Primary renal allograft dysfunction Kirk Foster, MD, David J Cohen, MD, Vivette D D'Agati, MD, Glen S Markowitz, MD  American Journal of Kidney Diseases  Volume 44, Issue 2, Pages 376-381 (August 2004) DOI: 10.1053/j.ajkd.2003.10.047 Copyright © 2004 National Kidney Foundation, Inc. Terms and Conditions

Fig 1 (A) Low-power view shows diffuse tubular degenerative changes characterized by luminal ectasia and cytoplasmic simplification. There is diffuse interstitial edema. A single glomerulus appears unremarkable. (Hematoxylin and eosin, original magnification ×100.) (B) On high-power view, tubular casts appear eosinophilic, display “lines of fracture,” and are surrounded by adherent mononuclear leukocytes. There is mild interstitial inflammation and focal, mild tubulitis. (Hematoxylin and eosin, original magnification ×250.) (C) Another tubular cast displays prominent adherent mononuclear leukocytes. (Hematoxylin and eosin, original magnification ×250.) (D and E) The tubular casts exhibited strong staining for κ light chain (D) but only weak and focal staining for λ light chain (E). (Both, original magnification ×250.) (F) On review, similar fractured tubular casts with adherent monocytes were present in the first allograft biopsy. Immunofluorescence had not been performed. (Hematoxylin and eosin, original magnification ×250.) American Journal of Kidney Diseases 2004 44, 376-381DOI: (10.1053/j.ajkd.2003.10.047) Copyright © 2004 National Kidney Foundation, Inc. Terms and Conditions