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J Am Soc Nephrol 14:1904-1926, 2003
© 2003 American Society of Nephrology

SPECIAL FEATURE

Pathways to Recovery and Loss of Nephrons in Anti-Thy-1 Nephritis

Wilhelm Kriz*, Bruni Hähnel*, Hiltraud Hosser*, Tammo Ostendorf{dagger}, Soeren Gaertner{dagger}, Bettina Kränzlin{ddagger}, Norbert Gretz{ddagger}, Fujio Shimizu§ and Jürgen Floege{dagger}

*Institute of Anatomy and Cell Biology, University of Heidelberg, Germany; {dagger}Division of Nephrology and Immunology, Klinikum Aachen, Germany; {ddagger}Medical Research Center, University of Heidelberg, Mannheim, Germany; and §Institute of Nephrology, Niigata University, Japan.

Correspondence to Prof. Dr. Wilhelm Kriz, Institute of Anatomy and Cell Biology, University of Heidelberg, Im Neuenheimer Feld 307, D-69120 Heidelberg, Germany. Phone: 49-6221-548680; Fax: 49-6221-544951;

ABSTRACT. The present histopathologic study of anti-Thy-1.1 models of mesangioproliferative glomerulonephritis in rats provides a structural analysis of damage development and of pathways to recovery and to nephron loss. As long as the disease remains confined to the endocapillary compartment, the damage may be resolved or recover with a mesangial scar. Irreversible lesions with loss of nephrons emerge from extracapillary processes with crucial involvement of podocytes, leading to tuft adhesions to Bowman‘s capsule (BC) and subsequent crescent formation. Two mechanisms appeared to be responsible: (1) Epithelial cell proliferation at BC and the urinary orifice and (2) misdirected filtration and filtrate spreading on the outer aspect of the nephron. Both may lead to obstruction of the tubule, disconnection from the glomerulus, and subsequent degeneration of the entire nephron. No evidence emerged to suggest that the kind of focal interstitial proliferation associated with the degeneration of injured nephrons was harmful to a neighboring healthy nephron. E-mail: wilhelm.kriz@urz.uni-heidelberg.de




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