Kidney sparing during surgical treatment of an adrenocortical carcinoma with renal vein invasion in a cat

Abstract

A 15-year-old domestic shorthair cat was presented with gastrointestinal signs, polyuria, polydipsia, and weakness. Abdominal bruit (“whooshing” sound from turbulent blood flow) and hypertension (systolic blood pressure: 200 mmHg) were present. A left adrenal gland mass was detected with abdominal ultrasonography; a subsequent CT examination identified a mass and a thrombus in the ipsilateral renal vein. Adrenalectomy and venotomy were completed but nephrectomy was not necessary. Histological diagnosis was an adrenocortical carcinoma. There were no clinical signs at a follow-up examination 30 mo after surgery.

Key clinical message:

This report describes successful surgical management of feline adrenocortical carcinoma with renal vein invasion without kidney damage. This case suggests that, after correct diagnosis and in well-selected cases, surgery to remove adrenal tumors and thrombi in cats, despite renal vein invasion, can be done with excellent short- and long-term outcomes.

Adrenal tumors are infrequent findings in cats, representing about 0.2% of all feline neoplasms, compared to 1 to 2% of all spontaneous canine neoplasms (1–4). Adrenal tumors are classified as either cortical tumors (adenoma or adenocarcinoma) or medullary tumors (pheochromocytoma). Cortical tumors can be functional, producing excessive adrenocortical hormones (cortisol, aldosterone, or sex hormones, alone or in combination) and resulting in a clinical syndrome, or they may be nonfunctional.

Primary hyperaldosteronism is a rare condition in cats. Hypersecretion of mineralocorticoids can be caused by bilateral hyperplasia of the zona glomerulosa of the adrenal cortex or, in rare cases, by an aldosterone-secreting tumor, defined as an aldosteronoma (5–7). This neoplasia is often associated with an expansive lesion, which may be accompanied by invasion of a neoplastic thrombus in the caudal vena cava, phrenicoabdominal vein, or, rarely, renal vein (4,8). Cats and dogs with adrenal gland neoplasia can undergo medical treatment to reduce clinical signs, but surgical treatment is preferred for this lesion and for any associated tumor thrombi. However, there are conflicting data regarding whether vascular invasion worsens short-term prognosis (2,8–12).

When small thrombi invade the phrenicoabdominal vein, they can be managed and removed concurrently with the vessel and tumor, though removal of more extended thrombi that enter the caudal vena cava usually require a caval venotomy (1,11,13). In rare cases with direct invasion of the renal vein from tumor thrombi, nephrectomy has been performed. In some studies, concurrent nephrectomy and adrenalectomy had a poor prognosis, with increased risk of renal failure and shorter survival (1,11,13). In a recent, noteworthy study of 5 dogs that had adrenal tumors with tumor thrombi present in the renal vein, nephrectomy was avoided by renal venotomy. These surgical treatments enabled kidney sparing and may have reduced morbidity associated with the procedure (14).

To our knowledge, this is the first report of adrenocortical carcinoma with invasion of the renal vein in a cat, with a syndrome of hyperaldosteronism treated with renal vein venotomy and thrombectomy without kidney damage.

CASE DESCRIPTION

A 15-year-old castrated male domestic shorthair cat weighing 5 kg was presented to the Clinica Veterinaria Camagna (Reggio Calabria, Italy) with a history of intermittent diarrhea, weakness, polyuria, and polydipsia.

Physical examination revealed abdominal bruit (“whooshing” sound from turbulent blood flow) and hypertension (systolic blood pressure: 200 mmHg). The remaining findings of the clinical evaluation were unremarkable. Further investigation was completed under sedation and included hematology, biochemistry, urinalysis, echocardiography, and abdominal ultrasound.

Hematology results were normal. For biochemistry and urinalysis, abnormal findings included hypokalemia [3.3 mmol/L; reference interval (RI): 3.5 to 5.8 mmol/L], hypernatremia (163 mmol/L; RI: 144 to 160 mmol/L), and urine specific gravity (USG) of 1.020.

Echocardiography findings were normal. Abdominal ultrasound revealed the presence of a structure of at least 1.5 cm in diameter on the left adrenal gland that was subjected to fine-needle aspiration. Cytological examination revealed a cell population compatible with adrenal neoplasia of cortical origin. All other structures, including the right adrenal gland, were normal.

The cat was returned 2 d later. An endocrinology panel detected an increased aldosterone concentration (930.5 ng/mL; RI: 11.3 to 294.3 ng/mL), though baseline cortisol concentration and concentrations after ACTH stimulation were normal. Contrast computed tomography (CT) identified a circular structure at least 1.3 cm in diameter on the left adrenal caudal pole; the ipsilateral renal vein was dilated and invaded by a thrombus (Figure 1). However, all other abdominal organs appeared normal and there was no evidence of pulmonary metastasis.

FIGURE 1.

Computed tomographic examination of the abdomen of a cat, showing the left adrenal mass. A — Axial plane, B — Sagittal plane, and C — Coronal plane.

Adrenalectomy was considered the treatment of choice. The owner was advised about surgical risks, particularly regarding renal vein invasion. After discussion with the owner and in accordance with their wishes, the surgical plan was to perform left adrenalectomy and try to spare the left kidney by attempting to remove the thrombus via venotomy.

Based on the anesthesiology examination, the cat was classified in the 4th class as defined by the American Society of Anesthesiologists. The cat was sedated (tiletaminezolazepam, 0.1 mg/kg, IV), induced with propofol (1 mL/kg, IV), intubated, and maintained under anesthesia with sevoflurane, with continuous monitoring during surgery.

The hair was clipped in the abdominal area, the cat was placed in dorsal recumbency, a routine presurgical scrub was done, and a cranial midline celiotomy was made. The left adrenal gland was identified, and the tumor was isolated from blood vessels and from numerous adhesions with cotton swabs and HarmonicWave (Ultracision; Johnson & Johnson, New Brunswick, New Jersey, USA), with care to avoid damage to the cranial mesenteric artery and caudal vena cava. A Satinsky vascular clamp was placed on the renal vein (Figure 2 A) to reduce the renal vein inflow and isolate the thrombus. A longitudinal venotomy (~5 mm) was made, and the thrombus was grasped with a DeBakey clamp and carefully removed by constant traction. The venotomy was then closed with a simple continuous suture of Prolene 7-0 (Ethicon) (Figure 2 B) and the vascular clamp removed. The venotomy was checked for residual hemorrhage. After lavage of the peritoneal cavity with sterile warm saline, the celiotomy was closed routinely. Recovery from anesthesia was uneventful, and the cat was discharged after 2 d of hospitalization. During hospitalization, the cat was given fluid therapy (NaCl, 10 mL/h, IV) and meloxicam (0.05 mg/kg, PO, q24h).

FIGURE 2.

A — Isolation of a thrombus in a cat with the use of a Satinsky vascular clamp on the renal vein. B — Renal vein suture.

At follow-up examinations (at 24 h and at 7, 10, and 30 d after surgery), the cat was doing clinically well and renal functions were within normal ranges (Table 1). Histological analysis confirmed the diagnosis of adrenocortical carcinoma. There was a multinodular, infiltrating structure composed of nests and trabeculae of polygonal cells, separated by a delicate fibrovascular stroma. Anisocytosis and anisokaryosis were moderate, and mitotic figures were occasional.

TABLE 1.

Progression of renal function values during the first 30 d of postsurgical follow-up in a cat with adrenocortical carcinoma with renal vein invasion.

	Preoperative	24 h postoperative	7 d postoperative	10 d postoperative	30 d postoperative
Creatine, mg/dL (RI: 0.6 to 1.6 mg/dL)	1.7	1.5	1.2	1.2	1.3
Blood urea nitrogen, mg/dL (RI: 27 to 75 mg/dL)	30	35	50	55	35
Sodium, mmol/L (RI: 144 to 160 mmol/L)	163	132	133	132.5	130
Chloride, mmol/L (RI: 110 to 125 mmol/L)	95.4	95.4	95.4	93	97
Potassium, mmol/L (RI: 3.5 to 5.5 mmol/L)	2.5	4.07	4.08	4.06	4
Glucose, mg/dL (RI: 80 to 120 mg/dL)	90	89	100	120	100

RI — Reference interval.

At a 20-month follow-up, physical examination and hematology, biochemistry, urinalysis, and ultrasound examinations were all normal. At a 30-month follow-up, physical examination and hematology were normal. There was a moderate increase in serum creatinine (2.7 mg/dL; RI: 0.8 to 2.4 mg/dL). Urinary specific gravity remained within normal limits (USG: 1.028). Ultrasonographically, both kidneys appeared normal, with no signs suggestive of left renal vein thrombosis.

DISCUSSION

We describe here preservation of the kidney during successful surgical management of feline adrenocortical carcinoma with invasion of the renal vein, with excellent short- and long-term outcomes.

Although adrenal neoplasia is infrequent in cats, there are some reports (3–5). However, to the best of our knowledge, this is the first report of an adrenal tumor with renal vein invasion in a cat surgically treated without nephrectomy.

Diagnostic imaging, particularly ultrasonography, was the first step to visualize the lesion. Adrenal size and asymmetry may help in confirming suspicion of endocrine diseases in cats, though ultrasonographic appearance of adrenal glands cannot be used to differentiate benign versus malignant lesions (15).

The CT examination identified a circular structure at least 1.3 cm in diameter on the left adrenal caudal pole, with the ipsilateral renal vein dilated and invaded by a thrombus. In patients with adrenal disease, the use of CT is important in determining adrenal gland size; identifying the relationship of the tumor with surrounding tissues, vessels, and organs; detecting the presence and size of a thrombus; issuing an oncologic grading; optimizing planning of the surgical approach and technique; and issuing a prognosis.

Hyperaldosteronism was marked in this cat. Cases of primary hyperaldosteronism are not rare in the literature and must be considered as a differential diagnosis in middle-aged and older cats with hypokalemic polymyopathy and/or systemic hypertension (8). Primary hyperaldosteronism was diagnosed in a 13-year-old cat with an adrenal cortical carcinoma. Adrenalectomy resolved the hypokalemia, hypertension, and other electrolyte abnormalities. Surgical excision of a tumor thrombus from the caudal vena cava was accomplished without pathological narrowing of the vena cava (9).

In the current case, surgery was our preferred approach. Surgical treatment for feline adrenal tumors (regardless of tumor type) is associated with good long-term survival, with preoperative adrenal generally recommended (4). Acute adrenal hemorrhage can occur as a consequence of tumor necrosis and rupture and can cause severe hypovolemia and anemia in cats with primary hyperaldosteronism (8,16,17). Caval thrombi associated with adrenal gland tumors are amenable to adrenalectomy and thrombectomy without significantly increased perioperative morbidity and mortality rates, assuming the surgeon is experienced in appropriate techniques (11).

Tumor thrombectomy is traditionally done in dogs with invasive adrenal tumors. This treatment is achieved through caudal vena cava or phrenicoabdominal venotomy; however, when the thrombi involve the renal vein, or if there is neoplastic infiltration of the renal parenchyma, ipsilateral nephrectomy may be done concurrently with adrenalectomy. Nephrectomy was done in 17 to 26% of cases in dogs with invasive adrenal tumors (1,10,12). Whereas these neoplasms are rare in humans, renal vein thrombosis was described in 9 to 19% of patients (18).

It is well-established that nephrectomy is associated with worse short- and long-term prognoses in dogs undergoing this surgical treatment (10). In a recent study (14), Chiti et al carried out adrenalectomy and renal vein thrombectomy on 5 dogs with invasive adrenal tumors. This enabled preservation of the kidney, obviated the requirement for nephrectomy, and potentially reduced surgical morbidity. Furthermore, this technique was associated with good short- and long-term outcomes.

The surgical technique described in this case report allowed us to successfully remove the adrenal tumor and renal vein thrombus through venotomy without nephrectomy. Renal venotomy in cats is technically demanding due to the small diameter of the renal vein compared to the vena cava and the delicate nature of the vessel. Potential complications can be caused by vessel wall damage and occlusion of renal vein inflow. Vascular and adrenal surgical experience is considered important for achieving good results.

In cases with an adrenocortical tumor, clinicians should investigate whether the tumor produces excessive blood concentrations of glucocorticoids, mineralocorticoids, sex steroids, or combinations of these hormones. Hypersecretion of > 1 adrenal hormone may occur in a cat with an adrenocortical tumor (5,19).

In conclusion, this clinical case confirmed in a cat what has been reported in the dog. Although the renal vein is narrower in the cat, it is possible to perform adrenalectomy with removal of a thrombus in the renal vein, thereby preserving kidney function and avoiding poorer outcomes associated with the nephroureterectomy procedure concurrent with adrenalectomy.