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Updated: Aug 10, 2026
Assessment of Kidney Function in Mouse Models of Glomerular Disease
Published on: June 30, 2018
Crescentic glomerulonephritis is diminished in fibrinogen-deficient mice
1Division of Developmental Biology, Children's Hospital Research Foundation, Cincinnati, Ohio 45229-3039, USA.
Insights
Fibrinogen plays a key role in crescentic glomerulonephritis, a kidney disease. Reducing fibrinogen levels in mice lessened disease severity and preserved kidney function.
Area of Science:
- Nephrology
- Immunology
- Pathology
Background:
- Crescentic glomerulonephritis involves fibrin and cell accumulation in Bowman's space, leading to rapid kidney function loss.
- Fibrin deposition in glomeruli is hypothesized to drive macrophage infiltration and subsequent glomerular injury.
Purpose of the Study:
- To investigate the direct role of fibrinogen in the pathogenesis of crescentic glomerulonephritis.
- To assess the impact of fibrinogen deficiency on disease development and renal function.
Main Methods:
- Antiglomerular basement membrane nephritis was induced in both fibrinogen-deficient and control mice.
- Disease severity, crescent formation, glomerular macrophage accumulation, and renal function (serum creatinine) were evaluated.
Main Results:
- Control mice exhibited severe glomerulonephritis with significant crescent formation (46.3%).
- Fibrinogen-deficient mice showed milder disease with reduced crescent formation (24.0%, P < 0.03).
- Macrophage accumulation and serum creatinine levels were significantly lower in fibrinogen-deficient mice.
Conclusions:
- Fibrinogen is not essential but significantly contributes to crescentic glomerulonephritis development.
- Fibrinogen promotes glomerular macrophage infiltration and impairs renal filtration, exacerbating kidney injury.
Abstract:
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.
