Vet Pathol Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by KolbjØrnsen, O.
Right arrow Articles by Jansen, J. H.
PubMed
Right arrow PubMed Citation
Right arrow Articles by KolbjØrnsen, O.
Right arrow Articles by Jansen, J. H.
Vet Pathol 45:467-474 (2008)
© 2008 American College of Veterinary Pathologists
IMMUNOINFLAMMATORY, DEGENERATIVE, NUTRITIONAL, TRAUMATIC, AND GENETIC DISEASES

End-Stage Kidney Disease Probably due to Reflux Nephropathy with Segmental Hypoplasia (Ask-Upmark Kidney) in Young Boxer Dogs in Norway. A Retrospective Study

Ø. KolbjØrnsen, M. Heggelund and J. H. Jansen

National Veterinary Institute, Department of Animal Health, Section for Pathology, Oslo, Norway (ØK), Oslo Animal Clinic, Oslo, Norway (MH), Norwegian School of Veterinary Science, Department of Basic Sciences and Aquatic Medicine, Section for Biochemistry and Physiology, Oslo, Norway (JHJ)

Abstract

This paper is a retrospective morphologic study of 7 young Boxer dogs, showing end-stage kidney lesions compatible with chronic pyelonephritis with severe segmental cortical atrophy and fibrosis, associated with chronic tubulointerstitial inflammation of varying degree. Azotemia was observed in 6 of the 7 cases. The gross kidney lesions were as follows: bilateral small kidneys with numerous segmental cortical scars causing depression of the renal cortical surface. Histologic examination revealed salient atrophy of nephrons, including paucity of glomeruli, glomerulocystic lesions, colloid-filled tubular microcysts, and a conspicuously increased occurrence of arteries with narrowed lumina caused by intimal thickening. These segmental abnormalities were accompanied by pronounced interstitial fibrosis. All but 1 dog showed salient tubulointerstitial lympho-plasmacytic infiltration, which in 3 cases also included diffuse infiltration of polymorphonuclear neutrophilic leukocyte (PMN)-cells and occurrence of tubular PMN-casts. Morphologic signs of abnormal metanephric differentiation (renal dysplasia) were observed in all cases in the form of atypical tubules or asynchronous nephronic development (immature glomeruli) or both. However, other morphologic primary dysplastic features were absent. Based on the morphologic features, it is concluded that the end-stage kidney disease in these young Boxer dogs was the result of chronic atrophic nonobstructive pyelonephritis, most probably caused by vesico-ureteral reflux, compatible with reflux nephropathy causing segmental hypoplasia (Ask-Upmark kidney) in man. It is proposed that atypical tubular epithelium in the form of adenomatoid proliferation of collecting duct epithelial cells should be considered an acquired compensatory lesion, rather than the result of disorganized metanephric development.

Key words: Blood chemical analysis; boxer; dogs; juvenile nephropathy; kidney failure; nephrosclerosis; pyelonephritis; retrospective studies; uremia; vesico-ureteral reflux.

Request reprints from Dr. Ø Kolbjørnsen, National Veterinary Institute, Department of Animal Health, Section for Pathology, PO Box 8156 Dep., NO-0033, Oslo (Norway). E-mail: oyvor.kolbjornsen{at}vetinst.no






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2008 by the American College of Veterinary Pathologists.