Baby's autopsy pictures


Abdomen full of fat.


Another picture to show how much fat was in the abdomen.





Baby's histopathology report:


Lethargy, inappetence, PD, abdominal distension, Splenomegaly not verified on post mortem.


Chronic Renal Failure


Prognosis Not Applicable

Histologic findings:

Kidney (slide 1, 2 sections): Several wdge-shaped areas in the renal cortex with a depressed capsular surface contain interstitial fibrosis, the tubules are either lost or distended and with attenuated epithelium, sometimes filled with hypereosinophilic material (protein casts). In one area, the tubular epithelium is completely lost and replaced by basophilic mineralized material. Glomeruli in these areas are absent or have a very thickened mesangium and shrunken tuft with variable degrees of fibrosis (glomerular sclerosis). Similar changes, i.e. thickened mesangium and some increase in cellularity are present in many other glomeruli across the sections examined. In some glomeruli, the epithelium of Bowmanís capsule is separated from the basement membrane by accumulation of palely eosinophilic amorphous material (Congo Red negative-not amyloid). The interstitium of the renal medulla has multifocal to coalescent fibroplasias (fibrosis) and compression or loss of collecting ducts.

Lymph node (slide 1, 1 section): There is a uniform population of medium size lymphocytes without clear germinal centers in the cortex and paracortex. The medullary sinuses are greatly distended by clear edema fluid. Several clusters of plasma cells are present in the septa. Within the sinuses, many macrophages are completely surrounded by erythrocytes that have attached to the outer surface of their cellular membrane.

Adrenal gland (slide 1, 1 section): A focal proliferation of cortical cells is present outside the adrenal capsule.

Liver (slide 2, 1 section): The surface contour is irregularly pitted. There are several clusters of oval cell proliferation with frequent differentiation towards small bile ducts present in the lobular parenchyma and, less often, in portal zones. Several small arterioles are also present within the lobular parenchyma (microvascular proliferation). Minimal areas of hepatocellular necrosis with some neutrophils are present.

No significant lesions are present in the pancreas.


The changes in the kidneys of this ferret are marked to severe and characteristic of chronic renal failure (CRF). CRF very possibly caused the clinical signs as glomerular injury is accompanied by protein loss and polyuria, which would have resulted in polydipsia. The cause of CRF is often difficult to pinpoint. Chronic inflammation with deposition of antigen-antibody complexes in the glomerular basement membranes is often associated with CRF development.
The liver had a mild bile duct hyperplasia and a multifocal microvascular proliferation. Microvascular proliferation in adult animals generally indicates some form of portal hypertension that stimulates the formation of alternative vessels to relief the pressure.
The appearance of the lymph node examined suggests an early stage of lymphosarcoma. There is cortical adrenal hyperplasia, not uncommon in ferrets.