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Biomedical subjects

G E Lees

Publications and source records attributed to G E Lees.

42 records · Page 3Linked to original sources
PubMed1978

Pulmonary edema in a dog with acute pancreatitis and cardiac disease.

Acute pancreatitis and cardiac disease were diagnosed in a dog with pulmonary edema. The early clinical course and initial thoracic radiographs suggested that the pulmonary edema was noncardiogenic. The late clinical course was complicated by heart failure. The dog died, and a necropsy was performed. Histologically, an acute, severe capillary-alveolar membrane lesion was found in the lungs. Review of the human medical literature indicated that respiratory complications, including pulmonary edema, are commonly recognized in people with acute pancreatitis. Furthermore, in acute pancreatitis of human beings, the existence of specific mechanisms of pulmonary injury is suspected. Retrospective consideration of this case suggested that the initial pulmonary edema was induced by acute pancreatitis.

Acute Disease↗
PubMedDate not supplied

Glomerular ultrastructural findings similar to hereditary nephritis in 4 English cocker spaniels.

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.

Animals↗
PubMedDate not supplied

Early diagnosis of familial nephropathy in English cocker spaniels.

Two litters of English cocker spaniels (ECSs) produced by familial nephropathy (FN) carriers were evaluated to characterize the early features of this disease. Three puppies developed FN. Proteinuria, which began when these puppies were five-to-eight months old, was the first abnormality detected. Proteinuria persisted while each puppy's growth rate slowed, and renal function gradually deteriorated. The interval from onset of proteinuria to development of azotemia was two-to-nine months. Characteristic glomerular capillary basement membrane (GCBM) lesions were seen with transmission electron microscopy (TEM) of renal biopsy specimens obtained during this interval. Ultrastructural GCBM lesions progressed substantially during the interval from biopsy to necropsy. However, routine light microscopic findings did not allow definitive diagnosis of FN in either biopsy or necropsy specimens. Detection of FN can be accomplished by screening at-risk ECSs for proteinuria. Renal biopsies are required to confirm the diagnosis in dogs for which proteinuria cannot be explained otherwise. Percutaneous needle biopsy specimens sufficient for TEM must be used to examine the GCBM to make a definitive diagnosis.

Aging↗