| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Articles in PresS, published online ahead of print August 21, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.0002.2001
Submitted on January 5, 2001
Accepted on July 5, 2001
1 Developmental Biology, Children's Hospital Research Foundation, Cincinnati, OH, USA
2 Pathology, Children's Hospital Research Foundation, Cincinnati, OH, USA
3 Medicine, Monash University, Melbourne, Victoria, Australia
* To whom correspondence should be addressed. E-mail: degej0{at}chmcc.org.
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, anti-glomerular 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 per glomerular cross-section) relative to control mice (3.9 ± 1.4 macrophages per 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 while 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.
This article has been cited by other articles:
|
|
 |
|
  J. Apostolopoulos, M. J. Hickey, L. Sharma, P. Davenport, L. Moussa, W. G. James, J. L. Gregory, A. R. Kitching, M. Li, and P. G. Tipping The cytoplasmic domain of tissue factor in macrophages augments cutaneous delayed-type hypersensitivity J. Leukoc. Biol., April 1, 2008; 83(4): 902 - 911. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. C. Banas, B. Banas, K. L. Hudkins, T. A. Wietecha, M. Iyoda, E. Bock, P. Hauser, J. W. Pippin, S. J. Shankland, K. D. Smith, et al. TLR4 Links Podocytes with the Innate Immune System to Mediate Glomerular Injury J. Am. Soc. Nephrol., April 1, 2008; 19(4): 704 - 713. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. A. Eddy and A. B. Fogo Plasminogen Activator Inhibitor-1 in Chronic Kidney Disease: Evidence and Mechanisms of Action J. Am. Soc. Nephrol., November 1, 2006; 17(11): 2999 - 3012. [Full Text] [PDF]
|
|
|
|
 |
|
 J I Shin, J M Park, Y H Shin, J S Lee, and H J Jeong Role of mesangial fibrinogen deposition in the pathogenesis of crescentic Henoch-Schonlein nephritis in children J. Clin. Pathol., November 1, 2005; 58(11): 1147 - 1151. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. Kriz, B. Hahnel, H. Hosser, T. Ostendorf, S. Gaertner, B. Kranzlin, N. Gretz, F. Shimizu, and J. Floege Pathways to Recovery and Loss of Nephrons in Anti-Thy-1 Nephritis J. Am. Soc. Nephrol., July 1, 2003; 14(7): 1904 - 1926. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. R. Kitching, Y. Z. Kong, X. Ru Huang, P. Davenport, K. L. Edgtton, P. Carmeliet, S. R. Holdsworth, and P. G. Tipping Plasminogen Activator Inhibitor-1 Is a Significant Determinant of Renal Injury in Experimental Crescentic Glomerulonephritis J. Am. Soc. Nephrol., June 1, 2003; 14(6): 1487 - 1495. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
