medicine, Minneapolis, Minnesota 55455

Department of Medicine, University of Connecticut School of Medicine, Farmington, Connecticut 06032

Find articles by Michael, A. in: PubMed | Google Scholar

Department of Pediatrics, University of Minnesota School of Medicine, Minneapolis, Minnesota 55455

Department of Medicine, University of Connecticut School of Medicine, Farmington, Connecticut 06032

Find articles by Hoyer, L. in: PubMed | Google Scholar

Published May 1, 1974 - More info

Published in Volume 53, Issue 5 on May 1, 1974
J Clin Invest. 1974;53(5):1375–1384. https://doi.org/10.1172/JCI107686.
© 1974 The American Society for Clinical Investigation
Published May 1, 1974 - Version history
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Abstract

Tissue localization of antihemophilic factor (AHF, factor VIII) antigen and fibrinogen by immunofluorescent microscopy was determined in 146 specimens of normal and diseased kidneys. AHF antigen was present in the endothelial cells of glomeruli, peritubular capillaries, arteries, and veins of normal kidneys; a distribution similar to that in other tissues. In scleroderma and malignant hypertension, deposition of AHF antigen and fibrinogen was limited to the markedly thickened endothelial layers of arteries. More extensive intense deposition of both AHF antigen and fibrinogen in glomeruli and in arterial walls were present in hyperacute renal homograft rejection, hemolyticuremic syndrome, postpartum renal failure, and in some cases of acute homograft rejection. In contrast, deposition of fibrinogen was observed in glomerular epithelial cresents in severe proliferative glomerulonephritis, but AHF deposition was not present in these lesions. Glomerular deposition of fibrinogen without increased AHF standing was also detected in renal tissue from patients with anaphylactoid purpura nephritis and in recurrent macroscopic hematuria with focal glomerulonephritis. Increased staining of peritubular capillaries with anti-AHF was seen in diseased kidneys irrespective of etiology. Immunofluorescent localization of AHF, a participant in the intrinsic coagulation pathway, offers a new way by which to analyze the mechanisms responsible for fibrinogen deposition in disease.

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