Minnesota Veterinary Diagnostic Laboratory
College of Veterinary Medicine
1333 Gortner Ave.
St. Paul, MN 551081-800-605-8787
612-625-8787
Fax: 612-624-8707
e-mail: mvdl@tc.umn.edu
Received: 11/28/01
Species: CANINE
Breed: MIX
Age: 13
Sex: FEMALE
Specimen: Necropsy samples of spleen, kidney, pancreas, glossal mucosa, liver, lung, and heart.
Kidney: Renal glomeruli throughout this section contained extensive deposits of amorphous, pale eosinophilic material consistent with amyloid. These deposits resulted in marked compression of glomerular vessels and reduced apparent perfusion. Renal proximal tubules showed mild atrophy and occasional hyaline casts were seen in distal tubules. There was also a wedge-shaped region of acute necrosis and hemorrhage extending from the renal capsule into the medulla, consistent with a renal infarct.
Spleen: The splenic parenchyma in this section showed diffuse necrosis and hemorrhage. A splenic artery adjacent to the necrotic region was mostly occluded by an organizing thrombus.
Pancreas: There was marked peripancreatic fat necrosis which showed extensive infiltrates of macrophages and some PMNs. Inflammation and edema tended to separate the pancreatic lobules and there was some extension of the inflammation into the pancreatic parenchyma- Along some margins there was formation of fibrous (scar) tissue around the periphery of necrotic zones.
Glossal mucosa: The mucosa in these sections was extensively ulcerated and the ulcerated surfaces covered with fibrinonecrotic exudate. Mucosa beneath the ulcers contained infiltrates of PMNs and macrophages and showed moderate granulation tissue proliferation. Additionally in the surrounding lamina propria there were deposits of homogeneous eosinophilic material consistent with amyloid in perivascular or interstitial locations.
Liver: In both sections of liver examined there were fairly well-delineated zones of acute coagulation necrosis of hepatic parenchyma. At the margins of these areas there were marked infiltrates of PMNs and macrophages. In hepatic lobules outside of the necrotic zones there was marked patchy vacuolar change of hepatocytes consistent with steroid hepatopathy.
Lung: There were a few widely scattered foci of interstitial mineralization and scattered anthracite pigment-laden macrophages in peribronchiolar locations. Both findings are common age-related findings in dogs.
Heart: Myocardial arteries in this section showed marked, irregular thickening of the arterial wall by deposits of homogeneous eosinophilic material consistent with amyloid. These deposits tended to narrow the arterial lumen and in some areas the deposits were invested with many small endothelial -lined channels. In the adjacent myocardium there were fairly well-delineated zones of myocardial fiber loss and infiltration by macrophages consistent with a myocardial infarct.
Diagnosis:
1. Systemic amyloidosis with renal glomerular, glossal mucosal, and cardiac vascular amyloid deposits
2. Thrombotic diathesis with multifocal splenic and hepatic infarcts probably secondary to #1
3. Myocardial infarction, secondary to #1 and #2
4. Pancreatitis, subacute, severe, with extensive peripancreatic fat necrosis
Comments: Immunohistochemistry will be done to establish the type of amyloid being deposited in the tissues of this dog. The most likely form is systemic AA amyloidosis which is usually secondary to chronicinflammatory processes; in this case long-standing autoimmune hemolytic anemia is the most likely cause. The renal amyloidosis was likely causing marked proteinuria which can result in a thrombotic diathesis due mainly to loss of antithrombin III in the urine. It appears likely, based upon the severity of the glomerular lesions, that this dog was also in chronic renal failure.
Timothy D. O'Brien, DVM, PhD, Diplomate, ACVP