Case summaryA 10-year-old, 5.1 kg (11.2 lb), male castrated cat was presented with signs of lethargy and decreased appetite at home after being previously healthy. Serum biochemical analysis identified normokalemia (5.1 mmol/l; reference interval [RI] 3.4–5.6 mmol/l) and severe hyponatremia (123 mmol/l; RI 145–158 mmol/l), with an Na/K ratio of 24 (RI 32–41). Baseline serum cortisol was low to normal, but serum aldosterone was markedly decreased with a pre-adrenocorticotropic hormone stimulation concentration of 13 pmol/l (RI 194–388 pmol/l) and post-adrenocorticotropic hormone stimulation concentration of 21 pmol/l (RI 277–721 pmol/l). Hematologic and biochemical analyses were otherwise unremarkable. Abdominal ultrasound revealed bilaterally enlarged adrenal glands with no other abnormalities noted; thoracic radiographs also did not identify any signs of metastasis. Fine-needle aspiration was strongly suggestive of lymphoma of the adrenal glands, and PCR for antigen receptor rearrangement was positive for B-cell clonal expansion; based on these findings, a diagnosis of primary adrenal B-cell lymphoma was made. Stable disease was achieved for a short period of time following vincristine, cyclophosphamide, prednisolone and fludrocortisone therapy, followed by progressive adrenal enlargement and electrolyte derangements that responded to neither doxorubicin nor adjustments in fludrocortisone dosage. Ultrasonographic metastasis was not identified at any time, and other organ derangements were not noted on hematologic or biochemical analyses. The cat was euthanized 55 days after initial presentation.Relevance and novel informationThis is the first report of primary adrenal lymphoma in a cat, with presenting signs compatible with hypoaldosteronism. Lymphoma should be a differential for cats presenting with adrenal enlargement or clinical signs and biochemical changes consistent with hypoaldosteronism or hypoadrenocorticism.

A 1.5-year-old, female, entire German shepherd dog was presented for evaluation of an abdominal mass. The dog had a 4-month history of polydipsia, polyuria, diarrhoea, and weight loss despite polyphagia. Abdominal ultrasound confirmed a large abdominal mass suspected to be uterine in origin. An exploratory celiotomy revealed a 4.3 kg, 26 × 17 × 17 cm multinodular mass entirely encompassing the uterus, left ovary and left kidney. A combined ovariohysterectomy and left nephrectomy were undertaken. Histopathology confirmed stage ΙΙ renal nephroblastoma with favourable histology. Chemotherapy was declined and 86 days following surgery, significant abdominal metastases were identified on a computed tomography scan. The patient was euthanased 113 days after surgery due to progressive disease. This is the first report to display the rapid presumed metastasis of a canine nephroblastoma, without gross metastasis at initial surgical resection, through advanced imaging. This is also the first reported case of polyphagia despite weight loss as a presenting clinical sign.

No abstract

Case summary A 5-year-old male neutered cat weighing 3.56 kg presented owing to the development of two masses over the dorsal cervical and cranial thoracic areas, as well as weight loss, inappetence and vomiting. Diagnostic tests revealed a grossly lipaemic sample with hypercholesterolaemia (440 mg/dl; reference interval [RI] 90.0–205.0), hypercalcaemia (>16.0 mg/dl [RI 8.0–11.8]) and urine specific gravity 1.022 (RI ⩾1.035). When re-presented 9 months later, fasted blood analyses revealed elevated ionised calcium (1.87 mmol/l [RI 1.11–1.38]), persistently elevated total calcium, normal phosphate and persistent minimally concentrated urine with calcium oxalate dihydrate crystals. Ultrasound-guided fine-needle aspiration of the masses produced blood-tinged purulent fluid with negative culture results. Excisional biopsies of both masses were undertaken, and histopathology was consistent with cutaneous xanthoma. No organisms were identified with special staining, and deep-tissue culture did not grow bacteria or fungi. Postoperatively, repeat fasted biochemical analysis revealed persistent hypercholesterolaemia with normal triglycerides, and normalisation of ionised and total calcium levels. Based on these findings, a diagnosis of cutaneous xanthoma causing hypercalcaemia due to primary dyslipidaemia was made. The cat was reported to be significantly improved in comfort and energy levels postoperatively and a transition to a fat-restricted diet was instituted. Eight months after xanthoma removal no recurrence was reported. Relevance and novel information To our knowledge, this is the first report of cutaneous xanthoma and associated granulomatous inflammation causing hypercalcaemia due to dyslipidaemia in a cat. Familial hypercholesterolaemia is an example of a primary condition that could cause dyslipidaemia in cats, and further studies are warranted to better describe the genetic characteristics. Xanthoma formation and the resultant granulomatous inflammation should be considered in cases of hypercalcaemia.

A nearly 2-year-old, male, neutered pug was referred for a 1-month duration of progressive gastrointestinal signs and lethargy, and possible seizure activity. Blood analyses before referral had shown marked increases in hepatocellular and hepatobiliary enzymes and increased pre-prandial and post-prandial bile acids, with normal bilirubin. Physical exam revealed a quiet mentation and blood analyses at the time of presentation found persistent increases in hepatic enzymes, and hypoalbuminaemia. Abdominal ultrasound identified intra-abdominal free fluid and ileocolic lymphadenopathy. Cytology of the abdominal effusion, liver and abdominal lymph nodes identified organisms of the Cryptococcus genus. The dog had a positive Cryptococcus antigen lateral flow assay titre of 1:>10,000, confirming cryptococcosis. The dog was euthanased following diagnosis. This is the first report describing a case of disseminated cryptococcosis causing liver dysfunction in a veterinary species. Cryptococcus infection should be considered in a young dog presenting with gastrointestinal signs and liver enzymopathy.