Small Animal Medicine and Surgery, College of Veterinary Medicine, Texas A & M University, College Station, TX 77843–4474.
Glomerular Ultrastructural Findings Similar to Hereditary Nephritis in 4 English Cocker Spaniels
Article first published online: 28 JUN 2008
Journal of Veterinary Internal Medicine
Volume 11, Issue 2, pages 80–85, March 1997
How to Cite
Lees, G. E., Wilson, P. D., Helman, R. G., Homco, L. D. and Frey, M. S. (1997), Glomerular Ultrastructural Findings Similar to Hereditary Nephritis in 4 English Cocker Spaniels. Journal of Veterinary Internal Medicine, 11: 80–85. doi: 10.1111/j.1939-1676.1997.tb00077.x
- Issue published online: 28 JUN 2008
- Article first published online: 28 JUN 2008
- Accepted September 23, 1996
Renal disease affecting 3 male and 1 female English Cocker Spaniels was studied. Clinical features of the disease included proteinuria and progressive deterioration of renal function. Dogs were 11 to 27 months old when euthanized because of severe chronic renal failure. Grossly, the renal cortices were thin. Light microscopic evaluation revealed diffuse glomerular disease characterized by mesangial thickening, glomerular fibrosis, periglomerular fibrosis, and glomerular obsolescence. Based on these clinical and pathologic features, familial nephropathy of English Cocker Spaniels was suspected despite the fact that the individual dogs were not closely related. On transmission electron microscopy, a distinctive ultrastructural lesion was observed in the glomerular basement membranes (GBM) of all dogs. The GBM exhibited extensive thickening, multilaminar splitting, and fragmentation. Electron dense deposits, suggestive of immunocomplex glomerular disease, were notably absent. A similar ultrastructural GBM lesion is found in human beings and Samoyeds with hereditary nephritis, diseases caused by mutations in the type IV collagen genes. Familial nephropathy in English Cocker Spaniels may be a form of hereditary nephritis caused by a mutation in one of the collagen IV genes.