Renal carcinoma

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Physical appearance of a renal carcinoma in a dog[1]
Renal carcinoma showing high cell density with diffuse necrosis (asterisk) and hemorrhage[2]

Renal carcinoma are a relatively uncommon metastatic neoplasia of the kidney in older dogs (> 8 years) and the most common form of renal neoplasia.

Renal adenocarcinoma are a less common variant involving glandular epithelial neoplastic cells.

Male dogs appear more predisposed to renal carcinoma than females (2:1) but no breed predilection has been noted. Middle-aged and older dogs are more likely to be affected, but renal carcinoma has been reported in dogs as young as 1 year of age[3].

The prevalence of primary renal neoplasia in dogs is estimated to be 0.3 – 1.5 % of all the canine neoplasms[4].

Although the specific cause of these tumors is unknown, the pathogenesis appears to involve mitogenic gene mutations that leads to protein kinase and matrix metalloproteinase activation[5]. This results in propagation of neoplastic cells throughout the renal parenchyma via release of macrophage-expressed COX-2[6], TNF-α and hypoxia inducible factor 1α[7]. Local invasion and distal metastasis of canine renal carcinoma are important predictors of clinical outcomes and increased expression of several matrix metalloproteinases are associated with a poor prognosis[8].

Renal carcinoma are usually classified by pathologists based on their histological (papillary, tubular, and solid type) and cytological (chromophobic, eosinophilic, and clear cell type) appearances, but the relevance of this clinically is open to debate[9].

These tumors are believed to originate from the epithelium of proximal convoluted tubules[10].

Affected dogs frequently present with a vague history of hematuria, anorexia and weight loss over a 1 - 3 month period. A palpable abdominal mass may sometimes be evident[11] and secondary hypertrophic osteoarthropathy, dermatofibrosis[12] and skin tumors have been reported.

Blood tests may reveal paraneoplastic increases in ALT, ALP[13], as well as leukocytosis, neutrophilia, eosinophilia, erythrocytosis, thrombocytopenia[14], hypercalcemia[15] and non-regenerative anemia but these signs are not always concurrent with clinical symptoms[16].

Even in bilateral cases, signs of renal failure may not be present, as adequate kidney function requires only 25% of the parenchyma to be normal[17].

Diagnosis is usually presumptive based on radiographic, CT and ultrasonographic imaging[18] and intravenous urography[19].

Since metastases to the caudal vena cava, lung, thoracic vertebrae[20], ribs and adrenal gland are common[21], abdominal radiographs aid in identifying the organ(s) primarily involved, the size and location of the neoplasm, and metastatic foci, which will influence treatment protocols. Generalized lymphedema and purpura have been reported in dogs where renal carcinoma have metastasied into the vena cava and caused secondary thromboembolism[22].

A definitive diagnosis requires post-operative histological examination of sample tissues[23]. Classification is based on cytological appearance and immunohistochemical staining with vimentin[24]cytokeratin and c-KIT[25].

In most cases, percutaneous biopsy of the mass is not recommended, due to the potential for iatrogenic metastasis along the needle tract[26]. Percutaneous biopsy is indicated, however, when bilateral involvement is detected.

A differential diagnosis would include renal lymphoma, nephroblastoma, renal pelvic squamous cell carcinoma[27], histiocytic sarcoma, oncocytoma, myxoma, adenocarcinoma, cysts and renal transitional cell carcinoma[28].

Treatment requires nephroureterectomy with removal of regional lymph nodes, affording a reasonable prognosis. Some studies report survival times up to 4 years after surgical excision of a unilateral malignant renal neoplasm[29].

In cases of highly aggressive or invasive bilateral renal carcinoma, cytotoxic chemotherapy should be considered as adjunctive therapy to surgery, but the prognosis is considered poor.

Renal carcinoma are generally considered resistant to multidrug chemotherapy, hormonal therapy and radiation therapy and response rates to chemotherapy are < 10% due to chemoresistance


  1. Vet surgery central
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  29. Peeters D et al (2001) Resolution of paraneoplastic leukocytosis and hypertrophic osteopathy after resection of a renal transitional cell carcinoma producing granulocyte-macrophage colony-stimulating factor in a young Bull Terrier. J Vet Intern Med 15:407–411