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Divisions of 1 Developmental Biology and 2 Pathology, Children's Hospital Research Foundation, Cincinnati, Ohio 45229-3039; and 3 Centre for Inflammatory Diseases, Monash Medical Centre, Department of Medicine, Monash University, Clayton 3168, Melbourne, Australia
First published August 21, 2001;
00.1152/ajprenal.0002.2001.
Crescentic forms of glomerulonephritis
are characterized by the accumulation of fibrin and cells in Bowman's
space and are associated with a rapid loss of renal function.
Accumulation of fibrin in the glomerular tufts is thought to promote
macrophage infiltration and glomerular injury. To directly explore the
role of fibrin(ogen) in the development of crescentic
glomerulonephritis, antiglomerular basement membrane nephritis was
induced in fibrinogen-deficient and control mice. Glomeruli from
control mice developed severe disease including fibrin deposits,
inflammatory cell accumulation, and crescent formation (46.3 ± 7.3% of glomeruli). Fibrinogen-deficient mice developed significantly
milder disease with fewer glomerular crescents (24.0 ± 4.7% of
glomeruli; P < 0.03). Glomerular macrophage accumulation was diminished in fibrinogen-deficient mice (0.9 ± 0.4 macrophages/glomerular cross section) relative to control mice
(3.9 ± 1.4 macrophages/glomerular cross section;
P < 0.03). Finally, renal function as assessed by
serum creatinine was better maintained in fibrinogen-deficient mice.
These results indicate that although fibrin(ogen) is not essential for
the development of glomerular crescents, it contributes significantly
to the pathogenesis of crescentic glomerulonephritis by promoting
glomerular macrophage accumulation and impairing filtration.
knockout; immune-mediated response
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