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A 12-year-old, female spayed, Domestic Shorthair was referred for an abdominal ultrasound following a history of intermittent vomiting of two months duration, hind limb weakness, weight loss and progressive hyporexia.  The patient had a history of diabetes mellitus (in remission).

  • On presentation, she was quiet, alert and responsive with signs of compensatory shock. She was non-ambulatory paraparetic with poor/absent femoral pulses and absent proprioception in both pelvic limbs.
  • A complete cell count and biochemistry panel showed a severe azotemia (BUN >140, Creat 6.5), and elevated hematocrit (59.6%), consistent with hemoconcentration. A SNAP FeLV/FIV ELISA assay was negative.
  • Urinalysis revealed isosthenuria, mild hematuria and mild pyuria. A urine culture was negative. • An ACTH stimulation test showed a low-normal basal serum cortisol with a minimal response following ACTH administration (pre: 2.6 μg/kg; post: 2.8 μg/kg), consistent with adrenocortical insufficiency.
  • Three view thoracic radiographs were unremarkable.
  • Spinal radiographs were performed to assess for osseous abnormalities that could be contributing to her paraparesis, which were also unremarkable.

View the multiple still images in the above carousel and the video clip of the urinary bladder below. 



  • The adrenal glands are severely enlarged, hypoechoic, and mildly heterogeneous, both measuring 1.0 cm in thickness. The right adrenal gland has a somewhat lobular appearance. The surrounding fat is hyperechoic bilaterally. No evidence of vascular invasion is noted upon Doppler interrogation.
  • Corticomedullary distinction is mildly decreased bilaterally. A round, subtly hypoechoic nodule is noted within the cortex of the caudal pole of the left kidney, measuring 0.7 cm in diameter. Two, similar nodules are seen in the right kidney measuring up to 0.5 cm in diameter.
  • The urinary bladder wall is irregularly marginated and thickened. The largest region of rounded thickening is along the dorsal aspect of the apex, measuring 1.9 cm in length and 0.6 cm in thickness. A smaller, rounded region of thickening is noted along the ventral mid bladder wall (0.7 cm in length and 0.3 cm in thickness). These lesions do not appear to efface the wall layering of the urinary bladder.
  • The muscularis layer of the small intestines is moderately, diffusely thickened. The stomach, ileocolic junction, and colon are normal.
  • Scant peritoneal effusion is noted adjacent to a few small intestinal segments.

1. Severe bilateral adrenomegaly with surrounding steatitis.

2. Bilateral renal nodules.

3. Multifocal urinary bladder wall thickening/nodules.

4. Moderate diffuse enteropathy.

5. Scant peritoneal effusion.

Given the constellation of findings, round cell neoplasia (e.g. Lymphoma) is prioritized. The possibility of metastatic urothelial carcinoma or adrenal carcinoma was thought much less likely but not completely excluded. The intestinal changes could represent inflammatory bowel disease or small cell lymphoma, as a separate process.

Fine needle aspirates of the left kidney, left adrenal gland and urinary bladder were obtained. Cytology of the left kidney and left adrenal gland were consistent with a diagnosis of large cell lymphoma (granular phenotype (LGL)), while cytology of the urinary bladder was inconclusive.

Based on this, disseminated/metastatic lymphoma was presumed to also be present within the right kidney and right adrenal gland. The marked thickening of the urinary bladder was thought likely related, despite the lack of confirmation on cytology. The patient continued to decline over the course of hospitalization despite fluid resuscitation and treatment with pressors, antibiotics and steroids. Given her lack of improvement and grave long term prognosis, the clients elected to pursue humane euthanasia. The cause for the patient’s paraparesis remained unclear, but was speculated to be secondary to possible aortic thromboembolism from paraneoplastic hypercoagulability or further neoplastic dissemination into the nervous system. A necropsy was not pursued.


Lymphoma is a common hematopoietic neoplasm of the cat, accounting for approximately one third of all tumors in cats.1 In the current case report, the patient had confirmed large granular lymphosarcoma of the left adrenal gland, which was also suspected on the right given the similar appearance.

Clinicopathologic evidence of adrenocortical insufficiency was supportive of hypoadrenocorticism secondary to neoplastic infiltration.  In humans, metastatic tumors are the most common neoplastic lesions in the adrenal glands.2 The prevalence of metastasis to the adrenal glands is thought to be related to the rich blood supply of the adrenal sinusoids.2

In domestic animals, histological metastases to the adrenal glands, are similarly common, seen on postmortem examination in up to 27% of canine and 60% of feline adrenal neoplasms.1,3 Metastases are commonly bilateral, including 55.1% of canine and 50% of feline cases.3 Lymphoma and metastatic carcinoma have been most commonly reported in cases of feline adrenal metastasis.3 When tumors metastasized to the adrenal glands, an average of 4.5 other organ systems were involved, including the lungs, liver, abdominal and thoracic lymph nodes, kidneys, intestines and pancreas.3 In a study by Labelle and De Cock (2005), gross lesions were seen only in 8.3% of cats with confirmed histological metastasis to the adrenal glands postmortem, suggesting that cases may be overlooked if histopathological examination of the adrenal glands is not pursued.3

Adrenal function must be compromised by at least 90% in order to detect clinical changes, hence the development of hypoadrenocorticism is more common when both adrenal glands are affected (i.e. in cases of lymphoma).5,6 Although hypoadrenocorticism secondary to neoplastic invasion of the adrenal glands is well-described in humans, it has only been reported in two cats, both of which were diagnosed with multicentric lymphoma with bilateral adrenal gland involvement.2,4,5,8,9 One cat had histologic evidence of concurrent infiltration into the lungs, liver and mesenteric lymph nodes, while the other had concurrent infiltration into the mesenteric lymph nodes, spleen, pancreas, liver, kidney, peritoneum and bone marrow.5


  1. Jacobs, R. M., Messick, J. B. & Valli, V. E. Tumors in Domestic Animals. 119–198 (2002) doi:10.1002/9780470376928.ch3.
  2. Lam, K. Y. The pathology of adrenal tumors. Cancer Journal 7, 181–187 (1994).
  3. Labelle, P. & Cock, H. E. V. D. Metastatic Tumors to the Adrenal Glands in Domestic Animals. Vet Pathol 42, 52–58 (2005).
  4. Romine, J. F., Kozicki, A. R. & Elie, M. S. Primary adrenal lymphoma causing hypoaldosteronism in a cat. J Feline Medicine Surg Open Reports 2, 2055116916684409 (2016).
  5. Parnell, N. K., Powell, L. L., Hohenhaus, A. E., Patnaik, A. K. & Peterson, M. E. Hypoadrenocorticism as the primary manifestation of lymphoma in two cats. J Am Vet Med Assoc 214, 1208–11, 1200 (1999).
  6. Holm, J., Breum, L., Stenfeldt, K. & Hitz, M. F. Bilateral Primary Adrenal Lymphoma Presenting with Adrenal Insufficiency. CaseReports Endocrinol 2012, 638298 (2012).
  7. Daniel, G. et al. Clinical findings, diagnostics and outcome in 33 cats with adrenal neoplasia (2002–2013). J Feline Med Surg 18, 77–84 (2016).
  8. Serrano, S. et al. Addisonian crisis as the presenting feature of bilateral primary adrenal lymphoma. Cancer 71, 4030–4033 (1993).
  9. Peterson, M. E., Greco, D. S. & Orth, D. N. Primary Hypoadrenocorticism in Ten Cats. J Vet Intern Med 3, 55–58 (1989).